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eLife Assessment

This study presents valuable evidence of sex differences in oxycodone relapse-related behavior alongside novel characterization of synaptic adaptations in the paraventricular thalamus - nucleus accumbens shell circuit. The authors show that females exhibit heightened cue-induced seeking after 14 days, but not 1 day, of abstinence, while both sexes display similar time-dependent strengthening of paraventricular thalamus - nucleus accumbens shell glutamatergic transmission. The revised manuscript strengthens the work through improved statistical analyses, clearer interpretation, and expanded integration with prior literature. The strength of evidence is solid. However, association among experiments is incomplete, as the sex-specific behavioral effect is not reflected in circuit-level plasticity, and no causal manipulations test pathway involvement in relapse. Future work could link these circuit adaptations to sex-specific relapse vulnerability.

Reviewer #1 (Public review):

Summary:

This manuscript by Alonso-Caraballo et al, is a novel piece of work that examines the impact of oxycodone self-administration on neural plasticity within paraventricular thalamic (PVT) to nucleus accumbens shell (Shell) pathway - two regions shown to play a key role in cue-induced drug seeking on their own, and whether this plasticity varies based on abstinence period and biological sex.

Strengths:

The authors show using a clinically relevant long-access model of opioid self-administration promotes dependence and acute withdrawal in both male and female rats. During subsequent cue-induced relapse tests at 1 or 14-days following the conclusion of self-administration, data show that while both male and females demonstrate drug-seeking behavior at both time points, females show a further elevation in responding on day 14 versus day 1 that is not observed in the males. When accounting for past work showing elevations in drug seeking in males after 30 days, these data indicate that craving-induced relapse for opioids may develop faster and may be more pronounced in females compared to males.

These behavioral findings were paralleled by use of ex vivo acute slice electrophysiology and circuit-specific ex vivo optogenetics to examine the impact of oxycodone self-administration on synaptic strength within the paraventricular thalamus (PVT) to nucleus accumbens shell (NAcSh) pathway(s). Data support a time-dependent but sex independent strengthening of glutamatergic signaling at PVT-to-NAcSh medium spiny neurons (MSNs) that is only present following a relapse test at 14 days post abstinence in males versus females, providing the first evidence that opioid self-administration and/or cue-induced drug-seeking augments this pathway. Using an extensive set of physiological measures, the authors show that this increased synaptic strength reflects a upregulation of presynaptic release probability. Further, this upregulation of excitatory signaling aligned temporally with an increase in MSN excitability, as assessed by increases in action potential firing frequency. Finally, the authors provide the first evidence that similar to other inputs to the NAcSh, PVT projections innervate both MSN as well as local interneurons, promoting a GABA-A specific feedforward inhibitory circuit. Interestingly, unlike direct excitatory inputs to MSNs, no changes were observed ostensibly within this feedforward circuit, highlighting a selective enhancement of excitatory drive and output of MSNs with protracted abstinence.

Overall, these data highlight a potential role for heightened synaptic strength within the PVT-NAcSh pathway in cue-induced relapse behavior during protracted abstinence and identify a potential therapeutic target during abstinence to reduce relapse risk in abstaining individuals.

Weaknesses:

Overall, the experimental approach and data provided appear rigorous and support their overall conclusions and achieve their goal of understanding how opioid self-administration impacts synaptic strength within the PVT-NAcSh pathway. Although not undermining these data, there are a few potential weaknesses that reduce the impact of the work. For example, the inability to directly assess whether cue-induced drug-seeking is in fact augmented compared to daily intake during self-administration in the maintenance face only permits the authors to denote that reexposure to cues and the context is sufficient to promote active lever pressing without demonstrating whether seeking behavior is in fact elevated further during a cue test. This is notably understandable as drug available sessions were 6-hours versus a 1hour relapse test. Importantly, it is clearly demonstrated that drug seeking is higher on average in female mice after 14 days versus 1 day.

With regard to interpretation of electrophysiology findings, the lack of inclusion of an abstinence only group does not permit interpretations to parse out whether observed increases in synaptic strength (or the lack of) reflect abstinence or an interaction between abstinence period and re-exposure to the operant chamber, as slices were taken 30-45 min post relapse test. While much literature has shown that drug induced adaptations in the NAc requires a post drug period for plasticity to measurably emerge, studies have also shown that re-exposure to heroin-associated cues following abstinence seemingly "reverses" increases in cell excitability in prelimbic-NAc pyramidal neurons (Kokane et al., 2023) and that depotentiation of morphine-induced increases in synaptic strength in the NAc shell can be depotentiated by drug re-exopsure -- an effect also observed with cocaine re-exposure (Madayag et al., 2019). Notably, the lack of effect at 14 but not 1 day supports the likelihood that the relapse test does not in fact influence the plasticity within the PVT-NAcSh circuit.

While the lack of effect on AMPAR:NMDAR ratio and rectification indices do support the notion that enhanced EPSC amplitudes in input-output curves do not reflect a change in AMPAR subunit expression (i.e., increased GluA2-lacking receptors that exhibit inward rectification at depolarized potential) nor a change in postsynaptic sensitivity to glutamate, without direct assessment of AMPAR-specific and NMDAR-specific input-output curves, it doesn't definitively exclude the possibility that both AMPA and NMDA receptor currents are being upregulated, thus negating an observable change in postsynaptic strength.

Overall, these findings provide novel insight into how the PVT-NAcSh pathway is altered by opioid self-administration and whether this is unique based on abstinence period and sex. Importantly, these were the primary objectives stated by the author. Data highlight a potential role for the observed adaptations in relapse behavior and identify a potential therapeutic target during abstinence to reduce relapse risk in abstaining individuals. However, it should be noted that no causal link is demonstrated without experiments to reduce/prevent relapse.

Comments on revisions:

The authors addressed previous concerns brought up, specifically by clarifying data interpretation as well as text modifications related to potential caveats of these interpretations. However, I recommend that the title be changed to not focus on sex differences to avoid misunderstanding. The authors should also address the lack of difference physiologically compared to the behavior as a caveat more clearly in the discussion (i.e. likely suggests this isn't the pathway driving the difference).

Reviewer #2 (Public review):

Summary:

This is an interesting paper from Alonso-Caraballo and colleagues that examines the influence of opioid use, acute and prolonged abstinence, and sex on cue-induced relapse and paraventricular thalamus (PVT) to nucleus accumbens shell (NAcSh) medium spiny neurons circuit physiology. The study presents a valuable finding that following prolonged, but not acute abstinence from oxycodone self-administration, female rodents exhibit higher relapse rates to drug paired cues. Additionally, the study presents the useful finding that prolonged abstinence increased PVT-NAcSh MSN synaptic strength in both sexes, an effect that is likely due to presynaptic adaptations. While the evidence to support these two findings is solid, further experiments are required to determine the functional role of the PVT-NAcSh MSN circuit in relapse following prolonged oxycodone abstinence, and the mechanism underlying the heightened relapse vulnerability in females in this model of opioid use disorder.

Strengths:

The paper is interesting, well written and presented, and the experiments are well designed and conducted. The revised analysis of spike count data that models the hierarchical structure of the data is appropriate to overcome low animal numbers and the potential for oversampling. The authors are transparent in reporting the results related to this analysis in figure 5 and acknowledge the study is underpowered to confirm the trend of increased intrinsic excitability in male MSNs following prolonged oxycodone analysis.

Weaknesses:

A major weakness of this study is the disconnect between the behavioral and neurophysiological data reported. While a striking sex difference in relapse-like behavior is observed, there are no statistically significant sex differences in any of the neurophysiological data reported. Moreover, without an experiment to functionally test the role of the PVT-NAc projection in relapse-like behavior following prolonged oxycodone these two arms of the study seem divorced.

While the authors don't directly conclude that the PVT-NAc MSN circuit is required for relapse following prolonged oxycodone abstinences, in the introduction the authors state they aim to test the hypothesis that increased synaptic strength in PVT-NAcSh projections are necessary for drug-seeking. This study does not include the required experiments to test this hypothesis.

Impact:

The topic is of interest to the field of substance use disorders and gives solid evidence for the need to consider targeted therapeutics aimed at relapse prevention in opioid use disorder.

Reviewer #3 (Public review):

Summary:

Alonso-Caraballo et al. use behavioral testing and ex vivo patch-clamp electrophysiology combined with circuit-specific optogenetic stimulation of PVT terminals to examine how oxycodone self-administration and abstinence duration shape cue-induced relapse and PVT-NAcSh synaptic transmission in male and female rats. In the revision, the authors reanalyzed intrinsic excitability using nested hierarchical GLMMs, acknowledged the low power in the male prolonged-abstinence group, and expanded the discussion of relevant PVT-NAc literature. These changes improve the manuscript. That said, most of the revisions are textual and the main experimental gap remains. Both sexes show increased oxycodone seeking compared to saline at 14 days, but only females show a time-dependent incubation from 1 to 14 days, and the PVT-NAcSh synaptic strengthening is the same in both sexes. Nothing in the revision brings those two observations closer together. The excitability data also come from NAcSh MSNs with no confirmation of PVT connectivity, which limits what circuit-specific conclusions can be drawn. The study is a solid characterization of abstinence-related synaptic changes in this pathway, but some of the conclusions still go further than the data allow.

Strengths:

The behavioral characterization is thorough and well-executed, covering self-administration, somatic withdrawal, and cue-induced relapse across two abstinence durations in both sexes. The sex-specific escalation in oxycodone seeking from 1 to 14 days in females but not males is a clear and compelling finding. The use of circuit-specific ex vivo optogenetics to isolate PVT terminal inputs onto NAcSh neurons is a genuine methodological strength, and the demonstration of feedforward inhibitory recruitment through local GABAergic interneurons adds meaningful novelty to the circuit characterization. The reanalysis of intrinsic excitability using nested hierarchical GLMMs appropriately accounts for the non-independence of cells recorded within the same animal and is a real improvement over the original approach. The expanded discussion of prior PVT-NAc work, particularly the more accurate treatment of Keyes et al. (2020) and Paniccia et al. (2024), better situates the findings within the existing literature.

Weaknesses:

The core limitation of the study remains unchanged after revision. The PVT-NAcSh synaptic strengthening after prolonged abstinence is statistically indistinguishable between sexes, while females but not males show a time-dependent escalation in oxycodone seeking from 1 to 14 days of abstinence. The Discussion proposes hormonal modulation or differences in upstream inputs as possible explanations, but none of these are tested and the gap is left unresolved. The intrinsic excitability recordings come from NAcSh MSNs with no confirmation that those neurons receive direct PVT input, which was raised in the original review, acknowledged in the revision, and not experimentally addressed. The male prolonged-abstinence excitability trend has approximately 20% statistical power and is non-significant, yet the Discussion interprets it as a potential neuroadaptation that could facilitate signal flow through the PVT-NAcSh circuit and contribute to relapse, which goes well beyond what the data support. The failure to distinguish between D1 and D2 MSNs remains a significant limitation given that cell-type-specific plasticity at PVT-NAc synapses has been shown to be directly relevant to opioid seeking in prior work. Finally, the Conclusion builds a mechanistic framework around D2 MSNs, PV interneurons, and D1 MSNs that is drawn from studies using different drugs or experimental designs, and none of these cell-type-specific mechanisms are tested in the present experiments.

Author response:

The following is the authors’ response to the original reviews.

Public Reviews:

Reviewer #1 (Public review):

(1) Although not undermining these data, there are a few potential weaknesses that reduce the impact of the work. For example, the inability to directly assess whether cue-induced drug-seeking is in fact augmented compared to daily intake during self-administration in the maintenance face only permits the authors to denote that re-exposure to cues and the context is sufficient to promote active lever pressing without demonstrating whether seeking behavior is in fact elevated further during a cue test. This is notably understandable as drug available sessions were 6-hours versus a 1-hour relapse test. Importantly, it is clearly demonstrated that drug seeking is higher on average in female mice after 14 days versus 1 day.

We agree that the current design does not allow us to directly assess whether cue induced drug-seeking is augmented relative to the average self-administration intake. However, this comparison was not a question examined in the manuscript and was not an intended interpretation of the data. Our analyses and interpretations focused on comparisons between saline and oxycodone groups tested under identical cue-induced relapse conditions. While it does not change or contradict the reviewer’s point, we would also like to clarify that the relapse test was 2 hours long.

(2) With regard to the interpretation of electrophysiology findings, the lack of inclusion of an abstinence-only group does not permit interpretations to parse out whether observed increases in synaptic strength (or the lack of) reflect abstinence or an interaction between abstinence period and re-exposure to the operant chamber, as slices were taken 30-45 min post relapse test.

The inclusion of an abstinence-only control group would have been required to definitively dissociate synaptic changes driven by abstinence alone from those arising from an interaction between abstinence and re-exposure to the operant context during the relapse test. In the present study, electrophysiological recordings were intentionally performed 30 to 45 minutes following the relapse test to capture synaptic modifications associated with cue-induced drug-seeking after abstinence. Accordingly, we interpret these findings as reflecting the neural state following relapse rather than abstinence alone, and we have revised the text accordingly to clarify this point.

(3) With regard to the interpretation of electrophysiology findings, the lack of inclusion of an abstinence-only group does not permit interpretations to parse out whether observed increases in synaptic strength (or the lack of) reflect abstinence or an interaction between abstinence period and re-exposure to the operant chamber, as slices were taken 30-45 min post relapse test. While much literature has shown that drug-induced adaptations in the NAc require a post-drug period for plasticity to measurably emerge, studies have also shown that re-exposure to heroin-associated cues following abstinence seemingly "reverses" increases in cell excitability in prelimbic-NAc pyramidal neurons (Kokane et al., 2023) and that depotentiation of morphine-induced increases in synaptic strength in the NAc shell can be depotentiated by drug re-exposure - an effect also observed with cocaine re-exposure (Madayag et al., 2019). Notably, the lack of effect at 14 but not 1 day supports the likelihood that the relapse test does not in fact influence the plasticity within the PVT-NAcSh circuit.

We thank the reviewer for highlighting relevant literature showing that drug or cue re exposure can modify or reverse drug-induced plasticity in NAc-related circuits. We want to clarify that, in our dataset, synaptic changes in the PVT-NAcSh pathway are seen after 14 days of abstinence, but not after 1 day. Therefore, the lack of effect at the earlier time point and its appearance after extended abstinence support the idea of time-dependent plasticity. Although electrophysiological recordings were taken soon after the relapse test, this temporal pattern argues against relapse testing alone as the primary driver of the observed synaptic changes. We have updated the text to clarify this point.

(4) While the lack of effect on AMPAR:NMDAR ratio and rectification indices do support the notion that enhanced EPSC amplitudes in input-output curves do not reflect a change in AMPAR subunit expression (i.e., increased GluA2-lacking receptors that exhibit inward rectification at depolarized potential) nor a change in postsynaptic sensitivity to glutamate, without direct assessment of AMPAR-specific and NMDAR-specific input output curves, it doesn't definitively exclude the possibility that both AMPA and NMDA receptor currents are being upregulated, thus negating an observable change in postsynaptic strength.

We agree that unchanged AMPAR/NMDAR ratios and rectification index suggest against altered AMPAR subunit composition or simple postsynaptic sensitivity changes. Although receptor-specific input-output analyses would be necessary to definitively rule out proportional increases in both AMPA and NMDA receptor currents, we have updated the manuscript to clarify that our conclusions are limited to the synaptic measures we obtained. The revised text now states that acute or prolonged abstinence “might have no detectable postsynaptic effects as assessed by these synaptic measures” at PVT-NAcSh synapses.

Reviewer #2 (Public review):

(5) While this paper is certainly interesting, and well-written, and the experiments seem to be well performed, the behavioral and physiological effects observed are somewhat divorced. Specifically, what accounts for the heightened relapse in females? Since no opioid-related sex differences were observed in PVT-NAcSh neurophysiology, it is unclear how the behavioral and neurophysiological data fit together. Furthermore, the lack of functional manipulation of PVT-NAcSh circuitry leaves one to wonder if this circuit is even important for the behavior that the authors are measuring. I would be more positive about this study if the authors were able to resolve either of the two issues noted above.

A key challenge in circuit-based studies of motivated behavior is connecting circuit-level plasticity to complex, sex-dependent behavioral phenotypes. In this study, we do not mean to imply that synaptic plasticity within the PVT-NAcSh projection alone explains the increased relapse seen in females. Instead, our electrophysiological data indicate that this projection experiences time-dependent, abstinence-dependent changes in synaptic strength, offering important insights into when and where circuit-level adaptations may occur. We also believe that the lack of obvious sex differences in PVT-NAcSh synaptic strength does not rule out this circuit's role in sex-specific behavior. Growing evidence suggests that sex differences in relapse and motivated behaviors may stem from different modulation of shared circuits (for example, via ovarian hormones, neuromodulatory tone, or upstream inputs), rather than from significant differences in baseline synaptic properties within a given projection. Regarding circuit relevance, extensive previous research has identified the PVTNAcSh pathway as a critical regulator of cue-induced reward seeking and relapse. Our findings expand on this by showing that this projection displays abstinence-dependent synaptic strengthening after oxycodone self-administration. Although functional manipulation of this circuit is needed to confirm its causal role, such experiments were beyond the scope of this study.

(6) There are insufficient animals in some cases. For example, in Figure 4, the Male Saline 14-day abstinence group (n = 3 rats) has less than half of the excitability as compared to the Male Saline 1-day abstinence group (n = 7 rats). This is likely due to variance between animals and, possibly, oversampling. Thus, more rats need to be added to the 14-day abstinence group. Additionally, the range of n neurons/rat should be reported for each experiment to ensure readers that oversampling from single animals is not occurring.

We appreciate the reviewer's concern regarding the number of animals and the potential for oversampling. We take this concern seriously and have substantially revised our statistical approach in response.

All spike count data were reanalyzed using nested hierarchical Poisson generalized linear mixed-effects models (GLMMs), fitted separately for each sex and abstinence duration. Each model included injected current (mean-centered), drug condition, and their interaction as fixed effects, with random intercepts and slopes for injected current at the animal level, and random intercepts for cells nested within animals. Importantly, this reanalysis changed several of our original conclusions. Effects that appeared significant under the conventional cell-level analysis were no longer statistically significant once the hierarchical structure of the data was properly modeled. We report these corrected results transparently throughout the revised manuscript.

However, in males after prolonged abstinence, oxycodone-treated animals showed a higher spike output than controls, with a large effect size. Post-hoc analysis showed only 20% power with current sample (3 saline, 4 oxycodone rats). To reach 80% power, 13 rats per group are needed. We report this as a trend that warrants further study and have revised related sections to reflect this. The data suggest a possible neuroadaptation in males that the study is underpowered to confirm, not a null effect.

In response to this comment, we have updated Figure 5, the Results and Discussion sections, and the Statistics/Methods section to clearly describe the nested hierarchical modeling approach, report corrected statistical values, and acknowledge the power limitation for the male prolonged abstinence group. The figure legend now reports the number of neurons recorded per rat, showing the distribution across animals rather than individual subjects.

(7) The IPSC data, for example in Figure 4, is one of the more novel experiments in the manuscript. However, it is quite challenging to see the difference between males and females, saline and oxycodone, at low stimulation intensities within the graph. Authors should expand this so that reviewers/readers can see those data, especially considering other work suggesting that PVT synaptic input onto select NAc interneurons is disrupted following opioid self-administration. Additional comment: It's also interesting that the IPSC amplitude seems to be maximal at ~2mW of light, whereas ~11 mW is required to evoke maximal EPSC amplitude. It would be interesting to know the authors' thoughts on why this may be.

While visual separation between conditions at low light levels is subtle, we addressed this directly using linear mixed-effects modeling, which evaluates IPSC amplitudes across the full range of stimulation intensities while accounting for repeated measurements from cells nested within animals. This approach provides greater sensitivity than visual inspection alone and avoids over interpretation of noise at individual stimulation levels.

Using this framework, we observed robust main effects of light intensity in both males and females, indicating preserved recruitment of inhibitory synaptic responses as stimulation increased. Importantly, no significant Light × Condition interactions were detected in either sex, indicating that the scaling of IPSC amplitudes with light intensity was not altered by oxycodone exposure.

With respect to the observation that IPSC amplitudes appear to reach near-maximal levels at lower light intensities (~2 mW) compared to EPSCs (~11 mW), we agree that this distinction is intriguing. One possible explanation is that the depend on the recruitment of local interneurons. However, the number of interneurons activated by PVT interneurons is limited and inhibitory responses may reach a plateau at relatively low light intensities once these interneurons are fully recruited.

On the other hand, the increased intensity of photostimulation would result in an increase of monosynaptic EPSC amplitude over a wider range of stimulation (light) intensities, as increased intensity of light would recruit more ChR2-expressing PVT fibers, resulting in larger EPSCs.

(8) There is an inadequate description of what has been done to date on the PVT-NAc projection regarding opioid withdrawal, seeking, disinhibition, and the effects on synaptic physiology therein. For example, a critical paper, Keyes et al., 2020 Neuron, is not cited. Additionally, Paniccia et al., 2024 Neuron is inaccurately cited and insufficiently described. Both manuscripts should be described in some detail within the introduction, and the findings should be accurately contextualized within the broader circuit within the discussion.

In the revised manuscript, we expanded the Discussion to give a more thorough overview of previous research on the PVT-NAc pathway in relation to opioid-related behaviors and synaptic changes. Specifically, we added more detail about Keyes et al., 2020 and Paniccia et al., 2024, clarifying their findings and placing them within the context of the circuit mechanisms studied in our work. We also revised the text to ensure the descriptions of these studies are accurate and that their conclusions are properly related to our findings.

(9) Related to the above, the authors should provide a more comprehensive description of how PVT synapses onto cell-type specific neurons in the NAc which expand beyond MSNs, especially considering that PVT has been shown to influence drug/opioid seeking through the innervation of NAc neurons that are not MSNs. For example, see PMIDs 33947849, 36369508, 28973852, 38141605.

In the revised manuscript, we expanded the Discussion to describe the diversity of PVT projections within the NAc and the potential role of non-MSN neuronal populations in drug-related behaviors. We added discussion on the broader circuit context and other cell types where relevant to the focus on synaptic transmission onto MSNs. Since our experiments specifically examined synaptic physiology in MSNs, we focused the literature discussion on studies most directly related to MSNtargeted PVT inputs and opioid-related behaviors.

Reviewer #3 (Public review):

(10) Additional experiments could strengthen the results and help clarify synaptic mechanisms underpinning behavioral sex differences.

We agree that additional experiments focused on identifying cell-type-specific mechanisms within the PVT-NAcSh circuit would further enhance understanding of the neural substrates behind the observed behavioral sex differences. In the revised manuscript, we have expanded the Discussion to explicitly acknowledge these limitations and clarify the scope of our current study. Specifically, we discuss the possibility that sex-specific adaptations might occur in particular neuronal subpopulations or circuit components that were not resolved in the present experiments. We also mention that future research using cell-type–specific approaches will be necessary to determine if such mechanisms contribute to the increased oxycodone seeking seen in females after prolonged abstinence. We appreciate the reviewer’s suggestions and have incorporated this perspective into the revised manuscript to better contextualize our findings and outline future directions.

eLife Assessment

This study investigates the role of the Z-disc protein Zasp52 in Drosophila flight muscles and provides evidence that an intrinsically disordered region (IDR) helps to stabilize and promote the localization of the protein to the Z-disc. Overall, this represents an important study that provides insights into Z-disc function and maintenance. The data are convincing, supported by strong genetic evidence and behavioral tests, well-controlled experiments, and detailed statistical analyses. Additional functional analyses designed to tease out specialized regions within the newly described isoform of Zasp52 would further strengthen models regarding the function of the protein.

Reviewer #1 (Public review):

The manuscript by Ho and Schock investigates the role of the Z-disc protein Zasp52 during Drosophila flight muscle development. It was known before, mainly by findings from this group, that Zasp52 is required for normal sarcomere morphogenesis, specifically Z-disc morphogenesis in indirect flight muscles. But the exact molecular mechanism by which Zasp52 contributes, apart from the fact that it is localised there and is somehow involved in multimerization/cross-linking, was not clear. This paper proposes that an intrinsically disordered region (IDR) in Zasp52 is needed for some of its functions, by stabilising Zasp52 localisation at the Z-disc. Specifically, the IDR in Zasp52 is proposed to be required for Z-disc maintenance during the mechanical challenges of flight, while being dispensable for the initial morphogenesis during development. This hypothesis is supported by strong genetic evidence and behavioural tests, deleting Zasp's IDR impairs flight from mid-age onwards, while a block in flight activity lifts the phenotype.

However, some of the phenotypic analysis, in particular the bending of the sarcomere, likely upon mechanical challenge by muscle contractions, needs more detailed investigations to be fully convincing.

Strengths:

(1) The linker in the alternatively spliced exon 15 of Zasp52 was deleted with a state-of-the-art genetic editing strategy. Surprisingly, flies are homozygous viable, showing that this long part of the Zasp52 protein is not essential for animal survival or sarcomere morphogenesis.

(2) The observed sarcomere phenotypes with age, especially the bending Z-discs, are new and exciting.

(3) The displayed EM images document interesting phenotypes.

(4) Most of the observed phenotypes can be rescued by re-expression of the long Zasp52 isoform, which does contain the IDR region, but not by a shorter one without it, suggesting that IDR is important.

(5) FRAP data measure the local turnover of a short-ZaspGFP and show that this increased in the Zasp mutant lacking the IDR domain, suggesting that Zasp-IDR might stabilise Zasp at the Z-disc.

(6) Interestingly, flight and sarcomere morphology phenotypes can be rescued by preventing the flies from flying, suggesting that they are mechanically induced.

Weaknesses:

(1) The western blot quantifications of Zasp isoform expression are weak. No error bars are indicated in the quantifications; the quantifications appear to be more qualitative than quantitative. According to band intensities, the long Zasp isoforms seem to be less present compared to the shorter ones, even in the flight muscles.

(2) The phenotypic analysis of the sarcomere appears somewhat superficial throughout the paper. Only Zasp52 and phalloidin are shown; no other Z-disc or thick filament proteins. At least myosin stainings and overview images are important to better judge the phenotypic variations. Are the variants between individuals or regional in the same muscle?

(3) EM images would benefit from better quantification.

(4) Other proteins were not analysed with the FRAP-based turnover assay for comparison in wild type and mutant. All Z-proteins might turn over faster in the mutant with the defective Z-disc.

Reviewer #2 (Public review):

Summary and Strengths:

This in-depth genetic analysis of Zasp52 function in Drosophila indirect flight muscle (IFM) provides an interesting perspective regarding the role of a partially disordered region (IDR) in exon 15e. This exon seems to be exclusively present in IFM and contributes to the prevention of myofibril disintegration during aging, likely due to interactions of this region with Z-disc insertion and/or stability. The addition of an isoform (PR) that lacks exon 15e serves as a nice control to illustrate the necessity of exon 15e in muscle structure and function. Overall, the manuscript is exceptionally well-written, logical, with nicely controlled experiments and detailed statistical analysis that largely support the conclusions drawn by the authors. While exon 15e is clearly involved in preventing muscle degeneration, a solid role for thin filament stability is not clearly shown (as mentioned in the abstract). In addition, which regions/how the proteins of the IDR may contribute are unclear.

Weaknesses:

(1) It is not clear in Figure S1A where exon 15e fits within the Zasp52 locus schematic. This is important as a premise of this paper describes this region to be key, and proof from multiple prediction programs would lend more weight to the prediction of the exon being largely disordered. Inclusion of the discussed short linear motifs, comparison with Canoe or LBD3 for similarities and/or an Alphafold structure would help make the authors' point (colorized with known domains).

(2) Interesting that immobilization rescues the deterioration phenotypes. The authors should explain in more detail how this was done to avoid dehydration/starvation of the flies.

(3) There is a lot of discussion about the potential function of the IDR region, specifically a putative actin binding motif or other 'ordered' regions that may contain short linear motifs. It would strengthen the findings to show which of these may be essential for Zasp52 function in the IFM. The ability to bind actin could be tested biochemically, and/or smaller deletions could be made to unequivocally test the role of the ABD vs other predicted motifs using genetics. If some of these regions are more ordered, where do they lie within, and do they form a predicted fold or structure that gives insight into function?

Author response:

Public Reviews:

Reviewer #1 (Public review):

The manuscript by Ho and Schock investigates the role of the Z-disc protein Zasp52 during Drosophila flight muscle development. It was known before, mainly by findings from this group, that Zasp52 is required for normal sarcomere morphogenesis, specifically Z-disc morphogenesis in indirect flight muscles. But the exact molecular mechanism by which Zasp52 contributes, apart from the fact that it is localised there and is somehow involved in multimerization/cross-linking, was not clear. This paper proposes that an intrinsically disordered region (IDR) in Zasp52 is needed for some of its functions, by stabilising Zasp52 localisation at the Z-disc. Specifically, the IDR in Zasp52 is proposed to be required for Z-disc maintenance during the mechanical challenges of flight, while being dispensable for the initial morphogenesis during development. This hypothesis is supported by strong genetic evidence and behavioural tests, deleting Zasp's IDR impairs flight from mid-age onwards, while a block in flight activity lifts the phenotype.

However, some of the phenotypic analysis, in particular the bending of the sarcomere, likely upon mechanical challenge by muscle contractions, needs more detailed investigations to be fully convincing.

Strengths:

(1) The linker in the alternatively spliced exon 15 of Zasp52 was deleted with a state-of-the-art genetic editing strategy. Surprisingly, flies are homozygous viable, showing that this long part of the Zasp52 protein is not essential for animal survival or sarcomere morphogenesis.

(2) The observed sarcomere phenotypes with age, especially the bending Z-discs, are new and exciting.

(3) The displayed EM images document interesting phenotypes.

(4) Most of the observed phenotypes can be rescued by re-expression of the long Zasp52 isoform, which does contain the IDR region, but not by a shorter one without it, suggesting that IDR is important.

(5) FRAP data measure the local turnover of a short-ZaspGFP and show that this increased in the Zasp mutant lacking the IDR domain, suggesting that Zasp-IDR might stabilise Zasp at the Z-disc.

(6) Interestingly, flight and sarcomere morphology phenotypes can be rescued by preventing the flies from flying, suggesting that they are mechanically induced.

Weaknesses:

(1) The western blot quantifications of Zasp isoform expression are weak. No error bars are indicated in the quantifications; the quantifications appear to be more qualitative than quantitative. According to band intensities, the long Zasp isoforms seem to be less present compared to the shorter ones, even in the flight muscles.

We will work on including quantifications with error bars for the Western blots in our resubmission. It is important to keep in mind that the main point in figure 1B is that there are plenty of exon15e-containing isoforms in IFM, in contrast to other tissues with very limited exon15e-containing isoforms. This is confirmed by the analysis of RNAseq data in figure 1C, and of course, by the flightless phenotype of the exon15e mutant.

(2) The phenotypic analysis of the sarcomere appears somewhat superficial throughout the paper. Only Zasp52 and phalloidin are shown; no other Z-disc or thick filament proteins. At least myosin stainings and overview images are important to better judge the phenotypic variations. Are the variants between individuals or regional in the same muscle?

Our images are representative of the observed phenotypes. We aim to provide overview images and other stainings to better illustrate the phenotypic variations in the revised version. Phenotypes are consistently present across all individuals, as reflected in our replicates. Interestingly, they appear to not be randomly interspersed among the sarcomeres but concentrated in certain regions of muscle more than others.

(3) EM images would benefit from better quantification.

We do not believe that EM images can be meaningfully quantified, because of the many selection steps preceding image acquisition.

(4) Other proteins were not analysed with the FRAP-based turnover assay for comparison in wild type and mutant. All Z-proteins might turn over faster in the mutant with the defective Z-disc.

This is the point we are trying to make. The Zasp52 IDR acts like a glue stabilizing all Z-disc proteins. We performed this experiment as a first step to explore whether an exon15e-lacking system exhibited modified dynamics, and we aim to provide more data in the revised version.

Reviewer #2 (Public review):

Summary and Strengths:

This in-depth genetic analysis of Zasp52 function in Drosophila indirect flight muscle (IFM) provides an interesting perspective regarding the role of a partially disordered region (IDR) in exon 15e. This exon seems to be exclusively present in IFM and contributes to the prevention of myofibril disintegration during aging, likely due to interactions of this region with Z-disc insertion and/or stability. The addition of an isoform (PR) that lacks exon 15e serves as a nice control to illustrate the necessity of exon 15e in muscle structure and function. Overall, the manuscript is exceptionally well-written, logical, with nicely controlled experiments and detailed statistical analysis that largely support the conclusions drawn by the authors. While exon 15e is clearly involved in preventing muscle degeneration, a solid role for thin filament stability is not clearly shown (as mentioned in the abstract). In addition, which regions/how the proteins of the IDR may contribute are unclear.

Weaknesses:

(1) It is not clear in Figure S1A where exon 15e fits within the Zasp52 locus schematic. This is important as a premise of this paper describes this region to be key, and proof from multiple prediction programs would lend more weight to the prediction of the exon being largely disordered. Inclusion of the discussed short linear motifs, comparison with Canoe or LBD3 for similarities and/or an Alphafold structure would help make the authors' point (colorized with known domains).

We will add a bar below figure S2A to show the region corresponding to exon 15e. We used three disorder prediction programs and one structure (order) prediction program. The majority of exon15e is completely disordered and of very low confidence score, and thus uninformative to display as an Alphafold structure. Likewise, IDR’s are very difficult to classify, therefore we cannot say much more than that LDB3, Zasp52, and Canoe contain IDRs, with Zasp52 and Canoe both having an actin-binding domain within the IDR. We will provide more data on the function of the ABD in the revised version.

(2) Interesting that immobilization rescues the deterioration phenotypes. The authors should explain in more detail how this was done to avoid dehydration/starvation of the flies.

We will provide more details in the revised version.

(3) There is a lot of discussion about the potential function of the IDR region, specifically a putative actin binding motif or other 'ordered' regions that may contain short linear motifs. It would strengthen the findings to show which of these may be essential for Zasp52 function in the IFM. The ability to bind actin could be tested biochemically, and/or smaller deletions could be made to unequivocally test the role of the ABD vs other predicted motifs using genetics. If some of these regions are more ordered, where do they lie within, and do they form a predicted fold or structure that gives insight into function?

We will provide data on the function of the ABD in the revised version.

Le passage me fait penser à une forme de projection : la présence de points communs semble rapidement interprétée comme une preuve de compatibilité profonde (« c’est lui »). Cette impression de familiarité permet-elle réellement de connaître l’autre ou peut-elle conduire à une idéalisation ?

Je me demande si ce phénomène peut être attribué uniquement aux sites de rencontres. L’idéalisation du partenaire semble exister bien avant l’apparition du numérique. Ca me fait penser à Stendhal, et la notion de cristalisation qu'il décrit comme étant la tendance à projeter sur l'être aimé des qualités idéales, dépassant la réalité. Amour et idéalisation vont je pense de pair, avec ou sans internet. Aussi, l’affirmation selon laquelle « les femmes recherchent un homme idéal » paraît assez générale. Existe-t-il des recherches empiriques permettant d’étayer cette différence entre hommes et femmes ?

Argument d’autorité : l’auteur s’appuie sur son expérience professionnelle (« dans mon cabinet, je constate »). Cela apporte une expertise, mais ne constitue pas à lui seul une preuve scientifique généralisable.

L’auteur défend ici l’idée qu’Internet aurait modifié notre représentation des relations amoureuses en nous faisant revenir vers une vision plus figée et idéalisée de l’amour.

Met-level extensibility as in OHS

a personal digital archive, to store and use whatever content the learner/knowledge worker need to gather, organize, explore, reuse in a form that meets personal needs, and produce artifact in a form that she specifies, to harness personal creativity to personal problem solving

!4 Conceptipedia

metaxy

http://bafybeiddch5xxgmi3dgk2kfn6fjs4gp5yjxvl2p5fes57n6chrhknyxewa.ipfs.dweb.link/metaxy/~/metaxy-copy.html

This is a good accessibility point as it presents how important simple language is. Utilizing simple words makes it easier for users to understand, especially those with reading disorders, short attention spans, memory challenges or those with poorer digital literacy. This form of simple, clear writing ensures the web content is much more accessible to a wider range of users.

This is a link with descriptive wording and is a good example of an accessible link as the link very clearly discusses where it will take them. As opposed to it saying "click here" it tells you where you will be redirected, naming the exact source; The Web Content Accessibility Guidelines (WCAG) 2.0. This helps all users, and the screen readers specifically to understand the link they click prior to opening it. This connects to this weeks theme as accessibility is not solely about internet access, it also is about making online information accessible and usable for those with various needs.

This statement relates to web accessibility as it has content that is not just about design, but also discusses how someone can understand and use the information they learn. This is a very useful tool as it considers all readers, and considers those with unique differences such as any physical or cognitive disabilities.

This is a strong accessibility feature that utilizes a clear heading to organize the information neatly so it is easy to follow. This helps readers see when what they are reading and where exactly they are in the paper. This is especially useful for those who are looking for a specific piece of information as it can save time and help map out the page.

This is a table of contents which is often at the beginning or the very end of a paper, and is a very crucial accessibility feature as it helps users navigate the paper easily, saving time and allows for ultimate efficiency as it eliminates the need to scroll endlessly. This is especially useful for those who struggle with large amounts of information all at once.

Happy to share our preprint on bioRxiv. We warmly welcome all comments and suggestions to further strengthen this manuscript.

DASHES

Reportedly comprising around 45 staff members in 2023

:

metaxy pdf

https://bafybeicmg6blrd3iog3fw5bvmmgkqrx6thpi5cwha45g4p3yb3kltm27da.ipfs.inbrowser.link/?filename=metaxy-copy.pdf

eLife Assessment

This important study identified Mex3a protein with dual RNA-binding protein/ubiquitin ligase function as a pivotal regulator of olfactory sensory neurons (OSN) differentiation and lineage fidelity. The authors employed a combination of systems biology approaches (e.g., single-cell RNA sequencing, proteomics) and newly developed animal models (e.g., HyperTRIBE) to provide solid evidence that abrogation of Mex3a disrupts cilia structure and polarity of OSNs. Notwithstanding that this article is of a broad potential interest across different biomedical disciplines ranging from RNA to developmental biology, additional mechanistic data connecting identified Mex3a mRNA targets and ensuing OSN phenotypes would further strengthen this study.

Reviewer #1 (Public review):

The study by Escamilla del Arenal et al. utilized a conditional knockout mouse model to study the role of Mex3a in immature olfactory sensory neurons (OSN). Mex3a is a dual-functional protein that has RNA-binding function and ubiquitin-E3 ligase activity. The results revealed that Mex3a expression is critical for proper OSN differentiation and contributes to cell surface protein trafficking and translation, cilia structure, and planar cell polarity in mature neurons. Moreover, Mex3a enforces lineage fidelity, selectively repressing sustentacular programs in neurons and neuronal programs in sustentacular cells.

In addition, the authors established an in vivo HyperTRIBE mouse model to identify Mex3a RNA targets and incorporated UbiFast into the Mex3a conditional knockout (cKO) model to find its protein targets to investigate how Mex3a regulates OSN differentiation. The experimental systems are laborious and comprehensive, which allowed the authors to identify new Mex3a putative targets in OSN.

The phenotypic results derived from the conditional Mex3a cKO mice are solid. Mechanistic findings also revealed that, in addition to facilitating protein degradation, Mex3a may confer K27 ubiquitin linkage on its target proteins, which has a non-proteolytic role but affects target protein activity, other post-translational modifications, or protein-protein interactions. However, among all Mex3a putative targets, the authors decided to emphasize on the Mex3a-mediated K27 ubiquitination on stress granule protein Serbp1 and ribosome protein Rps7, and the association between Mex3a expression and Serbp1 and p-eEF2 ribosome recruitment. This Mex3a-Serbp1-p-eEF2 ribosome recruitment axis, although it can be important in Unfolded Protein Response (UPR) signaling, seems rather general and cannot explain the striking lineage-specific phenotypes observed in the mouse model. The authors need to provide more solid evidence to demonstrate that K27-Ubiquitinylation of Serbp1 is a key step of Mex3a function in OSN differentiation to strengthen the relation between the phenotypes and mechanism presented in this study.

Reviewer #2 (Public review):

Summary:

In this manuscript, Arenal and colleagues demonstrate that loss of Mex3a leads to defects in cell surface protein trafficking, translation, ciliary structure, and planar cell polarity in mature neurons. Through proteomic analyses, the authors show that Mex3a depletion alters the abundance of proteins involved in vesicular transport, lipid metabolism, and ribosome biogenesis. Using the HyperTRIBE approach, the authors further identify targets of Mex3a and provide evidence supporting a role for K27-linked ubiquitination in regulating these substrates. Mechanistically, the study suggests that Mex3a levels influence the recruitment of SERBP1 and phosphorylated eEF2 (p-eEF2) to ribosomes, contributing to translational repression.

Strengths:

Overall, this is a very interesting and well-written manuscript that significantly advances our understanding of Mex3a function and its role in neuronal development, particularly in olfactory sensory neurons. The data are clearly presented and thoughtfully interpreted.

Weaknesses:

I have a few minor comments that may further strengthen the manuscript and improve its accessibility to a broader readership.

(1) In Figure 3B, the authors describe Mex3a localization to cytoplasmic granules. However, it is unclear how these compartments were defined. It would strengthen the conclusions if the authors included co-localization experiments using established cytoplasmic granule markers (e.g., stress granule markers) to define the identity of these structures more precisely. This would clarify whether Mex3a associates with stress granules, RNA processing bodies, or another class of ribonucleoprotein granules.

(2) Functional validation of K27-linked ubiquitination on SERBP1<br /> To further define the functional significance of K27-linked ubiquitination, it would be informative to mutate the relevant lysine residue(s) on SERBP1 and examine whether this alters its recruitment to ribosomes or affects translational repression. Such an experiment would provide more direct evidence that K27-linked ubiquitination of SERBP1 mediates the observed translational effects.

(3) Discussion of vesicular trafficking and lipid metabolism targets<br /> The identification of Mex3a targets involved in vesicular trafficking and lipid metabolism, including COPII coat components such as Sec31a and lipid regulatory proteins such as Sec14 and PIP5K1A, is particularly intriguing. The authors may wish to expand the Discussion to address how regulation of these proteins could contribute to defects in plasma membrane trafficking and planar cell polarity. Integrating these findings with the observed cell surface trafficking phenotypes would further enhance the mechanistic framework of the study.

Reviewer #3 (Public review):

Summary:

In this manuscript, the authors investigate the role of the KH and RING domain-containing protein Mex3a in the differentiation and maturation of olfactory sensory neurons. Using conditional knockout of Mex3a in immature neurons, they show that mature olfactory sensory neurons display defects in membrane protein trafficking, including olfactory receptors and Adcy3, together with abnormalities in ciliary radial organization and planar cell polarity. Through single-cell RNA sequencing and quantitative proteomics, the authors further show that Mex3a-deficient neurons fail to properly resolve the unfolded protein response and exhibit transcriptomic features suggestive of lineage mixing with sustentacular cells. The study also introduces a methodological advance by adapting HyperTRIBE for use in transgenic mice, which enables the identification of in vivo Mex3a RNA targets, including components of Wnt signaling that appear to be under translational repression by Mex3a. The authors then pursue one of these targets to further explore the role of Mex3a in translational repression.

Strengths:

First, it addresses an important biological and conceptual question. Mex3a is a multifunctional protein with the potential to couple RNA regulation, protein homeostasis, and key cellular processes, yet its in vivo role in neuronal differentiation remains poorly understood. By focusing on Mex3a in olfactory sensory neurons, the manuscript asks a timely and important question of how post-transcriptional regulation contributes to the maturation of highly specialized neurons, including the establishment of ciliary architecture, membrane protein trafficking, and cell polarity. Second, the generation and validation of an inducible in vivo mouse HyperTRIBE system represents a technical advance. By incorporating the Adar deaminase domain into a transgenic mouse model, the authors establish a rigorous and useful approach for identifying Mex3a RNA targets in vivo, which is likely to be valuable to the wider RNA biology community. Third, the study integrates the Mex3a knockout model with single-cell RNA sequencing, quantitative mass spectrometry-based proteomics, ubiquitin profiling, and ribosome-related analyses, providing a broad and multilayered view of the Mex3a knockout phenotype. Finally, the imaging analyses revealing altered ciliary content and organization in olfactory sensory neurons identify an interesting and potentially important link between Mex3a, cilia biology, and vesicular trafficking. More broadly, the manuscript reflects a very substantial experimental effort, and each individual dataset has the potential to be useful for the field.

Weaknesses:

A main weakness of the manuscript is that the mechanistic links between the major findings remain somewhat correlative, and the biological narrative is not fully sustained through the later figures. The study documents defects in membrane trafficking, ciliary radial organization, and planar cell polarity, and it identifies candidate targets with clear relevance to these processes, including factors linked to vesicle trafficking. However, the manuscript then shifts its mechanistic focus toward translational regulators such as Serbp1 and Rps7, without adequately connecting these later analyses back to the core phenotypes established earlier. As a result, there is a noticeable disconnect between the phenotypic emphasis of the study and the mechanistic validation that follows.

A second weakness is that, given the breadth and potential importance of the datasets generated, validation remains limited for several of the major conclusions. This reduces confidence in the interpretation of the single-cell, proteomic, ubiquitin-related, and ribosome-associated analyses, and also limits the future value of these datasets as a resource for the field. Because the manuscript aims to address several major questions at once, stronger validation and clearer integration across the different experimental arms are needed for the conclusions to feel fully supported.

Finally, the HEK293T overexpression experiments are less solid than the in vivo analyses and do not provide equally strong support for the proposed mechanisms. In this context, some of the observed effects on cytoskeletal organization, membrane-less granule formation, and ribosome profiles may be indirect, which makes it difficult to weigh these findings alongside the much stronger in vivo phenotypes.

DOI: 10.64898/2026.05.05.720208

Resource: RRID:Addgene_128055

Curator: @dhovakimyan1

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What is this?

DOI: 10.64898/2026.05.05.720208

Resource: (KCB Cat# KCB 90029YJ, RRID:CVCL_0004)

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What is this?

DOI: 10.64898/2026.05.05.720208

Resource: RRID:Addgene_128055

Curator: @scibot

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What is this?

DOI: 10.64898/2026.05.05.720208

Resource: RRID:SCR_026671

Curator: @scibot

SciCrunch record: RRID:SCR_026671

What is this?

DOI: 10.64898/2026.05.05.720208

Resource: Odyssey CLx (RRID:SCR_014579)

Curator: @scibot

SciCrunch record: RRID:SCR_014579

What is this?

DOI: 10.64898/2026.05.05.720208

Resource: BD FACSARIA III cell sorter (RRID:SCR_016695)

Curator: @scibot

SciCrunch record: RRID:SCR_016695

What is this?

DOI: 10.64898/2026.05.05.720208

Resource: (LI-COR Biosciences Cat# 926-68072, RRID:AB_10953628)

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What is this?

DOI: 10.64898/2026.05.05.720208

Resource: (LI-COR Biosciences Cat# 926-32213, RRID:AB_621848)

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What is this?

DOI: 10.64898/2026.04.13.718264

Resource: (MMRRC Cat# 033018-UCD,RRID:MMRRC_033018-UCD)

Curator: @AleksanderDrozdz

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What is this?

DOI: 10.3390/cells15090817

Resource: (MMRRC Cat# 032045-JAX,RRID:MMRRC_032045-JAX)

Curator: @AleksanderDrozdz

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What is this?

DOI: 10.3389/fimmu.2026.1774396

Resource: (MMRRC Cat# 030988-MU,RRID:MMRRC_030988-MU)

Curator: @AleksanderDrozdz

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (MMRRC Cat# 034840-JAX,RRID:MMRRC_034840-JAX)

Curator: @AleksanderDrozdz

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Proteintech Cat# SA00001-1, RRID:AB_2722565)

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Thermo Fisher Scientific Cat# A-31573, RRID:AB_2536183)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Thermo Fisher Scientific Cat# A48269, RRID:AB_2893137)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Thermo Fisher Scientific Cat# A-11057, RRID:AB_2534104)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Thermo Fisher Scientific Cat# A10042, RRID:AB_2534017)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Thermo Fisher Scientific Cat# A-11055, RRID:AB_2534102)

Curator: @scibot

SciCrunch record: RRID:AB_2534102

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Thermo Fisher Scientific Cat# A-21068, RRID:AB_2535729)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Proteintech Cat# SA00001-2, RRID:AB_2722564)

Curator: @scibot

SciCrunch record: RRID:AB_2722564

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Thermo Fisher Scientific Cat# A78948, RRID:AB_2921070)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Proteintech Cat# 10094-1-AP, RRID:AB_2210695)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (ABclonal Cat# A6344, RRID:AB_2766946)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Proteintech Cat# 66009-1-Ig, RRID:AB_2687938)

Curator: @scibot

SciCrunch record: RRID:AB_2687938

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Cell Signaling Technology Cat# 2251, RRID:AB_2106903)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Abcam Cat# ab5392, RRID:AB_2138153)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (UC Davis/NIH NeuroMab Facility Cat# 75-028, RRID:AB_2292909)

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Proteintech Cat# 60004-1-Ig, RRID:AB_2107436)

Curator: @scibot

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Cell Signaling Technology Cat# 2258, RRID:AB_2186909)

Curator: @scibot

SciCrunch record: RRID:AB_2186909

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Cell Signaling Technology Cat# 5606, RRID:AB_1903900)

Curator: @scibot

SciCrunch record: RRID:AB_1903900

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (DSHB Cat# 1d4b, RRID:AB_2134500)

Curator: @scibot

SciCrunch record: RRID:AB_2134500

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Thermo Fisher Scientific Cat# 51-6900, RRID:AB_2533914)

Curator: @scibot

SciCrunch record: RRID:AB_2533914

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: RRID:AB_3100585

Curator: @scibot

SciCrunch record: RRID:AB_3100585

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Abcam Cat# ab16659, RRID:AB_443419)

Curator: @scibot

SciCrunch record: RRID:AB_443419

What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Abcam Cat# ab7260, RRID:AB_305808)

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Sigma-Aldrich Cat# A8717, RRID:AB_258409)

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Wako Cat# 019-19741, RRID:AB_839504)

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What is this?

DOI: 10.1186/s12979-026-00565-9

Resource: (Novus Cat# NB100-1028, RRID:AB_3148646)

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What is this?

DOI: 10.1186/s12964-025-02483-7

Resource: E-CRISP (RRID:SCR_019088)

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What is this?

DOI: 10.1186/s12882-025-04572-8

Resource: GraphPad Prism (RRID:SCR_002798)

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What is this?

DOI: 10.1177/21925682211032559

Resource: IBM SPSS Statistics (RRID:SCR_016479)

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SciCrunch record: RRID:SCR_016479

What is this?

DOI: 10.1177/2192568220975384

Resource: IBM SPSS Statistics (RRID:SCR_016479)

Curator: @areedewitt04

SciCrunch record: RRID:SCR_016479

What is this?

DOI: 10.1177/17448069251376189

Resource: Python Programming Language (RRID:SCR_008394)

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SciCrunch record: RRID:SCR_008394

What is this?

DOI: 10.1177/17448069251376189

Resource: MATLAB (RRID:SCR_001622)

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SciCrunch record: RRID:SCR_001622

What is this?

DOI: 10.1177/17103568251368314

Resource: Stata (RRID:SCR_012763)

Curator: @areedewitt04

SciCrunch record: RRID:SCR_012763

What is this?

DOI: 10.1177/08919887251366638

Resource: Parkinson's Progression Markers Initiative (RRID:SCR_006431)

Curator: @areedewitt04

SciCrunch record: RRID:SCR_006431

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (ATCC Cat# CRL-2336, RRID:CVCL_0290)

Curator: @nmaralla

SciCrunch record: RRID:CVCL_0290

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (Thermo Fisher Scientific Cat# 02-6102, RRID:AB_2532938)

Curator: @scibot

SciCrunch record: RRID:AB_2532938

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (Abcam Cat# ab236137, RRID:AB_2827629)

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SciCrunch record: RRID:AB_2827629

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (Proteintech Cat# 60188-1-Ig, RRID:AB_10859484)

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What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: ImageJ (RRID:SCR_003070)

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SciCrunch record: RRID:SCR_003070

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (Proteintech Cat# 26158-1-AP, RRID:AB_2800447)

Curator: @scibot

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What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: GraphPad Prism (RRID:SCR_002798)

Curator: @scibot

SciCrunch record: RRID:SCR_002798

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (Proteintech Cat# 15073-1-AP, RRID:AB_2142033)

Curator: @scibot

SciCrunch record: RRID:AB_2142033

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (Abcam Cat# ab246514, RRID:AB_2891213)

Curator: @scibot

SciCrunch record: RRID:AB_2891213

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (Abcam Cat# ab220162, RRID:AB_2892231)

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What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (NCI-DTP Cat# MCF7, RRID:CVCL_0031)

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SciCrunch record: RRID:CVCL_0031

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (RRID:CVCL_3422)

Curator: @scibot

SciCrunch record: RRID:CVCL_3422

What is this?

DOI: 10.1158/0008-5472.CAN-24-4751

Resource: (RRID:CVCL_0063)

Curator: @scibot

SciCrunch record: RRID:CVCL_0063

What is this?

DOI: 10.1126/sciadv.adw4064

Resource: RRID:MMRRC_049020-UCD

Curator: @AleksanderDrozdz

SciCrunch record: RRID:MMRRC_049020-UCD

What is this?

DOI: 10.1126/sciadv.adw4064

Resource: RRID:Addgene_46782

Curator: @scibot

SciCrunch record: RRID:Addgene_46782

What is this?

DOI: 10.1126/sciadv.adw4064

Resource: RRID:Addgene_46781

Curator: @scibot

SciCrunch record: RRID:Addgene_46781

What is this?

DOI: 10.1126/sciadv.adw4064

Resource: RRID:Addgene_161912

Curator: @scibot

SciCrunch record: RRID:Addgene_161912

What is this?

DOI: 10.1126/sciadv.adw4064

Resource: RRID:Addgene_101046

Curator: @scibot

SciCrunch record: RRID:Addgene_101046

What is this?

DOI: 10.1126/sciadv.adw4064

Resource: RRID:Addgene_49154

Curator: @scibot

SciCrunch record: RRID:Addgene_49154

What is this?

DOI: 10.1126/sciadv.adw4064

Resource: RRID:Addgene_49476

Curator: @scibot

SciCrunch record: RRID:Addgene_49476

What is this?

DOI: 10.1111/jnc.70456

Resource: (Abcam Cat# ab98111, RRID:AB_10678894)

Curator: @areedewitt04

SciCrunch record: RRID:AB_10678894

What is this?

DOI: 10.1111/jnc.70456

Resource: (Abcam Cat# ab18258, RRID:AB_444362)

Curator: @areedewitt04

SciCrunch record: RRID:AB_444362

What is this?

DOI: 10.1111/jnc.70456

Resource: (Abcam Cat# ab65783, RRID:AB_1658870)

Curator: @areedewitt04

SciCrunch record: RRID:AB_1658870

What is this?

DOI: 10.1111/jnc.70456

Resource: (Abcam Cat# ab133265, RRID:AB_11158532)

Curator: @areedewitt04

SciCrunch record: RRID:AB_11158532

What is this?

DOI: 10.1111/jnc.70456

Resource: (Abcam Cat# ab109182, RRID:AB_10862307)

Curator: @areedewitt04

SciCrunch record: RRID:AB_10862307

What is this?

DOI: 10.1038/s41419-026-08670-9

Resource: (MMRRC Cat# 015500-UCD,RRID:MMRRC_015500-UCD)

Curator: @AleksanderDrozdz

SciCrunch record: RRID:MMRRC_015500-UCD

What is this?

DOI: 10.1016/j.xcrm.2026.102803

Resource: RRID:IMSR_CRL:027

Curator: @nmaralla

SciCrunch record: RRID:IMSR_CRL:027

What is this?

DOI: 10.1016/j.xcrm.2026.102803

Resource: (IMSR Cat# CRL_564,RRID:IMSR_CRL:564)

Curator: @nmaralla

SciCrunch record: RRID:IMSR_CRL:564

What is this?

DOI: 10.1016/j.mrfmmm.2026.111939

Resource: (ATCC Cat# CRL-4053, RRID:CVCL_9Q53)

Curator: @nmaralla

SciCrunch record: RRID:CVCL_9Q53

What is this?

DOI: 10.1016/j.devcel.2026.03.011

Resource: RRID:BDSC_5137

Curator: @nmaralla

SciCrunch record: RRID:BDSC_5137

What is this?

DOI: 10.1016/j.devcel.2026.03.011

Resource: RRID:BDSC_8443

Curator: @nmaralla

SciCrunch record: RRID:BDSC_8443

What is this?

DOI: 10.1093/nar/gkag447

Resource: Mutant Mouse Regional Resource Center (RRID:SCR_002953)

Curator: @AleksanderDrozdz

SciCrunch record: RRID:SCR_002953

What is this?

DOI: 10.1016/j.chom.2026.04.015

Resource: RRID:Addgene_12259

Curator: @nmaralla

SciCrunch record: RRID:Addgene_12259

What is this?

DOI: 10.1016/j.celrep.2026.117347

Resource: RRID:IMSR_JAX:034159

Curator: @nmaralla

SciCrunch record: RRID:IMSR_JAX:034159

What is this?

DOI: 10.1016/j.celrep.2026.117347

Resource: RRID:IMSR_JAX:000664

Curator: @nmaralla

SciCrunch record: RRID:IMSR_JAX:000664

What is this?

DOI: 10.1016/j.celrep.2026.117333

Resource: (NCI-DTP Cat# NCI-H1299, RRID:CVCL_0060)

Curator: @nmaralla

SciCrunch record: RRID:CVCL_0060

What is this?

DOI: 10.1016/j.celrep.2026.117333

Resource: (RRID:CVCL_S744)

Curator: @nmaralla

SciCrunch record: RRID:CVCL_S744

What is this?

DOI: 10.1007/s12264-025-01573-3

Resource: (MMRRC Cat# 017263-UCD,RRID:MMRRC_017263-UCD)

Curator: @AleksanderDrozdz

SciCrunch record: RRID:MMRRC_017263-UCD

What is this?

DOI: 10.1007/s10495-026-02310-5

Resource: RRID:Addgene_12259

Curator: @dhovakimyan1

SciCrunch record: RRID:Addgene_12259

What is this?

DOI: 10.1007/s10495-026-02310-5

Resource: RRID:Addgene_12260

Curator: @dhovakimyan1

SciCrunch record: RRID:Addgene_12260

What is this?

DOI: 10.1007/s10495-026-02310-5

Resource: (RRID:CVCL_0179)

Curator: @dhovakimyan1

SciCrunch record: RRID:CVCL_0179

What is this?

DOI: 10.1007/s10495-026-02310-5

Resource: (DSMZ Cat# ACC-305, RRID:CVCL_0045)

Curator: @dhovakimyan1

SciCrunch record: RRID:CVCL_0045

What is this?

DOI: 10.1007/s10495-026-02310-5

Resource: (ICLC Cat# HTL98017, RRID:CVCL_0032)

Curator: @dhovakimyan1

SciCrunch record: RRID:CVCL_0032

What is this?

DOI: 10.1007/s10495-026-02310-5

Resource: RRID:Addgene_1864

Curator: @dhovakimyan1

SciCrunch record: RRID:Addgene_1864

What is this?

DOI: 10.1007/s10495-026-02310-5

Resource: RRID:Addgene_170446

Curator: @dhovakimyan1

SciCrunch record: RRID:Addgene_170446

What is this?

DOI: 10.1002/rmb2.70055

Resource: Mutant Mouse Regional Resource Center (RRID:SCR_002953)

Curator: @AleksanderDrozdz

SciCrunch record: RRID:SCR_002953

What is this?

DOI: 10.1002/dvg.70054

Resource: WEBLOGO (RRID:SCR_010236)

Curator: @areedewitt04

SciCrunch record: RRID:SCR_010236

What is this?

DOI: 10.1002/cbdv.71334

Resource: (BCRC Cat# 60408, RRID:CVCL_3612)

Curator: @areedewitt04

SciCrunch record: RRID:CVCL_3612

What is this?

DOI: 10.1002/cbdv.71314

Resource: (ATCC Cat# CRL-1721, RRID:CVCL_0481)

Curator: @areedewitt04

SciCrunch record: RRID:CVCL_0481

What is this?

DOI: 10.1002/alz.71452

Resource: (MMRRC Cat# 034848-JAX,RRID:MMRRC_034848-JAX)

Curator: @AleksanderDrozdz

SciCrunch record: RRID:MMRRC_034848-JAX

What is this?

DOI: 10.1002/1878-0261.70268

Resource: (DSMZ Cat# ACC-256, RRID:CVCL_0395)

Curator: @areedewitt04

SciCrunch record: RRID:CVCL_0395

What is this?

DOI: 10.1002/1878-0261.70268

Resource: (RRID:CVCL_0062)

Curator: @areedewitt04

SciCrunch record: RRID:CVCL_0062

What is this?

DOI: 10.1002/1878-0261.70268

Resource: (ICLC Cat# HTL95026, RRID:CVCL_1700)

Curator: @areedewitt04

SciCrunch record: RRID:CVCL_1700

What is this?

DOI: 10.1002/1878-0261.70268

Resource: (BCRC Cat# 60005, RRID:CVCL_0030)

Curator: @areedewitt04

SciCrunch record: RRID:CVCL_0030

What is this?

DOI: 10.64898/2026.05.07.723605

Resource: University of California, Berkeley Biosciences Divisional Services Cell Culture Core Facility (RRID:SCR_017924)

Curator: @scibot

SciCrunch record: RRID:SCR_017924

What is this?

DOI: 10.64898/2026.05.07.723453

Resource: RRID:SCR_017773

Curator: @scibot

SciCrunch record: RRID:SCR_017773

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BioLegend Cat# 345110, RRID:AB_11203542)

Curator: @scibot

SciCrunch record: RRID:AB_11203542

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (R and D Systems Cat# AF933, RRID:AB_355722)

Curator: @scibot

SciCrunch record: RRID:AB_355722

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: RRID:AB_3696542

Curator: @scibot

SciCrunch record: RRID:AB_3696542

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: RRID:AB_3697569

Curator: @scibot

SciCrunch record: RRID:AB_3697569

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (Thermo Fisher Scientific Cat# MA5-32654, RRID:AB_2809931)

Curator: @scibot

SciCrunch record: RRID:AB_2809931

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: RRID:AB_10732633

Curator: @scibot

SciCrunch record: RRID:AB_10732633

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BioLegend Cat# 313610, RRID:AB_493637)

Curator: @scibot

SciCrunch record: RRID:AB_493637

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: RRID:AB_1079302

Curator: @scibot

SciCrunch record: RRID:AB_1079302

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: RRID:AB_2741691

Curator: @scibot

SciCrunch record: RRID:AB_2741691

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (Thermo Fisher Scientific Cat# A10542, RRID:AB_2534042)

Curator: @scibot

SciCrunch record: RRID:AB_2534042

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BioLegend Cat# 406421, RRID:AB_2563484)

Curator: @scibot

SciCrunch record: RRID:AB_2563484

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BioLegend Cat# 324224, RRID:AB_2562518)

Curator: @scibot

SciCrunch record: RRID:AB_2562518

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BioLegend Cat# 304024, RRID:AB_493761)

Curator: @scibot

SciCrunch record: RRID:AB_493761

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BioLegend Cat# 324208, RRID:AB_756082)

Curator: @scibot

SciCrunch record: RRID:AB_756082

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BioLegend Cat# 303132, RRID:AB_2566175)

Curator: @scibot

SciCrunch record: RRID:AB_2566175

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BD Biosciences Cat# 562804, RRID:AB_2687421)

Curator: @scibot

SciCrunch record: RRID:AB_2687421

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BioLegend Cat# 301720, RRID:AB_2616764)

Curator: @scibot

SciCrunch record: RRID:AB_2616764

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: RRID:AB_1518752

Curator: @scibot

SciCrunch record: RRID:AB_1518752

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BD Biosciences Cat# 563851, RRID:AB_2744391)

Curator: @scibot

SciCrunch record: RRID:AB_2744391

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (Santa Cruz Biotechnology Cat# sc-23950, RRID:AB_628409)

Curator: @scibot

SciCrunch record: RRID:AB_628409

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (BD Biosciences Cat# 560180, RRID:AB_1645464)

Curator: @scibot

SciCrunch record: RRID:AB_1645464

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (ATCC Cat# CRL-2700, RRID:CVCL_G654)

Curator: @scibot

SciCrunch record: RRID:CVCL_G654

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: FlowJo (RRID:SCR_008520)

Curator: @scibot

SciCrunch record: RRID:SCR_008520

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: GraphPad Prism (RRID:SCR_002798)

Curator: @scibot

SciCrunch record: RRID:SCR_002798

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: RRID:AB_3697641

Curator: @scibot

SciCrunch record: RRID:AB_3697641

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (RRID:CVCL_A5KB)

Curator: @scibot

SciCrunch record: RRID:CVCL_A5KB

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: RRID:AB_3658598

Curator: @scibot

SciCrunch record: RRID:AB_3658598

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (Sigma-Aldrich Cat# HPA020587, RRID:AB_1850452)

Curator: @scibot

SciCrunch record: RRID:AB_1850452

What is this?

DOI: 10.64898/2026.05.07.723425

Resource: (CCLV Cat# CCLV-RIE 1018, RRID:CVCL_0063)

Curator: @scibot

SciCrunch record: RRID:CVCL_0063

What is this?

DOI: 10.64898/2026.05.07.723257

Resource: Max Planck Institute of Biochemistry Imaging Facility (RRID:SCR_025739)

Curator: @scibot

SciCrunch record: RRID:SCR_025739

What is this?

DOI: 10.64898/2026.05.05.723095

Resource: Emory University NIH Tetramer Core Facility (RRID:SCR_026557)

Curator: @scibot

SciCrunch record: RRID:SCR_026557

What is this?

DOI: 10.64898/2026.05.05.723085

Resource: (RRID:CVCL_0179)

Curator: @scibot

SciCrunch record: RRID:CVCL_0179

What is this?

DOI: 10.3390/ijms27094113

Resource: (MMRRC Cat# 034829-JAX,RRID:MMRRC_034829-JAX)

Curator: @scibot

SciCrunch record: RRID:MMRRC_034829-JAX

What is this?

DOI: 10.1186/s40478-026-02240-y

Resource: (Sigma-Aldrich Cat# G3893, RRID:AB_477010)

Curator: @scibot

SciCrunch record: RRID:AB_477010

What is this?

DOI: 10.1186/s40478-026-02240-y

Resource: (EnCor Biotechnology Cat# MCA-5C10, RRID:AB_2572311)

Curator: @scibot

SciCrunch record: RRID:AB_2572311

What is this?

DOI: 10.1186/s40478-026-02240-y

Resource: RRID:AB_3678889

Curator: @scibot

SciCrunch record: RRID:AB_3678889

What is this?

DOI: 10.1186/s40478-026-02240-y

Resource: (EnCor Biotechnology Cat# CPCA-GFAP, RRID:AB_2109953)

Curator: @scibot

SciCrunch record: RRID:AB_2109953

What is this?

DOI: 10.1186/s40478-026-02240-y

Resource: (Enzo Life Sciences Cat# BML-FG6090-0100, RRID:AB_2050678)

Curator: @scibot

SciCrunch record: RRID:AB_2050678

What is this?

DOI: 10.1186/s40478-026-02240-y

Resource: RRID:AB_3678888

Curator: @scibot

SciCrunch record: RRID:AB_3678888

What is this?

DOI: 10.1186/s40478-026-02240-y

Resource: RRID:AB_3711244

Curator: @scibot

SciCrunch record: RRID:AB_3711244

What is this?

DOI: 10.1186/s40478-026-02240-y

Resource: (Agilent Cat# Z0334, RRID:AB_10013382)

Curator: @scibot

SciCrunch record: RRID:AB_10013382

What is this?

DOI: 10.1183/23120541.01305-2025

Resource: RRID:SCR_026314

Curator: @scibot

SciCrunch record: RRID:SCR_026314

What is this?

DOI: 10.1182/bloodadvances.2025016898

Resource: GraphPad Prism (RRID:SCR_002798)

Curator: @scibot

SciCrunch record: RRID:SCR_002798

What is this?

DOI: 10.1182/bloodadvances.2025016898

Resource: BioTek Synergy H1 Hybrid Multi-Mode Microplate Reader (RRID:SCR_019748)

Curator: @scibot

SciCrunch record: RRID:SCR_019748

What is this?

DOI: 10.1182/bloodadvances.2025016898

Resource: (RRID:CVCL_0063)

Curator: @scibot

SciCrunch record: RRID:CVCL_0063

What is this?

DOI: 10.1182/bloodadvances.2025016898

Resource: (ECACC Cat# 92111706, RRID:CVCL_2481)

Curator: @scibot

SciCrunch record: RRID:CVCL_2481

What is this?

DOI: 10.1182/bloodadvances.2025016898

Resource: (DSMZ Cat# ACC-608, RRID:CVCL_2187)

Curator: @scibot

SciCrunch record: RRID:CVCL_2187

What is this?