Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (ChIP-Seq)

ABSTRACT: ChIP-sequencing of human 697 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE107886 | GEO | 2019/07/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MTA2/NuRD Regulates B Cell Development and Cooperates with OCA-B in Controlling the Pre-B to Immature B Cell Transition.

Project description: Not available

| S-EPMC6690613 | biostudies-literature

Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition

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

2019-07-11 | GSE107888 | GEO

Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (RNA-Seq)

Project description:The goal of this study is to compare NGS-derived mouse B cell RNA profiling in Mta2 KO, Ocab KO, and double KO mice

2019-07-11 | GSE107885 | GEO

Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition

Project description:Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition

| PRJNA421876 | ENA

Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (ChIP-Seq)

Project description:Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (ChIP-Seq)

| PRJNA421874 | ENA

Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (RNA-Seq)

Project description:Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (RNA-Seq)

| PRJNA421873 | ENA

lncRNA LINC00941 modulates MTA2/NuRD occupancy to suppress premature human epidermal differentiation.

Project description: Not available

| S-EPMC11035861 | biostudies-literature

Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS

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

2023-11-05 | GSE246695 | GEO

Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [2month.ChIPseq]

Project description:Low nephron endowment at birth is a risk factor for chronic kidney disease. The prevalence of this condition is increasing due to higher survival rates of preterm infants and children with multi- organ birth defect syndromes that affect the kidney and urinary tract. We created a mouse model of congenital low nephron number due to deletion of Mta2 in nephron progenitor cells. Mta2 is a core component of the Nucleosome Remodeling and Deacetylase (NuRD) chromatin remodeling complex. These mice developed albuminuria at 4 weeks of age followed by focal segmental glomerulosclerosis (FSGS) at 8 weeks, with progressive kidney injury and fibrosis. Our studies reveal that altered mitochondrial metabolism in the post-natal period leads to accumulation of neutral lipids in glomeruli at 4 weeks of age followed by reduced mitochondrial oxygen consumption. We found that NuRD cooperated with Zbtb7a/7b to regulate a large number of metabolic genes required for fatty acid oxidation and oxidative phosphorylation. Analysis of human kidney tissue also supported a role for reduced mitochondrial lipid metabolism and ZBTB7A/7B in FSGS and CKD. We propose that an inability to meet the physiological and metabolic demands of post-natal somatic growth of the kidney promotes the transition to CKD in the setting of glomerular hypertrophy due to low nephron endowment.

2023-11-05 | GSE246693 | GEO

Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [2month.RNAseq]

2023-11-05 | GSE246692 | GEO