Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bulk RNASeq S64F MAFA male islets

ABSTRACT: Mice harboring the S64F mutation in the endogenous MafA gene ("Het") on a mixed genetic background (SJL x C57/Bl6J) show impaired glucose tolerance then overt diabetes by 5 weeks of age. Moreover, when backcrossed to the C57/Bl6J background, mutant Het mice are euglycemic similar to their wild type littermates, suggesting compensation which can prevent diabetes.

ORGANISM(S): Mus musculus

PROVIDER: GSE299343 | GEO | 2025/12/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling of MafA, MafB, and MafA/MafB Mutants in E18.5 pancreas

Project description:MafA and MafB transcription factors have been shown to be key regulators of insulin and glucagon transcription. MafB is essential for alpha and beta cell differentiation, as MafB deficient mice produced fewer insulin+ and glucagon+ cells during development, with MafA expressed in remaining insulin+ cells. In contrast, beta cell development was reported to be normal in a total MafA knock out, although the animals developed beta cell dysfunction and diabetes as adults. However, we have found that MafB expression is elevated during development and retained in adult insulin+ cells after conditional removal of MafA in the pancreas. These studies will evaluate the broader significance of these insulin and glucagon regulators in alpha and beta cell development and function. Our efforts will focus on determining if the concerted actions of MafA and MafB factors are significant to beta cell formation, and we specifically plan to: Determine how alpha and beta cell differentiation is affected in MafA/MafB compound mutant mice during pancreas development. cDNA microarray studies (pancchip 6.0) with wild type, MafAKO, MafB-/-, and MafAKOMafB-/- mutant E18.5 pancreata will be performed to comprehensively identify genes controlled by MafA and MafB in developing alpha and beta cells.

2014-11-04 | E-MTAB-3070 | biostudies-arrayexpress

Mafa-MHC

Project description:Mafa-MHC alleles

| PRJEB43388 | ENA

Male biased islet b cell dysfunction is caused by the MODY MAFA S64F variant by inducing premature aging and senescence

Project description:A heterozygous missense mutation producing a variant of the islet β-cell-enriched MAFA transcription factor (p.Ser64Phe (S64F)) was identified in patients who developed adult-onset, β-cell dysfunction (diabetes or insulinomatosis), with men more prone to diabetes than women. This mutation engenders increased stability to the normally unstable MAFA protein. To obtain insight into how this variant impacts β cell function, we developed a mouse model expressing S64F MafA and found sex-dependent phenotypes, with heterozygous mutant males (MafAS64F/+) displaying impaired glucose tolerance while females were slightly hypoglycemic with improved blood glucose clearance. Only MafAS64F/+ males showed transiently higher MafA protein levels preceding the onset of glucose intolerance and sex-dependent, differential expression of genes involved in Ca2+ signaling, DNA damage, aging, and senescence. Functional changes in islet Ca2+ handling and signs of islet aging and senescence processes were uniquely observed in male animals. In addition, MAFAS64F production in male human β cells accelerated cellular senescence and increased production of senescence-associated secretory proteins compared to cells expressing MAFAWT. Together, these results implicate a conserved mechanism of accelerated islet aging and senescence in promoting diabetes in MAFAS64F carriers in a sex-dependent manner.

2021-09-10 | GSE183561 | GEO

Species-specific roles for the MAFA and MAFB transcription factors in regulating islet β cell identity

Project description:Type 2 diabetes (T2D) is associated with compromised identity of insulin-producing pancreatic islet beta (β) cells, characterized by inappropriate production of other islet cell-enriched hormones. Here we examined how hormone misexpression was influenced by the MAFA and MAFB transcription factors, closely related proteins that maintain islet cell function. Mice specifically lacking MafA in β cells demonstrated broad, population-wide changes in hormone gene expression with an overall gene signature closely resembling islet gastrin (Gast)-positive cells generated under conditions of chronic hyperglycemia and obesity. A human b cell line deficient in MAFB, but not one lacking MAFA, also produced a gastrin (GAST)-positive gene expression pattern. In addition, GAST was detected in human T2D β cells with low levels of MAFB. Moreover, evidence is provided that human MAFB can directly repress GAST gene transcription. These results support a novel, species-specific role for MafA and MAFB in maintaining adult mouse and human β cell identity, respectively, by repressing expression of Gast/GAST and other non-b cell hormones.

2023-05-01 | GSE230728 | GEO

Regulation of gene expression by MafA phosphorylation in transformed cells.

Project description:Transformation of Chicken Embryo fibroblast by MafA is dependent on its phosphorylation status. Using microarray analysis, we identify a gene expression subprogram regulated by MafA phosphorylation. Keywords: phosphorylation mediated transcriptional regulation

2007-12-25 | GSE9045 | GEO

RNA sequencing for PDX1, NGN3 and MAFA transduced iPSCs cell

Project description:Global gene expression profiling identifies accelerated induction of genes upon PDX1, NGN3 and MAFA transduction.

2019-07-03 | GSE133731 | GEO

GPRC5B preserves a mature β-cell state in obesity by controlling MafA expression [dof92_RNA-seq]

Project description:In vitro studies have implicated orphan receptor GPRC5B in β-cell survival, proliferation and insulin secretion, but its relevance for glucose homeostasis in vivo is largely unknown. Using tamoxifen-inducible, β-cell-specific GPRC5B knockout mice (Ins-G5b-KOs) we show here that loss of GPRC5B does not affect β-cell function in the lean state, but results in strongly reduced insulin secretion and disturbed glucose tolerance in mice subjected to high fat diet for 16 weeks. Flow cytometry and single-cell expression analyses in islets from obese mice show a reduced β-cell abundance and a less mature β-cell phenotype in Ins-G5b-KOs. Expression of β-cell-specific transcription factor MafA is reduced both on the RNA and protein level, as are transcripts of MafA target genes. Mechanistically, we show that phosphorylation of cAMP response element-binding protein (CREB), a major regulator of MafA expression, is reduced in islets of obese Ins-G5b-KOs, and that this phenotype precedes the downregulation of MafA and MafA target genes. Taken together, GPRC5B helps to maintain mature β-cell function in obesity through cAMP/CREB-dependent regulation of MafA expression.

2025-08-26 | GSE305580 | GEO

GPRC5B preserves a mature β-cell state in obesity by controlling MafA expression [dof105_scRNA-seq]

2025-08-26 | GSE305588 | GEO

Bulk RNASeq S64F MAFA male islets

Project description:Bulk RNASeq S64F MAFA male islets

| PRJNA1273941 | ENA

Gene expression following transverse aortic constriction in mice housed under normoxic or hypoxic conditions

Project description:mRNA expression profiles from C57/Bl6J mouse hearts 3 days after transverse aortic constriction (TAC) or sham surgery. Mice were house under normoxic (21% O2) or hypoxic conditions (12% O2).

2024-12-02 | GSE218522 | 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