KAP1 ChIP-seq in hESC
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA602892 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10958236.fastq.gz | Fastqsanger.gz | |||
| SRR10958237.fastq.gz | Fastqsanger.gz |
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Project description:endogenous KAP1 ChIPseq remapping (previously published in GSE57989)
2020-01-24 | GSE144150 | GEO
Project description:We have performed ChIP seq analysis to obtain the positions of KAP1 and ZFP57 binding sites in mouse ES cells. By comparing the two lists, we were able to find bona fide sites. ChIP-Seq of HA tagged ZFP57 and KAP1 in mouse ES cells
2011-11-07 | E-GEOD-31181 | biostudies-arrayexpress
Project description:Chromatin remodeling is fundamental for B cell differentiation. Here, we explored the role in this process of KAP1, the cofactor of KRAB-ZFP transcriptional repressors. B lymphoid-specific Kap1 knockout mice displayed reduced numbers of mature B cells, lower steady-state levels of antibodies and accelerated rates of decay of neutralizing antibodies following viral immunization. Transcriptome analyses of Kap1-deleted B splenocytes revealed an upregulation of PTEN, the enzymatic counter-actor of PIK3 signaling, and of genes encoding DNA damage response factors, cell-cycle regulators and chemokine receptors. ChIP/seq studies established that KAP1 bound at or close to a number of these genes, and controlled chromatin status at their promoters. Genome-wide, KAP1-binding sites avoided active B cell-specific enhancers and were enriched in repressive histone marks, further supporting a role for this molecule in gene silencing in vivo. Likely responsible for tethering KAP1 to at least some of these targets, a discrete subset of KRAB-ZFPs is enriched in B lymphocytes. This work thus reveals the role of KRAB/KAP1-mediated epigenetic regulation in B cell development and homeostasis. Examination of KAP1 binding sites and H3K9me3 enriched regions in KAP1 wild type and KO mouse B splenocytes.
2012-05-16 | E-GEOD-36850 | biostudies-arrayexpress
Project description:A current model for the genomic recruitment of Kap1 is via its interaction with KRAB domain-containing zinc finger transcription factors. We have performed ChIP-seq for various mutant KAP1 proteins and shown that this recruitment mechanism mediates binding of KAP1 only to the 3M-CM-"M-BM-^@M-BM-^Y ends of zinc finger genes and that other factors are involved in recruiting KAP1 to promoter regions. 17 total ChIP-seq datasets; three different FLAG-KAP1 mutants, one FLAG-KAP1 wild type, and four different Input datasets from 4 different stable cell lines derived from HEK293 cells: 1 FLAG-KAP1 wild type dataset and 1 Input dataset done from HEK293 stable cells; 1 FLAG-KAP1 HP1BDmut dataset and 1 Input dataset done from HEK293 stable cells, 1 FLAG-KAP1 N-ter RBCC{delta}mut dataset and 1 Input dataset done from HEK293 stable cells, 1 FLAG-KAP1 C-ter PB{delta}mut dataset and 1 Input dataset done from HEK293 stable cells. One FLAG-KAP1 N/C-ter (RBCC+PB){delta}mut dataset done from T-REx HEK293 stable cells. One endogenous KAP1 dataset done from HEK293 cells. Two independent ELK4 datasets done from duplicate HEK293 cells. One endogenous Kap1 dataset and one Input dataset from a stable cell line derived from U2OS cells.
2011-05-24 | E-GEOD-27929 | biostudies-arrayexpress
Project description:We show that a hitherto poorly characterized KRAB domain-containing zinc-finger (ZF) transcription factor, ZFP30, positively regulates adipogenesis. We demonstrate ZFP30’s function in murine in vitro and in vivo models, as well as in human stromal vascular fraction cells. We reveal through mechanistic studies that ZFP30 directly targets and activates Pparg2 by binding a retrotransposon-derived enhancer, suggesting a process of adipogenic exaptation. We further show that ZFP30 recruits the co-regulator KRAB-associated protein 1 (KAP1), which, surprisingly, acts as a ZFP30 co-activator in this adipogenic context. As neither the commercial ZFP30 antibodies nor four batches of customized ZFP30 antibodies recognized it specifically (data not shown), we performed ChIP-seq in 3T3-L1 cells expressing HA-tagged ZFP30 in a tetracycline-inducible manner, as also previously employed for ZEB1 (Gubelmann et al., 2014). The mRNA expression of exogenous Zfp30 was induced to a similar level as the endogenous Zfp30 by adjusting the amount of Doxycycline (data not shown), to avoid potential artefacts due to protein overexpression. To further characterize its role in adipogenesis and as a ZFP30 partner, we performed KAP1 ChIP-seq in undifferentiated (day 0) and differentiated (day 2) 3T3-L1 cells, as described above for HA-ZFP30. We first confirmed the high enrichment obtained with the employed KAP1 antibody.
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Project description:We used ChIP-seq to assess how abolition of KRAB binding by KAP1 (through structure-guided mutations in the KAP1-KRAB binding interface) changed the distribution of KAP1 on chromatin genome-wide.
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Project description:The ATP dependent chromatin remodeler SMARCAD1 and the co-repressor KAP1 (Trim28/Tif1 beta) interact directly. We wanted to understand the interplay between these two proteins in the context of chromatin; in particular at repetitive sequences. Therefore, we carried out an investigation in E14 ES cells of the genome wide binding behaviour of KAP1 and FLAG-tagged SMARCAD1; both wild-type SMARCAD1 and a catalytically inactive mutant. The E14 cells analysed were either wild-type or depleted for endogenous SMARCAD1 protein. FLAG and KAP1 ChIP was performed on double-cross linked chromatin and sequenced on an Illumina HiSeq1500 with matched input controls. A FLAG antibody precipitation was carried out on cells not expressing FLAG tagged protein as an additional control.
2019-02-17 | E-MTAB-7011 | biostudies-arrayexpress
Project description:A current model for the genomic recruitment of Kap1 is via its interaction with KRAB domain-containing zinc finger transcription factors. We have performed ChIP-seq for various mutant KAP1 proteins and shown that this recruitment mechanism mediates binding of KAP1 only to the 3â ends of zinc finger genes and that other factors are involved in recruiting KAP1 to promoter regions.
2011-05-24 | GSE27929 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE34447: Gene expression analysis of wild type and KAP1 KO mouse T cell progenitors GSE38579: ChIP-seq analysis of KAP1 binding and H3K9me3 modifications in mouse T cell progenitors Refer to individual Series
2012-08-07 | E-GEOD-38580 | biostudies-arrayexpress
Project description:We have performed ChIP seq analysis to obtain the positions of KAP1 and ZFP57 binding sites in mouse ES cells. By comparing the two lists, we were able to find bona fide sites.
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