Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcript expression level in control and Setd1a-knockdown mouse explant retina

ABSTRACT: Transcript expression level in control and Setd1a-knockdown mouse explant retina

PROVIDER: PRJNA646500 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12229969.fastq.gz	Fastqsanger.gz
	SRR12229970.fastq.gz	Fastqsanger.gz
	SRR12229971.fastq.gz	Fastqsanger.gz
	SRR12229972.fastq.gz	Fastqsanger.gz
	SRR12229973.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 7

Similar Datasets

Transcript expression level in control and Setd1a-knockdown mouse explant retina

Project description:Knockdown of Kmt2f in a embryonic mouse retina caused increased apoptosis and decreased proliferation. To investigate downstream molecular mechanisms of Kmt2f in retina, RNA-sequencing was performed with control or shKmt2f-expressing retina. Mouse retinas at embryonic dat 17 were electroporated with plasmids and cultured for 2 days. EGFP-expressing cells were purified by a cell sorter, and RNA-seq was carried out.

2021-05-19 | GSE154498 | GEO

Arrayed gene expression analysis of the SETD1A depleted cancer cells

Project description:Investigation of gene expression level changes in the SETD1A depleted cancer cells (shSETD1A), compared to the GFP depleted cancer cells (shGFP) as control. This analysis was performed to gain an understanding of the transcriptional changes induced by chromation modifications through H3K4 methyltransferase SETD1A. Key Word: SETD1A, Epigenetics

2017-07-18 | GSE71498 | GEO

IPs of SETD1A COMPASS-HUMAN LC-MSMS

Project description:Mapping physical interactions of SETD1A COMPOASS in HEK293T cells using endogenous immunoprecipitation followed by label-free quantitative proteomics. We found a novel protein interacts with SETD1A, which is RAD18 (DNA damage repair protein).

2019-06-13 | PXD012549 | Pride

RNA-Seq: assessment of transcript level analysis tools

Project description:RNA-Seq: assessment of transcript level analysis tools

| PRJNA302625 | ENA

Recapitulation and reversal of schizophrenia-related phenotypes in Setd1a-deficient mice

Project description:SETD1A, a histone methyltransferase, is a key schizophrenia susceptibility gene. Mutant mice carrying a heterozygous loss-of-function mutation of the orthologous gene exhibit alterations in axonal branching and cortical synaptic dynamics, accompanied by specific deficits in working memory that recapitulates SCZ-related alterations. We show that Setd1a targets mostly enhancers and reveal a striking overlap between Setd1a and Mef2 chromatin targets. Setd1a targets are highly expressed in pyramidal neurons and enriched for genes with postnatally-biased expression involved in synaptic structure and function. Notably, evolutionary conserved Setd1a binding sites and target genes are strongly associated with neuropsychiatric genetic risk burden. Reinstating Setd1a expression in adulthood rescues working memory deficits. We identify LSD1 as a major demethylase counteracting the effects of Setd1a methyl transferase activity and show that LSD1 antagonism in adult Setd1a-deficient mice results in a full rescue of the behavioral abnormalities and axonal branching deficits. Our findings advance our understanding of how SETD1A mutations predispose to SCZ and point to therapeutic interventions.

2019-10-09 | GSE123652 | GEO

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [ChIP-Seq]

Project description:Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce rapid SETD1A degradation in AML cell lines. SETD1A degradation results in immediate downregulation of transcripts associated with DNA repair and heme biosynthesis pathways. CRISPR-based functional analyses and metabolomics revealed an essential role of SETD1A to maintain mitochondrial respiration in AML cells. These SETD1A targets are enriched in head-to-head (H2H) genes. SETD1A degradation disturbs a non-enzymatic SETD1A domain-dependent cyclin K function, increases the mono-Ser5P RNA polymerase II (RNAP2) at TSS, and induces the promoter-proximal pausing of RNAP2 in a strand-specific manner. This study reveals a non-enzymatic role for SETD1A in transcriptional pause release and provides insight into the mechanism of RNAP2 pausing and its function in cancer.

2022-12-09 | GSE190994 | GEO

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [RNA-seq]

2022-12-09 | GSE189893 | GEO

BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (RNA-seq)

Project description:The H3K4 methyltransferase SETD1A plays an essential role in both development and cancer. However, essential components involved in SETD1A chromatin binding remain unclear. Here, we discovered that BOD1L exhibits the highest correlated co-dependency with SETD1A in human cancer cell lines. BOD1L knockout reduces leukemia cells in vitro and in vivo, and mimics the transcriptional profiles observed in SETD1A knockout cells. The loss of BOD1L immediately reduced SETD1A distribution at transcriptional start sites (TSS) and induces transcriptional elongation defect along with the increasing of RNA polymerase II at TSS, but did not cause the reduction of H3K4me3. The Shg1 domain of BOD1L has a DNA binding ability, and recruit SETD1A to chromatin through the association with SETD1A FLOS domain. In addition, the BOD1L-SETD1A complex associates with transcriptional regulators, including E2Fs. These results reveal that BOD1L mediates chromatin and SETD1A, and regulates the non-canonical function of SETD1A in transcription.

2024-06-25 | GSE258789 | GEO

BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (ChIP-seq)

2024-06-25 | GSE258788 | GEO

Epigenetic modification of GR enhancers by SETD1A/COMPASS complex in murine macrophages

Project description:Nuclear interaction studies by ChIP coupled with mass spectrometry identified the COMPASS/SETD1A complex as interaction partner of the glucocorticoid receptor (GR) in murine bone marrow-derived macrophages (BMDMs). Here, we profiled the occupancy of SETD1A and CXXC1, two subunits of the COMPASS/SETD1A complex in murine macrophages after LPS and Dex+LPS stimulation. We show, that GR recuits SETD1A and CXXC1 to GR enhancer and that SETD1A recruitment does correlate with changes in H3K4methylation at some of those enhancers.

2020-12-31 | GSE136070 | GEO

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