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    1. karim2001khoury 19 Feb 2026
      Oncogenic mutations of PIK3CA lead to increased membrane recruitment driven by reorientation of the ABD, p85 and C-terminus

      [Paper-level Aggregated] PMCID: PMC9837058

      Evidence Type(s): Oncogenic, Functional, Predictive

      Justification: Oncogenic: The text discusses multiple mutations (e.g., H1047R, G1049R, M1043L, N1068fs) that are frequently observed in cancer and describes their role in activating the PI3K pathway, indicating their oncogenic potential. Functional: The evidence describes how specific mutations (H1047R, G1049R, M1043L) lead to increased ATPase activity and enhanced membrane binding, demonstrating their functional impact on the PI3K enzyme activity. Predictive: The identification of specific mutations associated with increased membrane binding and PI3K activity suggests that these mutations could be used to predict the behavior of tumors and their response to therapies targeting the PI3K pathway.

      Gene→Variant (gene-first): PIK3CA(5290):D915N PIK3CA(5290):E726K PIK3CA(5290):G1049R PIK3CA(5290):H1047R PIK3CA(5290):H1047R/L PIK3CA(5290):M1043L PIK3CA(5290):M1043L/I PIK3CA(5290):N1044K PIK3CA(5290):N1068fs PIK3CA(5290):M1043I/L PIK3CA(5290):G106V PIK3CA(5290):G118D PIK3CA(5290):N345K PIK3CA(5290):His1047 PIK3CA(5290):Met1043

      Genes: PIK3CA(5290)

      Variants: D915N E726K G1049R H1047R H1047R/L M1043L M1043L/I N1044K N1068fs M1043I/L G106V G118D N345K His1047 Met1043

      CIViC paper-level aggregated PMC9837058
    2. karim2001khoury 19 Feb 2026
      PIK3CA encoding the phosphoinositide 3-kinase (PI3K) p110alpha catalytic subunit is frequently mutated in cancer, with mutations occurring widely throughout the primary sequence. The full set of mechanisms underlying how

      [Paragraph-level] PMCID: PMC9837058 Section: ABSTRACT PassageIndex: 1

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses how mutations in PIK3CA, including G1049R, H1047R, and M1043I/L, contribute to the activation of the PI3K pathway, indicating their role in tumor development or progression. Functional: The passage describes how specific mutations alter the conformation and binding properties of the p110alpha subunit, indicating that these variants affect molecular function related to PI3K activation.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043I/L

      Genes: 5290

      Variants: G1049R H1047R M1043I/L

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    3. karim2001khoury 19 Feb 2026
      We also compared HDX-MS differences in full-length p110alpha-p85alpha between WT, H1047R and DeltaC in the presence and absence of pY (Supplementary Fig. 6). The binding of pY led to significant increases for all three c

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 19

      Evidence Type(s): Functional

      Justification: Functional: The passage discusses how the H1047R variant alters the binding interactions and structural dynamics of the protein in response to pY binding, indicating a change in molecular function.

      Gene→Variant (gene-first): 5290:H1047R

      Genes: 5290

      Variants: H1047R

      CIViC paragraph-level PMC9837058 Functional
    4. karim2001khoury 19 Feb 2026
      The H1047R, G1049R, and the DeltaCter constructs showed similar significant increases compared to the WT in the kinase domain (Fig. 5A-C). These included regions covering 850-858 (hinge between the N and C lobes), the ac

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 18

      Evidence Type(s): Functional, Oncogenic

      Justification: Functional: The passage discusses how the H1047R and G1049R variants alter the molecular interactions and conformations within the kinase domain, indicating a change in biochemical function related to the protein's activity. Oncogenic: The evidence suggests that the H1047R and G1049R variants contribute to activation through disruption of the inhibitory conformation, which is indicative of their role in tumor development or progression.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043L 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R M1043L N1068fs

      CIViC paragraph-level PMC9837058 Functional Oncogenic
    5. karim2001khoury 19 Feb 2026
      HDX-MS experiments were carried out for 4-5 timepoints of exchange (3 s at 1 C, 3, 30, 300, and 3000 s at 20 C) for each complex. The full set of all peptides analysed for both p110alpha and p85alpha are shown in the Sou

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 17

      Evidence Type(s): Functional

      Justification: Functional: The passage discusses changes observed for the H1047R variant in the context of HDX-MS experiments, indicating that it alters molecular or biochemical function, specifically in terms of perturbations in conformation.

      Gene→Variant (gene-first): 5290:H1047R

      Genes: 5290

      Variants: H1047R

      CIViC paragraph-level PMC9837058 Functional
    6. karim2001khoury 19 Feb 2026
      To test if C-terminal mutations worked by disrupting the inhibitory interaction with the C-terminus, we carried out HDX-MS studies on six constructs of full-length p110alpha (WT, M1043L, H1047R, G1049R, N1068fs, and a co

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 16

      Evidence Type(s): Functional, Oncogenic

      Justification: Functional: The passage discusses how C-terminal mutations, including M1043L, H1047R, G1049R, and N1068fs, affect the inhibitory interaction with the C-terminus, indicating an alteration in molecular function. Oncogenic: The mention of "oncogenic mutation" in relation to M1043L, H1047R, and G1049R suggests that these somatic variants contribute to tumor development or progression.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043L 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R M1043L N1068fs

      CIViC paragraph-level PMC9837058 Functional Oncogenic
    7. karim2001khoury 19 Feb 2026
      For these mutants, we had difficulty in obtaining sufficient yield of the proteins for extensive biophysical analysis. To circumvent this, we used the kinase dead variants to characterise their membrane binding using pro

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 14

      Evidence Type(s): Functional, Oncogenic

      Justification: Functional: The passage discusses how the variants H1047R, G1049R, M1043L, and N1068fs alter membrane binding and ATPase activity, indicating changes in molecular function. Oncogenic: The variants are described in the context of their effects on membrane binding and ATPase activity, which suggests a role in tumor development or progression.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043L 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R M1043L N1068fs

      CIViC paragraph-level PMC9837058 Functional Oncogenic
    8. karim2001khoury 19 Feb 2026
      We characterised the intrinsic ATPase activity of each p110alpha mutant (Fig. 4A + B), and while this assay does not measure biologically relevant PIP3 activity, it can measure intrinsic differences in PI3K activity inde

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 13

      Evidence Type(s): Functional, Oncogenic

      Justification: Functional: The passage discusses the intrinsic ATPase activity of the p110alpha mutants, indicating that the variants G1049R, H1047R, and M1043L alter molecular function by exhibiting significantly increased ATPase activity compared to wild type. Oncogenic: The context of the passage implies that the variants are somatic mutations in a cancer-related gene, contributing to tumor development or progression through their altered biochemical activity.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043L 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R M1043L N1068fs

      CIViC paragraph-level PMC9837058 Functional Oncogenic
    9. karim2001khoury 19 Feb 2026
      To understand the regulatory mechanisms underlying the inhibitory interface with the C-terminus we analysed the most frequent oncogenic mutants that occur at or near this interface. While H1047R/L is the most frequent mu

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 12

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses frequent oncogenic mutants and their role in tumor samples, indicating that these variants contribute to tumor development or progression. Functional: The analysis of the mutants and their binding to full-length p85alpha suggests that these variants alter molecular or biochemical function, specifically in the context of their interaction with regulatory complexes.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:H1047R/L 5290:M1043L 5290:M1043L/I 5290:N1044K 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R H1047R/L M1043L M1043L/I N1044K N1068fs

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    10. karim2001khoury 19 Feb 2026
      While the disengagement of the ABD and p85 being involved in membrane binding provides a molecular rationale for activation by oncogenic mutations in the ABD, C2, and helical domains, it does not fully explain the molecu

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 11

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses the H1047R mutation in the context of its role in activating the kinase domain and increasing membrane binding, indicating its contribution to tumor development or progression. Functional: The passage describes how the H1047R mutation alters the molecular interactions and structural organization of the kinase domain, affecting its binding properties and functionality.

      Gene→Variant (gene-first): 5290:H1047R 5290:His1047 5290:Met1043

      Genes: 5290

      Variants: H1047R His1047 Met1043

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    11. karim2001khoury 19 Feb 2026
      When comparing our data to the full set of missense oncogenic mutations in the ABD, ABD-RBD linker, C2, helical and the N-lobe of the kinase domain we find that all mutations found in >30 tumours except one (E726K) are l

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 9

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses the E726K variant in the context of oncogenic mutations and its association with conformational changes that contribute to tumor development, indicating its role in cancer progression. Functional: The passage describes how the E726K variant leads to conformational changes affecting the interaction between the ABD and p85 with the catalytic core, suggesting an alteration in molecular function.

      Gene→Variant (gene-first): 5290:E726K

      Genes: 5290

      Variants: E726K

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    12. karim2001khoury 19 Feb 2026
      We have extensively characterised the membrane binding of the p110alpha/p85alpha complex using HDX-MS, however, the disengagement of the ABD and p85 from the catalytic core has likely complicated the analysis of membrane

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 8

      Evidence Type(s): Functional

      Justification: Functional: The passage discusses how the N345K variant affects the molecular interactions and binding of the p110alpha/p85alpha complex to membranes, indicating an alteration in biochemical function.

      Gene→Variant (gene-first): 5290:N345K

      Genes: 5290

      Variants: N345K

      CIViC paragraph-level PMC9837058 Functional
    13. karim2001khoury 19 Feb 2026
      This data comparing the full-length heterodimer vs p110alpha core allowed us to define the effect of ABD removal on the contact site at the ABD-RBD linker. This region still is protected from exchange at early time point

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 4

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses oncogenic mutants (N345K, G106V, and G118D) and their expected role in promoting ABD/iSH2 disengagement, indicating their contribution to tumor development or progression. Functional: The data suggests that the variants alter the dynamics of the ABD-p85 complex and its interaction with the p110alpha catalytic core, indicating a change in molecular function related to binding and mobility.

      Gene→Variant (gene-first): 5290:G106V 5290:G118D 5290:N345K

      Genes: 5290

      Variants: G106V G118D N345K

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    14. karim2001khoury 19 Feb 2026
      To investigate the role of the ABD domain/p85 regulatory subunit in controlling PI3K enzyme activity, we needed a construct that allowed us to interrogate the dynamic effects of full ABD disengagement. We engineered and

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 2

      Evidence Type(s): Functional

      Justification: Functional: The passage discusses the D915N mutation in the context of its effect on protein conformation and membrane binding, indicating that it alters molecular function as assessed by HDX-MS experiments.

      Gene→Variant (gene-first): 5290:D915N

      Genes: 5290

      Variants: D915N

      CIViC paragraph-level PMC9837058 Functional
    15. karim2001khoury 19 Feb 2026
      PIK3CA encoding the phosphoinositide 3-kinase (PI3K) p110alpha catalytic subunit is frequently mutated in cancer, with mutations occurring widely throughout the primary sequence. The full set of mechanisms underlying how

      [Paragraph-level] PMCID: PMC9837058 Section: ABSTRACT PassageIndex: 1

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses how mutations in PIK3CA, including G1049R, H1047R, and M1043I/L, contribute to the activation of the PI3K pathway, indicating their role in tumor development or progression. Functional: The passage describes how specific mutations alter the conformation and binding properties of the p110alpha subunit, indicating that these variants affect molecular function related to PI3K activation.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043I/L

      Genes: 5290

      Variants: G1049R H1047R M1043I/L

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    16. karim2001khoury 19 Feb 2026
      We also compared HDX-MS differences in full-length p110alpha-p85alpha between WT, H1047R and DeltaC in the presence and absence of pY (Supplementary Fig. 6). The binding of pY led to significant increases for all three c

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 19

      Evidence Type(s): Functional

      Justification: Functional: The passage discusses how the H1047R variant alters the binding interactions and structural dynamics of the protein in response to pY binding, indicating a change in molecular function.

      Gene→Variant (gene-first): 5290:H1047R

      Genes: 5290

      Variants: H1047R

      CIViC paragraph-level PMC9837058 Functional
    17. karim2001khoury 19 Feb 2026
      The H1047R, G1049R, and the DeltaCter constructs showed similar significant increases compared to the WT in the kinase domain (Fig. 5A-C). These included regions covering 850-858 (hinge between the N and C lobes), the ac

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 18

      Evidence Type(s): Functional, Oncogenic

      Justification: Functional: The passage discusses how the H1047R and G1049R variants alter the molecular interactions and conformations within the kinase domain, indicating a change in biochemical function related to the protein's activity. Oncogenic: The evidence suggests that the H1047R and G1049R variants contribute to activation through disruption of the inhibitory conformation, which is indicative of their role in tumor development or progression.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043L 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R M1043L N1068fs

      CIViC paragraph-level PMC9837058 Functional Oncogenic
    18. karim2001khoury 19 Feb 2026
      HDX-MS experiments were carried out for 4-5 timepoints of exchange (3 s at 1 C, 3, 30, 300, and 3000 s at 20 C) for each complex. The full set of all peptides analysed for both p110alpha and p85alpha are shown in the Sou

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 17

      Evidence Type(s): Functional

      Justification: Functional: The passage discusses changes observed for the H1047R variant in the context of HDX-MS experiments, indicating that it alters molecular or biochemical function, specifically in terms of perturbations in conformation.

      Gene→Variant (gene-first): 5290:H1047R

      Genes: 5290

      Variants: H1047R

      CIViC paragraph-level PMC9837058 Functional
    19. karim2001khoury 19 Feb 2026
      To test if C-terminal mutations worked by disrupting the inhibitory interaction with the C-terminus, we carried out HDX-MS studies on six constructs of full-length p110alpha (WT, M1043L, H1047R, G1049R, N1068fs, and a co

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 16

      Evidence Type(s): Functional, Oncogenic

      Justification: Functional: The passage discusses how C-terminal mutations, including M1043L, H1047R, G1049R, and N1068fs, affect the inhibitory interaction with the C-terminus, indicating an alteration in molecular function. Oncogenic: The mention of "oncogenic mutation" in relation to M1043L, H1047R, and G1049R suggests that these somatic variants contribute to tumor development or progression.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043L 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R M1043L N1068fs

      CIViC paragraph-level PMC9837058 Functional Oncogenic
    20. karim2001khoury 19 Feb 2026
      For these mutants, we had difficulty in obtaining sufficient yield of the proteins for extensive biophysical analysis. To circumvent this, we used the kinase dead variants to characterise their membrane binding using pro

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 14

      Evidence Type(s): Functional, Oncogenic

      Justification: Functional: The passage discusses how the variants H1047R, G1049R, M1043L, and N1068fs alter membrane binding and ATPase activity, indicating changes in molecular function. Oncogenic: The variants are described in the context of their effects on membrane binding and ATPase activity, which suggests a role in tumor development or progression.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043L 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R M1043L N1068fs

      CIViC paragraph-level PMC9837058 Functional Oncogenic
    21. karim2001khoury 19 Feb 2026
      We characterised the intrinsic ATPase activity of each p110alpha mutant (Fig. 4A + B), and while this assay does not measure biologically relevant PIP3 activity, it can measure intrinsic differences in PI3K activity inde

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 13

      Evidence Type(s): Functional, Oncogenic

      Justification: Functional: The passage discusses the intrinsic ATPase activity of the p110alpha mutants, indicating that the variants G1049R, H1047R, and M1043L alter molecular function by exhibiting significantly increased ATPase activity compared to wild type. Oncogenic: The context of the passage implies that the variants are somatic mutations in a cancer-related gene, contributing to tumor development or progression through their altered biochemical activity.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:M1043L 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R M1043L N1068fs

      CIViC paragraph-level PMC9837058 Functional Oncogenic
    22. karim2001khoury 19 Feb 2026
      To understand the regulatory mechanisms underlying the inhibitory interface with the C-terminus we analysed the most frequent oncogenic mutants that occur at or near this interface. While H1047R/L is the most frequent mu

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 12

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses frequent oncogenic mutants and their role in tumor samples, indicating that these variants contribute to tumor development or progression. Functional: The analysis of the mutants and their binding to full-length p85alpha suggests that these variants alter molecular or biochemical function, specifically in the context of their interaction with regulatory complexes.

      Gene→Variant (gene-first): 5290:G1049R 5290:H1047R 5290:H1047R/L 5290:M1043L 5290:M1043L/I 5290:N1044K 5290:N1068fs

      Genes: 5290

      Variants: G1049R H1047R H1047R/L M1043L M1043L/I N1044K N1068fs

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    23. karim2001khoury 19 Feb 2026
      While the disengagement of the ABD and p85 being involved in membrane binding provides a molecular rationale for activation by oncogenic mutations in the ABD, C2, and helical domains, it does not fully explain the molecu

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 11

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses the H1047R mutation in the context of its role in activating the kinase domain and increasing membrane binding, indicating its contribution to tumor development or progression. Functional: The passage describes how the H1047R mutation alters the molecular interactions and structural organization of the kinase domain, affecting its binding properties and functionality.

      Gene→Variant (gene-first): 5290:H1047R 5290:His1047 5290:Met1043

      Genes: 5290

      Variants: H1047R His1047 Met1043

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    24. karim2001khoury 19 Feb 2026
      When comparing our data to the full set of missense oncogenic mutations in the ABD, ABD-RBD linker, C2, helical and the N-lobe of the kinase domain we find that all mutations found in >30 tumours except one (E726K) are l

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 9

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses the E726K variant in the context of oncogenic mutations and its association with conformational changes that contribute to tumor development, indicating its role in cancer progression. Functional: The passage describes how the E726K variant leads to conformational changes affecting the interaction between the ABD and p85 with the catalytic core, suggesting an alteration in molecular function.

      Gene→Variant (gene-first): 5290:E726K

      Genes: 5290

      Variants: E726K

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    25. karim2001khoury 19 Feb 2026
      We have extensively characterised the membrane binding of the p110alpha/p85alpha complex using HDX-MS, however, the disengagement of the ABD and p85 from the catalytic core has likely complicated the analysis of membrane

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 8

      Evidence Type(s): Functional

      Justification: Functional: The passage discusses how the N345K variant affects the molecular interactions and binding of the p110alpha/p85alpha complex to membranes, indicating an alteration in biochemical function.

      Gene→Variant (gene-first): 5290:N345K

      Genes: 5290

      Variants: N345K

      CIViC paragraph-level PMC9837058 Functional
    26. karim2001khoury 19 Feb 2026
      This data comparing the full-length heterodimer vs p110alpha core allowed us to define the effect of ABD removal on the contact site at the ABD-RBD linker. This region still is protected from exchange at early time point

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 4

      Evidence Type(s): Oncogenic, Functional

      Justification: Oncogenic: The passage discusses oncogenic mutants (N345K, G106V, and G118D) and their expected role in promoting ABD/iSH2 disengagement, indicating their contribution to tumor development or progression. Functional: The data suggests that the variants alter the dynamics of the ABD-p85 complex and its interaction with the p110alpha catalytic core, indicating a change in molecular function related to binding and mobility.

      Gene→Variant (gene-first): 5290:G106V 5290:G118D 5290:N345K

      Genes: 5290

      Variants: G106V G118D N345K

      CIViC paragraph-level PMC9837058 Oncogenic Functional
    27. karim2001khoury 19 Feb 2026
      To investigate the role of the ABD domain/p85 regulatory subunit in controlling PI3K enzyme activity, we needed a construct that allowed us to interrogate the dynamic effects of full ABD disengagement. We engineered and

      [Paragraph-level] PMCID: PMC9837058 Section: RESULTS PassageIndex: 2

      Evidence Type(s): Functional

      Justification: Functional: The passage discusses the D915N mutation in the context of its effect on protein conformation and membrane binding, indicating that it alters molecular function as assessed by HDX-MS experiments.

      Gene→Variant (gene-first): 5290:D915N

      Genes: 5290

      Variants: D915N

      CIViC paragraph-level PMC9837058 Functional
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