hmChIP: a database and web server for exploring publicly available human and mouse ChIP-seq and ChIP-chip data

Chen, Li; Wu, George Y.; Ji, Hongkai

doi:10.1093/bioinformatics/btr156

Cited by 47 publications

(48 citation statements)

References 14 publications

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“…For each gene, we defined the promoter region as the 1000 bases upstream of the start of the longest gene transcript, as annotated in the RefSeq database(Pruitt et al, 2009). We compiled a total of 1867 TF binding motif models (in the form of position weight matrices) from the following sources (Transfac(Matys et al, 2006); JASPAR(Portales-Casamar et al, 2010); FactorBook(Wang et al, 2013); UniProbe(Robasky and Bulyk, 2011); hmCHIP(Chen et al, 2011); Jolma(Jolma et al, 2013)), which in total cover 623 distinct human TFs. We then used the Pscan software package(Zambelli et al, 2009) to rank all TF motifs based on their enrichment in the chr 5q gene set, as compared to random expectation based on background distributions obtained by scanning all RefSeq promoters.…”

Section: Methodsmentioning

confidence: 99%

Myeloid Malignancies with Chromosome 5q Deletions Acquire a Dependency on an Intrachromosomal NF-κB Gene Network

Fang¹,

Barker²,

Bolanos³

et al. 2014

Cell Reports

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Summary Chromosome 5q deletions (del(5q)) are common in high-risk (HR) myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML); however, the gene regulatory networks that sustain these aggressive diseases are unknown. Reduced miR-146a expression in del(5q) HR-MDS/AML and miR-146a−/− hematopoietic stem/progenitor cells (HSPC) results in TRAF6/NF-kB activation. Increased survival and proliferation of HSPC from miR-146alow HR-MDS/AML is sustained by a neighboring haploid gene, SQSTM1 (p62), expressed from the intact 5q allele. Overexpression of p62 from the intact allele occurs through NF-kB-dependent feedforward signaling mediated by miR-146a deficiency. p62 is necessary for TRAF6-mediated NF-kB signaling, as disrupting the p62-TRAF6 signaling complex results in cell cycle arrest and apoptosis of MDS/AML cells. Thus, del(5q) HR-MDS/AML employs an intrachromosomal gene network involving loss of miR-146a and haploid overexpression of p62 via NF-kB to sustain TRAF6/NF-kB signaling for cell survival and proliferation. Interfering with the p62-TRAF6 signaling complex represents a therapeutic option in miR-146a-deficient and aggressive del(5q) MDS/AML.

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Section: Methodsmentioning

confidence: 99%

Myeloid Malignancies with Chromosome 5q Deletions Acquire a Dependency on an Intrachromosomal NF-κB Gene Network

Fang¹,

Barker²,

Bolanos³

et al. 2014

Cell Reports

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“…The regulatory relationships were inferred based on ChIP-Seq data collected under 777 different conditions in the hmChip database [43] and transcription factors from the UCSC Genome Browser [40].…”

Section: Methodsmentioning

confidence: 99%

Elucidation of How Cancer Cells Avoid Acidosis through Comparative Transcriptomic Data Analysis

Mao

Mehta

et al. 2013

PLoS ONE

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The rapid growth of cancer cells fueled by glycolysis produces large amounts of protons in cancer cells, which tri mechanisms to transport them out, hence leading to increased acidity in their extracellular environments. It has been well established that the increased acidity will induce cell death of normal cells but not cancer cells. The main question we address here is: how cancer cells deal with the increased acidity to avoid the activation of apoptosis. We have carried out a comparative analysis of transcriptomic data of six solid cancer types, breast, colon, liver, two lung (adenocarcinoma, squamous cell carcinoma) and prostate cancers, and proposed a model of how cancer cells utilize a few mechanisms to keep the protons outside of the cells. The model consists of a number of previously, well or partially, studied mechanisms for transporting out the excess protons, such as through the monocarboxylate transporters, V-ATPases, NHEs and the one facilitated by carbonic anhydrases. In addition we propose a new mechanism that neutralizes protons through the conversion of glutamate to γ-aminobutyrate, which consumes one proton per reaction. We hypothesize that these processes are regulated by cancer related conditions such as hypoxia and growth factors and by the pH levels, making these encoded processes not available to normal cells under acidic conditions.

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“…All of the STAT1 targets detected in HeLa cells were used and downloaded from published supplementary data (Satoh and Tabunoki, 2013). The top 500 genes from NFκB targets in macrophages (Barish et al, 2010) and STAT3 targets in embryonic stem cells (Chen et al, 2008) were used and downloaded from HmChip database (Chen et al, 2011). The increase in STAT1 ChIP-seq peaks after LPS stimulation (Figure 4B) was calculated by summing the binding scores of all associated STAT1 peaks in both 0 h and 2 h time points and then subtracting the former from the latter.…”

Section: Methodsmentioning

confidence: 99%

Simultaneous Pathway Activity Inference and Gene Expression Analysis Using RNA Sequencing

et al. 2016

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Summary Reporter gene assays are a venerable tool for studying signaling pathways, but they lack the throughput and complexity necessary to contribute to a systems-level understanding of endogenous signaling networks. Here we present a parallel reporter assay, Transcription Factor activity sequencing (TF-seq), built on synthetic DNA enhancer elements, which enables parallel measurements in primary cells of the transcriptome and transcription factor activity from more than 40 signaling pathways. Using TF-seq in Myd88−/− macrophages, we captured dynamic pathway activity changes underpinning the global transcriptional changes of the innate immune response. We also applied TF-seq to investigate small-molecule mechanisms of action and find a role for NFκB activation and coordination of the STAT1 response in the macrophage response to the anti-inflammatory natural product halofuginone. Simultaneous TF-seq and global gene expression profiling presents an integrative approach for gaining mechanistic insight into pathway activity and transcriptional changes that result from genetic and small molecule perturbations.

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hmChIP: a database and web server for exploring publicly available human and mouse ChIP-seq and ChIP-chip data

Abstract: http://jilab.biostat.jhsph.edu/database/cgi-bin/hmChIP.pl.

Cited by 47 publications

References 14 publications

Myeloid Malignancies with Chromosome 5q Deletions Acquire a Dependency on an Intrachromosomal NF-κB Gene Network

Myeloid Malignancies with Chromosome 5q Deletions Acquire a Dependency on an Intrachromosomal NF-κB Gene Network

Elucidation of How Cancer Cells Avoid Acidosis through Comparative Transcriptomic Data Analysis

Simultaneous Pathway Activity Inference and Gene Expression Analysis Using RNA Sequencing

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