592 Matching Annotations
  1. Dec 2017
  2. alleledb.gersteinlab.org alleledb.gersteinlab.org
  3. Nov 2017
    1. These results suggest that deep sequencing is necessary for accurate determination of the expression level of genes

      or better quantification methods

    1. EGR2 peaks overlapped with a SOX10 peak when allowing separation distance as large as 1000 bp and 11.09% of the SOX10 peaks overlapped with an EGR2 peak with the same separation distance

      unclear

    1. CRISPR screening has emerged as a powerful method for identifying critical functional dependencies in vitro (Koike-Yusa et al., 2014xGenome-wide recessive genetic screening in mammalian cells with a lentiviral CRISPR-guide RNA library. Koike-Yusa, H., Li, Y., Tan, E.-P., Velasco-Herrera, Mdel.C., and Yusa, K. Nat. Biotechnol. 2014; 32: 267–273Crossref | PubMed | Scopus (285)See all References, Shalem et al., 2014xGenome-scale CRISPR-Cas9 knockout screening in human cells. Shalem, O., Sanjana, N.E., Hartenian, E., Shi, X., Scott, D.A., Mikkelson, T., Heckl, D., Ebert, B.L., Root, D.E., Doench, J.G., and Zhang, F. Science. 2014; 343: 84–87Crossref | PubMed | Scopus (936)See all References)
    1. Clone 1 is the founding clone; 12.74% of the tumour cells contain only this set of mutations

      derivation unclear; not provided in supplemental information

    1. tier 1 contains all changes in the amino acid coding regions of annotated exons, consensus splice-site regions, and RNA genes (including microRNA genes). Tier 2 contains changes in highly conserved regions of the genome or regions that have regulatory potential. Tier 3 contains mutations in the nonrepetitive part of the genome that does not meet tier 2 criteria, and tier 4 contains mutations in the remainder of the genome
  4. Oct 2017
    1. Using their expression data and the same fold-change categories, we investigated the influence of both affinity and cooperative effects based on GraphProt predictions of Ago2 binding sites in comparison to the available CLIP-seq data.

      Could do the same since expression microarray data are available, but they show complete lack of differential expression when over-expressing our proteins of interest.

    2. allows the evaluation of putative binding sites with a meaningful score that reflects the biological functionality

      score = prediction margin Part of standard GraphProt output?

    3. The following describes a typical biological application of computational target detection. A published CLIP-seq experiment for a protein of interest is available for kidney cells, but the targets of that protein are required for liver cells. The original CLIP-seq targets may have missed many correct targets due to differential expression in the two tissues and the costs for a second CLIP-seq experiment in liver cells may not be within the budget or the experiment is otherwise not possible. We provide a solution that uses an accurate protein-binding model from the kidney CLIP-seq data, which can be used to identify potential targets in the entire transcriptome. Transcripts targeted in liver cells can be identified with improved specificity when target prediction is combined with tissue-specific transcript expression data.

      use case

    4. Peak detection leads to high-fidelity binding sites; however, it again increases the number of false negatives. Therefore, to complete the RBP interactome, computational discovery of missing binding sites is essential.

      iCLIP data are not comprehensive

    1. equal to the frequency of the higher expressed eQTL allele in the population

      should be equal to product of frequency of high eQTL allele and major coding allele, though the latter will be close to 1 for the rare coding mutations studied here

  5. Sep 2017
  6. Aug 2017
  7. Jul 2017
  8. Jun 2017
  9. Apr 2017
  10. Sep 2016
    1. The P. tetraurelia MAC genome [1] was assembled from 13× Sanger sequencing reads from different insert size librairies of strain d4-2 DNA. Strain d4-2 only differs from strain 51 at a few loci.

      SRA accession ERR138952

    1. You must quit IGV and restart for this preference to take effect. The genome should appear in the drop-down list.

      restart may be insufficient; had to modify prefs.properties in ~/igv (removing old cached genome values) before i could see my genomes

  11. Aug 2016
    1. One currentproject in Dr Schulz’s lab is to characterise a selection of interesting loci in detailusingisoform specific primers and qRT-PCR.

      Would be better to end with making an explicit connection between the ENCODE tissue-specific RNAseq data and the Setd2 knock-down RNAseq data. Would it make sense to focus on loci showing evidence for tissue-specific polyA as well as being dependent on Setd2 for correct splicing?

    2. For some loci even the used tissues can differ in terms of strainand developmental stage between the qRT-PCRand bisulfite sequencing.

      German sentence structure: splitting the predicate (differ ... between). Not done in English. very awkward to read.

    3. Presumed that themechanism of poly(A) site selection/alternative polyadenylation may operate genome-wide in a tissue-specificmanner,and thus, contribute to the complexity of the mammalian transcriptome,

      use of very long prepositional phrases at the start of sentences makes reading difficult. stick to simple subject- predicate- object sentence structure.

    4. AAA indicates poly(A) site

      nice and useful figure but: you primed the cDNA synthesis with random hexamers. the qRT-PCR results are therefore not specific to polyadenylated transcripts. so, above figure shows models consistent with the data rather than summarisations of the data (you did not directly measure polyA).

    5. Based on the RNA-seq data

      depends in this case on whether you look at the scatter plot or the UCSC genome browser: they are not telling the same story for some reason. my corrections below reflect what UCSC shows, which results in flipping of placenta and thymus.

    6. Adck2 encodes for a kinase

      The host transcript of the CGI is non-coding. Your upstream primers amplify both the coding transcript and the non-coding host transcript. That is a limitation. Could explain the inconsistencies re the RNAseq data.

    7. qRT-PCR

      qRT-PCR cannot show transcription termination: all it can do is verify the RNAseq data, i.e., more relatively more transcription upstream of an active CGI compared to transcription across the CGI. It is important to be precise about what qRT-PCR can and cannot do.

    8. 1) Tissue with high CGI activity and more transcripts terminating upstream than across and 2) Tissue with lowCGI activity and more transcripts terminating across than upstream, as described in the chapter ‘Loci selection’.

      The data do not show transcripts terminating upstream or downstream of the CGI, they are merely consistent with the hypothesis.

    Tags

    Annotators