BiFET

ImmunoOncology

BiFET identifies TFs whose footprints are over-represented in target regions compared to background regions after correcting for the bias arising from the imbalance in read counts and GC contents between the target and background regions. For a given TF k, BiFET tests the null hypothesis that the target regions have the same probability of having footprints for the TF k as the background regions while correcting for the read count and GC content bias. For this, we use the number of target regions with footprints for TF k, t_k as a test statistic and calculate the p-value as the probability of observing t_k or more target regions with footprints under the null hypothesis.

Source attribution

  • BioconductorBiFET

Related resources

TENET identifies key transcription factors (TFs) and regulatory elements (REs) linked to a specific cell type by finding significantly correlated differences in gene expression and RE DNA methylation between case and control input datasets, and identifying the top genes by number of significant RE DNA methylation site links. It also includes many tools for visualization and analysis of the results, including plots displaying and comparing methylation and expression data and methylation site link counts, survival analysis, TF motif searching in the vicinity of linked RE DNA methylation sites, custom TAD and peak overlap analysis, and UCSC Genome Browser track file generation. A utility function is also provided to download methylation, expression, and patient survival data from The Cancer Genome Atlas (TCGA) for use in TENET or other analyses.

Integrates various levels of epigenomic information, including ChIP-seq, histone modification, ATAC-seq, and RNA-seq data. Regulatory network analysis uses combinatory approaches to infer regions of significance, such as enhancers. Downstream analysis identifies co-occurrence of epigenomic data at regions of interest. Visualization functions display multi-track genomic views with signal overlays. Please contact <ammawla@ucdavis.edu> for suggestions, feedback, or bug reporting.

This package provides ISoLDE a new method for identifying imprinted genes. This method is dedicated to data arising from RNA sequencing technologies. The ISoLDE package implements original statistical methodology described in the publication below.

Compute differentially bound sites from multiple ChIP-seq experiments using affinity (quantitative) data. Also enables occupancy (overlap) analysis and plotting functions.

Genetic variants associated with diseases often affect non-coding regions, thus likely having a regulatory role. To understand the effects of genetic variants in these regulatory regions, identifying genes that are modulated by specific regulatory elements (REs) is crucial. The effect of gene regulatory elements, such as enhancers, is often cell-type specific, likely because the combinations of transcription factors (TFs) that are regulating a given enhancer have cell-type specific activity. This TF activity can be quantified with existing tools such as diffTF and captures differences in binding of a TF in open chromatin regions. Collectively, this forms a gene regulatory network (GRN) with cell-type and data-specific TF-RE and RE-gene links. Here, we reconstruct such a GRN using single-cell or bulk RNAseq and open chromatin (e.g., using ATACseq or ChIPseq for open chromatin marks) and optionally (Capture) Hi-C data. Our network contains different types of links, connecting TFs to regulatory elements, the latter of which is connected to genes in the vicinity or within the same chromatin domain (TAD). We use a statistical framework to assign empirical FDRs and weights to all links using a permutation-based approach.

Provides an interface to several normalization and statistical testing packages for RNA-Seq gene expression data. Additionally, it creates several diagnostic plots, performs meta-analysis by combinining the results of several statistical tests and reports the results in an interactive way.