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Genome-wide mapping of Myc binding site (K562)

ABSTRACT: Proto-oncogene c-myc encodes a bHLH leucine-zipper containing transcription factor which has a DNA binding domain and a transactivation domain. Myc can dimerize with other factors like Max, Mad, Mnt and Miz and can influence transcription of genes. The c-myc oncogene contributes to the genesis of a wide variety of human tumors. A higher than normal level of c-myc gene expression has been observed in 50-80% of colon and breast cancers and a large proportion of human mortality from cancer is caused by abnormal expression of c-myc. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Map binding sites of transcription factor Myc in the genome of K562 cells. The K562 input data has been deposited in GEO as GSM325934.

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Wilson

PROVIDER: E-GEOD-19547 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Close association of RNA polymerase II and many transcription factors with Pol III genes.

Raha Debasish D Wang Zhong Z Moqtaderi Zarmik Z Wu Linfeng L Zhong Guoneng G Gerstein Mark M Struhl Kevin K Snyder Michael M

Proceedings of the National Academy of Sciences of the United States of America 20100205 8

Transcription of the eukaryotic genomes is carried out by three distinct RNA polymerases I, II, and III, whereby each polymerase is thought to independently transcribe a distinct set of genes. To investigate a possible relationship of RNA polymerases II and III, we mapped their in vivo binding sites throughout the human genome by using ChIP-Seq in two different cell lines, GM12878 and K562 cells. Pol III was found to bind near many known genes as well as several previously unidentified target ge ...[more]

PMID: 20139302

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Genome-wide mapping of Jun binding site (K562)

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2009-12-31 | E-GEOD-19545 | biostudies-arrayexpress

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2009-12-31 | E-GEOD-19546 | biostudies-arrayexpress

Genome-wide mapping of RNA Pol III binding site (K562)

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2009-12-31 | E-GEOD-19548 | biostudies-arrayexpress

Genome-wide mapping of RNA Polymerase II binding sites

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Genome-wide mapping of RNA Pol II binding site (GM12878)

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2009-12-31 | E-GEOD-19550 | biostudies-arrayexpress

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2009-12-31 | E-GEOD-19549 | biostudies-arrayexpress

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2008-09-16 | E-GEOD-12781 | biostudies-arrayexpress

STAT1 transcription factor in Human HeLa S3

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2008-09-15 | E-GEOD-12782 | biostudies-arrayexpress

Non-canonical PRC1.1 targets active genes independent of H3K27me3 and is essential for leukemogenesis

Project description:Polycomb proteins are classical regulators of stem cell self-renewal and cell lineage commitment and are frequently deregulated in cancer. Here we find that the non-canonical PRC1.1 complex, as identified by mass spectrometry-based proteomics, is critically important for human leukemic stem cells. Downmodulation of PRC1.1 complex members, like the DNA-binding subunit KDM2B, strongly reduces cell proliferation in vitro and delays or even abrogates leukemogenesis in vivo in humanized xenograft models. PRC1.1 components are significantly overexpressed in primary AML CD34+ cells. Besides a set of genes that is co-targeted by PRC1 and PRC2, ChIP-seq studies show that PRC1.1 also binds a distinct set of genes that are devoid of H3K27me3 suggesting a gene regulatory role independent of PRC2. This set encompasses genes involved in metabolism, which have transcriptionally active chromatin profiles. These data indicate that PRC1.1 controls distinct gene clusters involved in unique cell biological processes required for leukemic cell viability. K562 cells were transduced with lentiviral GFP-fusion vectors encoding GFP-CBX2, PCGF1-GPF, PCGF2-GFP, PCGF4-GFP, GFP-RING1A or GFP-RING1B. K562 cells expressing GFP-fusions at relatively low levels were sorted and expanded and subsequently crosslinked. ChIP reactions were performed using the following antibodies: anti-GFP (ab290, Abcam), anti-H3K27me3 (07-449, Millipore), anti-H3K4me3 (ab8580, Abcam), anti-H2AK119ub (D27C4, Cell Signaling Technology), and anti-KDM2B (ab137547, Abcam). Furthermore, ChIP reactions were performed using primary AML CD34+ and Peripheral Blood (PB) CD34+ cells using anti-H3K27me3 (07-449, Millipore), anti-H3K4me3 (ab8580, Abcam), anti-H2AK119ub (D27C4, Cell Signaling Technology), anti-KDM2B (ab137547, Abcam).

2015-11-24 | E-GEOD-54580 | biostudies-arrayexpress

Global analysis of in vivo EGR1-binding sites in erythroleukemia cell K562 using chromatin immunoprecipitation and massively parallel sequencing

Project description:Early growth response gene 1 (EGR1) has been implicated in megakaryocyte differentiation induced by PMA (phorbol 12-myristate 13-acetate). The identification of direct EGR1 target genes in global scale is critical for our understanding of how EGR1 contributes to this process. In this study, we provide a global survey on the binding location of EGR1 in the K562 cell treated by PMA using chromatin immunoprecipitation and massively parallel sequencing (ChIP-Seq). K562 is a human erythroleukemia cell line, which is situated in the common progenitor stage of megakaryocytic and erythroid lineages of the hematopoietic stem cell differentiation and its normally following differentiation is blockaded. Upon exposure to PMA stimuli, K562 cell can be induced into megakaryocytic cell, which provides a model for the study of transcriptional control networks. Over 14 000 highly confident in vivo EGR1 binding sites were identified in PMA treated K562 cell. More than 70% of these genomic sites associated with EGR1 binding were located around annotated gene regions. This whole genome study on the EGR1 targets may help a better understanding of the EGR1 regulated genes and the downstream pathway in megakaryocyte differentiation. The in vivo binding locations of EGR1 in K562 cell treated with PMA (phorbol 12-myristate 13-acetate, 10 ng/ml for 2 hours) were identified using chromatin immunoprecipitation combing with massively parallel sequencing (ChIP-Seq) based on AB SOLiD System 2.0.

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