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  1. ...) and tissues (Fig. 3D–G). We find that in promoters the proportion of TEs in open chromatin decreases toward a transcription start site (TSS) and the gene body, probably reflecting increased purifying selection pressure (less tolerance for TE insertions) inside the gene body.Furthermore, we find that close...
  2. ...correction applied).TE-chimeric transcript–derived peptides are validated as putative neoantigensTo overcome the resistance associated with LTR7-PLAAT4 and target lethal cancers driven by aberrant epigenetic activation of TEs, we turned to recent investigations that revealed the capacity of TEs in harboring...
  3. .... 2021). Similarly, we calculated the promoter nucleosome occupancy for the same fragment size range 250 bp upstream of every TSS to capture differences in promoter architecture.View larger version: In this window In a new window Figure 2. Chromatin occupancy profiling simultaneously reveals nucleosome...
  4. ...may enable extruding cohesin motors to bypass individual sites. In vivo, however, no existing approach can concomitantly track multiple genomic positions, cohesin, and CTCF and read out their instantaneous occupancy in real time.View larger version: In this window In a new window Figure 1. Dynamic...
  5. ...as a major contributing caller to reach final consensus calls by The Cancer Genome Atlas (TCGA) PanCanAtlas project (Ellrott et al. 2018), across approximately 13,000 tumor samples, and the International Cancer Genome Consortium Pan-Cancer Analysis of Whole Genomes (ICGC-PCAWG) initiative (The ICGC/TCGA Pan...
  6. ...suspected, in particular for the latter, that those sites were the result of genotyping error. An inspection of quality metrics indeed revealed significantly lower quality in the offspring (Supplemental Fig. S2A) as well as significantly lower depth and genotype quality in the parent for sites that would...
  7. ....2 ×10 −16) shows that binding-site composition and helical orientation refine accessibility-driven predictions, underscoring their interconnected roles in collectively influencing TP53 family-nucleosome binding. Our current model focuses on explaining in vitro binding; extending it to predict in vivo...
  8. ...to mediate 57 consistent phenotypic outcomes there must also be consistent regulation of such genes by 58 cis-regulatory modules (CRMs). CRMs consist of clusters of transcription factor binding sites 59 (TFBSs) that regulate the expression of target genes through collective or competitive binding 60...
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  9. ...selection (Supplemental Fig. S7). It revealed that the largest fraction of nucleosomes repositioned in CLL versus NBCs resides in 700,000 regions of 100-bp size. These loci were termed “variable” because their nucleosome occupancy significantly varied across CLL patients while being stable across all NBC...
  10. ...sequences, both in UV-irradiated yeast cells and in human skin cancers. CPD deamination is suppressed near the transcription start and end sites of yeast genes, which may in part by mediated by DNA-bound transcription factors. Finally, we show that the wrapping of DNA in nucleosomes modulates CPD...
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