Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Phospho-antibody microarray analyses for islets of control and Mettl14 knock-out mice

ABSTRACT: β-cell specific Mettl14 knock-out mice display reduced N6-methyladenosine (m6A) levels and recapitulate human Type II diabetes (T2D) islet phenotype with early diabetes onset and mortality secondary to decreased β-cell proliferation and insulin degranulation. To gain insights into the role of m6A in regulating the IGF1/insulin -> AKT - > PDX1 pathway and to dissect the signaling networks modulating AKT phosphorylation, we subjected freshly isolated islets from control and Mettl14 knock-out mice to phospho-antibody microarrays.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE132111 | GEO | 2019/08/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Adipose METTL14-elicited N6-methyladenosine promotes obesity, insulin resistance, and NAFLD by suppressing β adrenergic signaling and lipolysis

Project description:Obesity is associated with impaired β-adrenergic receptor (Adrb1-3) signaling and lipolysis, leading to aberrant white adipose tissue (WAT) growth. WAT research has been centered on transcriptional and posttranslational regulations, but posttranscriptional regulation and mRNA modifications are poorly understood. Here, we unveil a METTL14/N6-methyladenosine (m6A) paradigm guiding β-adrenergic signaling and lipolysis. METTL14 complex installs m6A on RNA, regulating mRNA fate and translation. We found that feeding and insulin increased adipose Mettl14 and m6A levels. Adipose Mettl14 and m6A were upregulated in high fat diet (HFD)-induced obesity. Ablation of adipose Mettl14 decreased Adrb2, Adrb3, Atgl (encoding lipase), and Cig-58 (Atgl activator) transcript m6A contents while increasing their translation and protein levels, thereby enhancing adipose β-adrenergic signaling and lipolysis. Consequently, adipocyte-specific Mettl14 knockout mice were resistant to HFD-induced obesity, insulin resistance, glucose intolerance, and NAFLD. These results unravel a METTL14/m6A-based epitranscriptomic mechanism governing β-adrenergic signaling, lipolysis, and adipose growth in health and disease.

2023-06-04 | GSE233782 | GEO

METTL14 regulates neuroblastoma through the m6A modification

Project description:RNA methylation is involved in the regulation of cell response and cell fate, and is closely related to the development of tumors. METTL14 is considered to be a m6A methyltransferase. Studies have found that METTL14 is associated with the occurrence and development of a variety of tumors, but the mechanism in neuroblastoma is not clear. The expression of METTL14 in high risk patients was significantly higher than that in low risk patients. Interference with METTL14 expression in SK-N-BE(2) cells significantly interfered with cell cycle and inhibited cell proliferation, migration and invasion. In neuroblastoma, METTL14 activates the PI3K/AKT signaling pathway by targeting YWHAH by upregulating m6A levels in mRNA transcripts. In all findings, it was suggested that METTL14 has a cancer-promoting function in neuroblastoma.

2024-05-10 | GSE244350 | GEO

METTL14-mediated m6A differentially orchestrates brown and white adipose tissue transcriptomes to regulate systemic metabolism

Project description:Human brown and white adipocytes (hBAT and hWAT) display markedly distinct m6A landscapes; besides, in insulin-resistant humans and mice, methyltransferase like 14 (METTL14) expression differs significantly between BAT and WAT in the context of its correlation with insulin sensitivity. We therefore employed independent BAT- and WAT-specific METTL14 knockout models to unveil the cell-type specificity of m6A mRNA methylation. Mettl14 knockout via Ucp1-cre or Adipoq-cre drivers in BAT and WAT, respectively, yields divergent metabolic outcomes in mouse.

2024-11-08 | GSE250137 | GEO

m6A-sequencing of Mettl14-conditional knock-out retinas and matched control.

Project description:m6A-sequencing of Mettl14-conditional knock-out retinas and matched control.

| PRJNA848799 | ENA

Expression profiling of METTL14 depleted human pancreatic β-like cells

Project description:N6-methyladenosine (m6A) is the most abundant chemical modification in mRNA, and plays important roles in human embryonic stem cell pluripotency, maintenance, and differentiation. However, the role of m6A and the precise mechanisms involved during the development of β-cells are unexplored. Here, we explored the requirement of METTL14-mediated m6A RNA methylome in human pancreatic β-like cells by simultaneously inducing METTL14 knockdown in H1 human embryonic stem cells (hESCs) with doxycycline (Dox) treatment and differentiating hESCs towards pancreatic β-like cells in vitro.

2024-06-13 | GSE236323 | GEO

N6-methyladenosine (m6A) profiling of EndoC-bH1 cell line and RNA seq of Mettl14 knockout mice beta cell

Project description:In type 2 diabetes, pancreatic beta-cells fail to compensate for the presence of insulin resistance in target tissues and represent a central player in the disease development. Identifying and studying innovative molecular mechanisms that lead to beta-cell failure in diabetes represent an interesting line of research and are necessary. N6-Methyladenosine (m6A) is the most abundant modification in mRNA and is found virtually in all mammals. Through m6A-profiling of m6A methyltransferase depleted animal model and human beta cell model, we aim to characterize the pathways affected by m6A methylation in the beta cells.

2019-08-09 | GSE132306 | GEO

METTL14-mediated N6-methyladenosine modification of Col17a1/Itgα6/Itgβ4 governs epidermal homeostasis [MeRIP-seq]

Project description:To elucidate the role of METTL14-mediated m6A modification in epidermal development, we conditionally knocked out the m6A methyltransferase METTL14 in mouse epidermal keratinocytes. We then performed MeRIP-seq analysis of epidermal keratinosis from P0 control mice (K14Cre,Mettl14F/+).

2023-12-31 | GSE246652 | GEO

METTL14-mediated N6-methyladenosine modification of Col17a1/Itgα6/Itgβ4 governs epidermal homeostasis [RNA-Seq]

Project description:To elucidate the role of METTL14-mediated m6A modification in epidermal development, we conditionally knocked out the m6A methyltransferase METTL14 in mouse epidermal keratinocytes. We then performed RNA-seq analysis of epidermal keratinosis from P0 control mice (K14Cre,Mettl14F/+) and cKO mice (K14CreMettl14F/F).

2023-12-31 | GSE246720 | GEO

METTL14-mediated N6-methyladenosine modification of Col17a1/Itgα6/Itgβ4 governs epidermal homeostasis [Ribo-Seq]

Project description:To elucidate the role of METTL14-mediated m6A modification in epidermal development, we conditionally knocked out the m6A methyltransferase METTL14 in mouse epidermal keratinocytes. We then performed ribosome-profiling analysis of epidermal keratinosis from P0 control mice (K14Cre,Mettl14F/+) and cKO mice (K14CreMettl14F/F).

2023-12-31 | GSE246653 | GEO

Primarily Dissecting the Autonomous and Cooperative Functions of METTL3 and METTL14 in mRNA Modification and Tumor Progression

Project description:METTL3 and METTL14 are considered to faithfully form the m6A writing complex in a 1:1 ratio, regulating the fate of mRNA by adding m6A modifications. However, recent studies have shown inconsistent expression and prognostic value of METTL3 and METTL14 in some tumors, suggesting that they may not be faithful in tumors. Pan-cancer analysis based on TCGA data reveals significant differences in expression, function, tumor burden correlation, and immune correlation between METTL3 and METTL14, especially in esophageal squamous cell carcinoma (ESCC). Knockdown of METTL3 significantly inhibits the cell proliferation in vitro and in vivo in ESCC EC109 cells, while the impact of METTL14 knockdown on proliferation is limited, and it cannot abolish the expression of METTL3 protein. mRNA-seq results indicate that METTL3 independently regulates the expression of 1615 genes, while only 776 genes are co-regulated by METTL3 and METTL14. Furthermore, through immunofluorescence co-localization, it is observed that METTL3 and METTL14 have certain inconsistencies in cellular localization. HPLC-MS results show that METTL3 independently binds to the Nop56p-associated pre-rRNA complex and mRNA splicing complex, separate from METTL14. Through bioinformatics and various omics studies, we have preliminarily discovered that METTL3 independently regulating tumor cell proliferation, and the participation in mRNA splicing may be a critical molecular mechanism. Our study provides an experimental basis and theoretical foundation for further understanding of the m6A writing complex and tumor therapy targeting METTL3.

2024-02-01 | PXD048886 | Pride

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