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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [ChIP-Seq]

ABSTRACT: KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [ChIP-Seq]

PROVIDER: PRJNA1108273 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28919400_1.fastq.gz	Fastqsanger.gz
	SRR28919400_2.fastq.gz	Fastqsanger.gz
	SRR28919401_1.fastq.gz	Fastqsanger.gz
	SRR28919401_2.fastq.gz	Fastqsanger.gz
	SRR28919402_1.fastq.gz	Fastqsanger.gz

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [PRO-Seq]

Project description:KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [PRO-Seq]

| PRJNA1108276 | ENA

KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [TT-Seq]

Project description:KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [TT-Seq]

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [RNA-Seq]

Project description:KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [RNA-Seq]

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KAP1 regulates elongation kinetics to activate signal-induced transcription

Project description:KAP1 regulates elongation kinetics to activate signal-induced transcription

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [TT-Seq]

Project description:Signal-induced transcriptional programs regulate critical biological processes through the precise spatiotemporal activation of Immediate Early Genes (IEGs); however, the mechanisms of transcription induction are still unfolding. By combining an acute depletion system with high resolution genomics approaches to interrogate synchronized, temporal transcription, we reveal that KAP1/TRIM28 is a first responder that fulfills the temporal and heightened transcriptional demand of IEGs. Unexpectedly, acute KAP1 loss triggers an increase in RNA Polymerase II elongation kinetics during early stimulation time points. This elongation defect derails the normal progression through the transcriptional cycle during late stimulation time points, ultimately leading to decreased recruitment of the transcription apparatus for re-initiation and dampening IEG transcription. Collectively, KAP1 plays a counterintuitive role by negatively regulating transcription elongation to support full activation across multiple transcription cycles of genes critical for cell physiology and organismal functions.

2024-05-07 | GSE266694 | GEO

KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [RNA-Seq]

2024-05-07 | GSE266693 | GEO

KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [ChIP-Seq]

2024-05-07 | GSE266691 | GEO

KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [PRO-Seq]

2024-05-07 | GSE266692 | GEO

KAP1 regulates elongation kinetics to activate signal-induced transcription

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-07 | GSE246218 | GEO

Functional analysis of Kap1 genomic recruitment

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

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