Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MORC2 promotes renal carcinogenesis via epigenetically downregulating DAPK1

ABSTRACT: epigenetic regulation plays a vital role in renal carcinogenesis. Here，we found epigenetic regulator MORC2 promoted carcinogenesis in kidney. Mechanistically, MORC2 functioned as oncogene via epigenetically silencing canonical tumor suppressor DAPK1 in kidney. Therefore, aMORC2—DAPK1 pro—oncogenic axis was identified in kindey.

ORGANISM(S): Homo sapiens

PROVIDER: GSE221129 | GEO | 2023/10/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MORC2 promotes renal carcinogenesis via epigenetically downregulating DAPK1

Project description:MORC2 promotes renal carcinogenesis via epigenetically downregulating DAPK1

| PRJNA913012 | ENA

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex

Project description:The human silencing hub (HUSH) complex binds to transcripts of LINE-1 retrotransposons (L1s) and other genomic repeats, recruiting MORC2 and other effectors to remodel chromatin. However, how HUSH and MORC2 operate alongside DNA methylation, a central epigenetic regulator of repeat transcription, remains poorly understood. Here we interrogate this relationship in human neural progenitor cells (hNPCs), a somatic model of brain development that tolerates removal of DNA methyltransferase DNMT1. Upon loss of MORC2 or HUSH subunit TASOR in hNPCs, L1s remain silenced by robust promoter methylation. However, genome demethylation and activation of evolutionarily-young L1s attracts MORC2 binding. Simultaneous depletion of DNMT1 and MORC2 causes massive accumulation of L1 transcripts. We identify the same mechanistic hierarchy at pericentromeric α-satellites and clustered protocadherin genes, repetitive elements important for chromosome structure and neurodevelopment respectively. Our data delineate the independent epigenetic control of repeats in somatic cells, with implications for understanding the vital functions of HUSH-MORC2 in hypomethylated contexts throughout human development.

2024-03-26 | GSE242143 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [CUT&RUN]

2024-03-26 | GSE240384 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [Bulk RNA-seq]

2024-03-26 | GSE240386 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [ONT cDNA sequencing]

2024-03-26 | GSE262483 | GEO

Assessing the genome-wide occupancy of MORC2

Project description:By comparing HeLa cells expressing V5 epitope-tagged MORC2 constructs, the goal of the experiment was to determine the genome-wide localisation of MORC2 in the presence or absence of the HUSH complex and upon inactivation of the CW domain. The occupancy of V5-MORC2 was also compared to that of endogenous TASOR.

2017-05-29 | GSE95451 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [ONT whole genome DNA]

2024-03-26 | GSE262482 | GEO

Assessing the impact of loss of MORC2 on the transcriptome

Project description:By comparing HeLa cells lacking MORC2 generated through CRISPR/Cas9-mediated gene disruption to wild-type HeLa cells, the goal of the experiment was to determine the effect of loss of MORC2 on the transcriptome.

2017-05-29 | GSE95452 | GEO

Epigenetic reprogramming in hepatic carcinogenesis

Project description:Epigenetic reprogramming in hepatic carcinogenesis

| PRJNA450821 | ENA

Identification and characterization of a human MORC2 DNA binding region that is required for gene silencing

Project description:The eukaryotic microrchidia (MORC) protein family are DNA gyrase, Hsp90, histidine kinase, MutL (GHKL)-type ATPases involved in gene expression regulation and chromatin compaction. We identified a DNA binding site in the C-terminus of the protein. Here we generated dox-inducible GFP, GFP-MORC2, and GFP-MORC2 DNA-binding mutants and performed RNA-sequencing. We show that the MORC2 C-terminal DNA binding region is required for gene silencing in cells. Our data provide a model to understand how MORC2 engages with DNA substrates to mediate gene silencing.

2024-12-13 | GSE262311 | 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