Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: A novel KRAB zinc finger gene has changed the balance of HES1 autoregulation during primate evolution

PROVIDER: PRJNA700073 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13645575_1.fastq.gz	Fastqsanger.gz
	SRR13645575_2.fastq.gz	Fastqsanger.gz
	SRR13645576_1.fastq.gz	Fastqsanger.gz
	SRR13645576_2.fastq.gz	Fastqsanger.gz
	SRR13645577_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

A novel KRAB zinc finger gene has changed the balance of HES1 autoregulation during primate evolution

Project description:A novel KRAB zinc finger gene has changed the balance of HES1 autoregulation during primate evolution

| PRJNA701019 | ENA

A novel KRAB zinc finger gene has changed the balance of HES1 autoregulation during primate evolution

Project description:KRAB zinc finger (KZNF) proteins are a class of transcriptional repressors important for epigenetic silencing of specific genomic regions. About 170 primate-specific KZNFs are present in the human genome. While KZNFs are primarily associated with repressing retrotransposon-derived DNA, evidence is emerging that they can be co-opted for other gene regulatory processes. We focused on the 19p12 locus, which shows copy-number variations associated with neurodevelopmental disorders, implying it is required for human brain development. The two genes in this locus, ZNF675 and ZNF681, arose via duplication in primates. Genetic deletion of ZNF675 caused developmental defects in cortical organoids and our data suggest that the observed neurodevelopmental phenotype is mediated by ZNF675 binding to the promoter of the neurodevelopmental gene HES1. We show that ZNF675 interferes with HES1 auto-inhibition, a process essential for maintenance of neural progenitors. As a striking example of how some KZNFs have integrated into pre-existing gene expression networks, these findings suggest the emergence of ZNF675 has caused a change in balance of HES1 autoregulation. The association of ZNF675 CNV with human developmental disorders suggests that this new balance has become essential for normal human brain development.

2021-02-10 | GSE166471 | GEO

ZNF676 ChIP-seq in HEK293T and H1 cells

Project description:Genome-wide binding profile of the primate-specific KRAB zinc finger protein ZNF676 in cell lines overexpressing the protein.

2022-01-28 | GSE163541 | GEO

ZNF676 and ZNF728 ChIP-exo in HEK293T cells

Project description:Genome-wide binding profile of the primate-specific KRAB zinc finger proteins ZNF676 and ZNF728 in cell lines overexpressing the proteins.

2022-01-28 | GSE163540 | GEO

ZNF728 ChIP-seq in HEK293T cells

Project description:Genome-wide binding profile of the primate-specific KRAB zinc finger protein ZNF728 in a HEK293T cell line overexpressing the protein.

2022-01-28 | GSE163542 | GEO

Adaptive evolution of gene promoters driven by primate-specific KRAB zinc finger proteins

Project description:Adaptive evolution of gene promoters driven by primate-specific KRAB zinc finger proteins

| PRJNA830860 | ENA

Primate-restricted KRAB zinc finger proteins control gene expression in human brain

Project description:Primate-restricted KRAB zinc finger proteins control gene expression in human brain

| PRJNA602996 | ENA

Human stem cell and mouse transchromosomic (hsa11) embryonic stem cell (with and without ectopic ZNF91 expression) ChIP-seq

Project description:We compared the binding patterns in embryonic stem cells of KAP1 and KRAB Zinc Finger (KZNF) proteins as well as H3K4me3 DNA under several conditions. Native human stem cells. Mouse stem cells containing a transchromosomic copy of human chromosome 11, with and without the introduction of plasmids containing KRAB Zinc Finger sequences. We show that certain KZNFs are responsible for the repression of certain retrotransposons in embryonic stem cells, preventing their spread across the genome. ChIP-seq of HESCs and mouse TC11 ESCs with ZNF91 plasmids and with empty vector plasmids. ChIP of KAP1, ZNF486, H3K4me3. At least 2 replicates of each condition.

2014-09-29 | E-GEOD-60210 | biostudies-arrayexpress

Genome-wide analysis of differential transcription in KRAB-ZFP cluster knock-out ES cells and mouse tissues

Project description:Mammalian genomes encode several hundred Krüppel-associated box zinc finger proteins (KRAB-ZFPs) that bind DNA in a sequence-specific manner through tandem arrays of C2H2-type zinc fingers and repress transcription via KRAB-dependent recruitment of the silencing cofactor KAP1. The KRAB-ZFP family rapidly amplified and diversified in mammals by segmental gene duplications, mutations, and zinc finger rearrangements likely in response to continued transposable element invasions, but the biological functions and in vivo requirement of these proteins has gone largely unexplored. We determined the genomic binding sites of 61 murine KRAB-ZFPs and genetically deleted five large KRAB-ZFP gene clusters encoding more than 100 of the approximately 360 mouse KRAB-ZFPs. We demonstrate that most KRAB-ZFPs bind to specific retrotransposon families and that many of these retrotransposons are transcriptionally activated in KRAB-ZFP cluster KO ESCs, licensing retrotransposon-derived enhancers to activate nearby genes.

2019-06-27 | GSE115288 | GEO

Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements

Project description:Reverse transcription-derived sequences account for at least half of the human genome. Although these retroelements are formidable motors of evolution, they can occasionally cause disease, and accordingly are inactivated during early embryogenesis through epigenetic mechanisms. In the mouse, at least for endogenous retroviruses, important mediators of this process are the tetrapod-specific KRAB-containing zinc finger proteins (KRAB-ZFPs) and their cofactor TRIM28. The present study demonstrates that KRAB/TRIM28-mediated regulation is responsible for controlling a very broad range of human-specific endogenous retroelements (EREs) in human embryonic stem (ES) cells and that it exerts, as a consequence, a marked effect on the transcriptional dynamics of these cells. It further reveals reciprocal dependence between TRIM28 recruitment at specific families of EREs and DNA methylation. It finally points to the importance of persistent TRIM28-mediated control of ERE transcriptional impact beyond their presumed inactivation by DNA methylation. Analyses of epigentic effectors and marks in KAP1 WT and KD human embryonic stem cells

2014-05-29 | E-GEOD-57989 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data