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FOXK2 ChIP-seq

ABSTRACT: FOXK2 ChIP-seq

PROVIDER: PRJEB2447 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR030904.fastq.gz	Fastqsanger.gz
	ERR030905.fastq.gz	Fastqsanger.gz
	ERR030906.fastq.gz	Fastqsanger.gz
	ERR030907.fastq.gz	Fastqsanger.gz
	ERR030908.fastq.gz	Fastqsanger.gz

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FOXK2 ChIP-seq

Project description:Chromatin immunoprecipitation of FOXK2 (tagged with Flag and His tags) in U2OS cells detected by SOLiD sequencing. ***Correction March 2014: The sample “FOXK2_Dox_treated” has been renamed, it was originally named “FOXK2_rep2”. A new sample “FOXK2_rep2” has been added, with new files. It has come to our attention that one of the FOXK2 ChIP-seq replicates 'FOXK2_rep2' that we used in our paper recent paper (Ji, Z., Donaldson, I.J., Liu, J., Hayes, A., Zeef, L.A.H. and Sharrocks, A.D. (2012) The forkhead transcription factor FOXK2 promotes AP-1-mediated transcriptional regulation. Mol. Cell. Biol. 32, 385-398. doi:10.1128/MCB.05504-11) was incorrect. The replicate was actually treated with doxorubicin prior to ChIP-seq analysis resulting in the loss of many FOXK2 binding events.***

2011-01-20 | E-MTAB-565 | biostudies-arrayexpress

FOXK2 ChIP-seq Illumina

Project description:Chromatin immunoprecipitation of FOXK2 (tagged with Flag and His tags) in U2OS cells detected by Illumina sequencing

2014-07-23 | E-MTAB-2204 | biostudies-arrayexpress

ChIP-seq of FOXK2 in human embryonic stem cells H1 ESC, and the differentiated mesendoderm cells and and NPC cells

Project description:In order to investigate the genome-wide binding profile of the forkhead transcription factor FOXK2 in human embryonic stem cells (ESCs) and downstream cell types, we generated the ChIP-seq data of FOXK2 in H1 ESC cells and two differentiated types of cells, mesendoderm cells and NPC cells.

2020-12-21 | E-MTAB-9630 | biostudies-arrayexpress

FOXK2 ChIP-chip

Project description:Chromatin immunoprecipitation of FOXK2 (tagged with Flag and His tags) in U2OS cells detected by Affymetrix human promoter array 1.0R.

2011-11-03 | E-MEXP-3116 | biostudies-arrayexpress

Genome-wide maps of chromatin state in LbetaT2 cells or in the pituitary tissues of wild-type and Foxk2 knockout mice.

Project description:First, we report a series of ChIP-seq results in LbetaT2 cells. Briefly, we performed ChIP-seq experiments with antibodies specific for Foxk2, Sin3a, Tet1 and Uhrf1 in LbetaT2 cells. We found that a total of 343 different promoters including Nab2 that are co-targeted by Foxk2, Sin3a, Tet1 and Uhrf1. Next, hMeDIP-seq and ChIP-seq experiments with antibodies specific for 5hmC and H3K18ub in the pituitary tissues of wild-type and Foxk2 knockout mice were performed. The results showed that compared to the wild-type mice, knockout of Foxk2 reduced the enrichment of 5hmC and H3K18ub on the Foxk2 target gene.This study revealed a critical switch control of FOXK2 for GnRH pulse frequency-dependent LH production and gave us a new understanding of the role of Foxk2 in chromatin status and gene transcription.

2020-05-01 | GSE130615 | GEO

FOXK2 ChIP sequencing in non-treated MCF-7 cells

Project description:Although clinically associated with severe intellectual disability, West syndrome, Dandy-Walker malformation, and syndactyly, the biological function of FOXK2 remains poorly explored. Here we report that FOXK2 acts as a transcription repressor. Strikingly, FOXK2 interacts with multiple transcription corepressor complexes including NCoR/SMRT, SIN3A, NuRD, and REST/CoREST. FOXK2 assembles these transcription programs to repress a cohort of genes including HIF1 and EZH2 and to regulate several signaling pathways including the hypoxic response that is critically implicated in tumor development and progression. We showed that FOXK2 inhibits the proliferation and invasion of breast cancer cells in vitro and suppresses the growth and metastasis of breast cancer in vivo. Interestingly, FOXK2 is transactivated by ERand transrepressed via reciprocal successive feedback by HIF1/EZH2. Significantly, the expression of FOXK2 is progressively lost during breast cancer progression, leading to elevated expression of EZH2, an eminent feature of aggressive breast cancer. Indeed, the expression of FOXK2 is inversely correlated with that of EZH2 and HIF1in breast carcinomas, and low FOXK2 expression is strongly correlated with higher histologic grades, positive lymph nodes, and ER/PR/Her2 status, all indicators of poor prognosis. Our experiments revealed that FOXK2 is massively involved in transcription repression, providing a molecular basis for the understanding of the mechanistic action of FOXK2. Our study identified the ER-FOXK2-HIF1/EZH2 axis in breast cancer progression, supporting the pursuit of these molecules as therapeutic targets for breast cancer intervention.

2016-11-08 | GSE84241 | GEO

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Project description:This study characterized the genome-wide binding of FOXK2 in ovarian cancer (OC) cell OVCAR-5 and investigated the expression profile of OVCAR5 cells with FOXK2 knocking-down.

2022-05-18 | GSE173777 | GEO

FOXK2 transcriptionally activating VEGFA induces apatinib resistance in anaplastic thyroid cancer through VEGFA/VEGFR1 pathway (ChIP-seq)

Project description:Chromatin immunoprecipitation -seq analysis of FOXK2 was performed on(Anaplastic thyroid cancer cell line) CAL-62 cells(WT).

2023-01-01 | GSE165777 | GEO

Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha

Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.

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FOXK2 promotes AP-1 mediated transcriptional regulation - transcription profiling FOXK2 induction

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