Author: Timothy A. Dinh; Ramja Sritharan; F. Donelson Smith; Adam B. Francisco; Rosanna K. Ma; Rodica P. Bunaciu; Matt Kanke; Charles G. Danko; Andrew P. Massa; John D. Scott; Praveen Sethupathy
Title: Hotspots of aberrant enhancer activity in fibrolamellar carcinoma reveal molecular mechanisms of oncogenesis and intrinsic drug resistance Document date: 2020_1_18
ID: bf4qpsy7_59
Snippet: Gene definitions were obtained from GENCODE v25 annotations. To avoid counting reads from the paused polymerase peak, ChRO-seq signal was quantified on the sense strand from 500 bp downstream of the gene start until the annotated end of the gene. Genes were eliminated from the analysis if they were shorter than 1000 bp and if they were not protein coding, pseudogene, lincRNA, antisense, or miRNA genes. Like TRE counts, gene body counts from ChRO-.....
Document: Gene definitions were obtained from GENCODE v25 annotations. To avoid counting reads from the paused polymerase peak, ChRO-seq signal was quantified on the sense strand from 500 bp downstream of the gene start until the annotated end of the gene. Genes were eliminated from the analysis if they were shorter than 1000 bp and if they were not protein coding, pseudogene, lincRNA, antisense, or miRNA genes. Like TRE counts, gene body counts from ChRO-seq followed a negative binomial distribution. Therefore, differential transcription analysis of genes was performed using DESeq2.
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