Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes

ABSTRACT: To understand the mechanism underlying the role of MOTS-c in protecting pancreatic islets from senescence, we performed gene microarray analyses in pancreatic islet cells treated with either MOTS-c or a scrambled peptide

ORGANISM(S): Mus musculus

PROVIDER: GSE305383 | GEO | 2025/09/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes

Project description:Mitochondria are principal metabolic organelles that are increasingly unveiled as immune regulators. However, it is currently not known whether mitochondrial-encoded peptides modulate T cells to induce changes in phenotype and function. Here, we found that MOTS-c prevented autoimmune β-cell destruction via phenotypical and functional changes of T cells in NOD mice, a type 1 diabetes (T1D) animal model. MOTS-c ameliorated the development of hyperglycemia and reduced islet-infiltrating immune cells. Furthermore, adoptive transfer of T cells from MOTS-c-treated NOD mice significantly decreased the incidence of diabetes in NOD-SCID mice. Metabolic and genomic analysis revealed that MOTS-c modulated T cell phenotype and function by regulating TCR/mTORC1 pathway. We observed that T1D patients had a lower serum MOTS-c level than healthy controls. Furthermore, MOTS-c reduced T cell activation by alleviating T cells from the glycolytic stress in T1D patients suggesting a potential therapeutic implication. Our findings indicate that the MOTS-c acts as a regulator of T cell phenotype and function in autoimmune diabetes.

2021-03-06 | GSE168324 | GEO

MOTS-c peptide binding protein

Project description:To elucidate the molecular mechanism of MOTS-c against NASH progression, we screened for potential MOTS-c binding proteins using biotin-labeled MOTS-c and HuProt human proteome microarray.

2024-01-18 | GSE253264 | GEO

The mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes

Project description:The mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes

| PRJNA706909 | ENA

MOTS-c: A Novel Peptide Encoded by a Short Mitochondrial Open Reading Frame Regulates Metabolic Homeostasis

Project description:Mitochondria are known to be functional organelles, but their role as a signaling unit is increasingly being appreciated. The recent identification of a short open reading frame (sORF) in the mitochondrial DNA (mtDNA) that encodes a signaling peptide, humanin, suggests the possible existence of additional sORFs in the mtDNA that yield bioactive peptides. Here we report the identification of a sORF within the mitochondrial 12S rRNA encoding a 16-amino-acid peptide named MOTS-c (mitochondrial open-reading-frame of the twelve S rRNA -c) that regulates insulin sensitivity and metabolic homeostasis. MOTS-c is detected in various tissues and in circulation in an age-dependent manner. Its primary target organ appears to be the skeletal muscle and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, causing a significant accumulation of AICAR levels concomitantly with AMPK activation. MOTS-c treatment in mice prevented age-dependent and high-fat diet-induced insulin resistance, as well as diet-induced obesity. These results suggest that mitochondria may be more actively engaged in regulating metabolic homeostasis than previously recognized, through the production of peptides encoded within its genome that act at the cellular and organismal level. Human embryonic kidney cells (HEK293 cell line) were cultured in 10-cm dishes in 7 mL of phenol-free DMEM supplemented with 10% FBS and incubated with water (controls) or the 16-amino-acid peptide mitochondrial open-reading-frame of the twelve S rRNA-c (MOTS-c, 10 uM) for 4 or 72 hours prior to RNA extraction.

2015-03-07 | E-GEOD-65068 | biostudies-arrayexpress

Mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes.

Project description:Mitochondria are principal metabolic organelles that are increasingly unveiled as immune regulators. However, it is currently not known whether mitochondrial-encoded peptides modulate T cells to induce changes in phenotype and function. In this study, we found that MOTS-c (mitochondrial open reading frame of the 12S rRNA type-c) prevented autoimmune β cell destruction by targeting T cells in non-obese diabetic (NOD) mice. MOTS-c ameliorated the development of hyperglycemia and reduced islet-infiltrating immune cells. Furthermore, adoptive transfer of T cells from MOTS-c-treated NOD mice significantly decreased the incidence of diabetes in NOD-severe combined immunodeficiency (SCID) mice. Metabolic and genomic analyses revealed that MOTS-c modulated T cell phenotype and function by regulating T cell receptor (TCR)/mTOR complex 1 (mTORC1) signaling. Type 1 diabetes (T1D) patients had a lower serum MOTS-c level than did healthy controls. Furthermore, MOTS-c reduced T cell activation by alleviating T cells from the glycolytic stress in T1D patients, suggesting therapeutic potential. Our findings indicate that MOTS-c regulates the T cell phenotype and suppresses autoimmune diabetes.

| S-EPMC10083145 | biostudies-literature

MOTS-c: A Novel Peptide Encoded by a Short Mitochondrial Open Reading Frame Regulates Metabolic Homeostasis

2015-03-07 | GSE65068 | GEO

MOTS-c peptide binding protein

Project description:MOTS-c peptide binding protein

| PRJNA1064922 | ENA

Effect of MOTS-c treatment on cast immobilization-induced skeletal muscle atrophy

Project description:To understand the effect of MOTS-c treatment on cast immobilization-induced skeletal muscle atrophy, we injected MOTS-c into casted mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of three groups: non-immobilization group, immobilization control group, and immobilization and MOTS-c treated group.

2024-07-03 | GSE212709 | GEO

Effect of K14Q MOTS-c treatment on cast immobilization-induced skeletal muscle atrophy

Project description:To understand the effect of K14Q MOTS-c treatment on cast immobilization-induced skeletal muscle atrophy, we injected K14Q MOTS-c into casted mice.

2025-08-15 | GSE274924 | GEO

Mitochondrial-Encoded Peptide MOTS-c, Diabetes, and Aging-Related Diseases.

Project description:Mitochondria are complex metabolic organelles with manifold pathophysiological implications in diabetes. Currently published mitochondrial-encoded peptides, which are expressed from the mitochondrial open reading frame of the 12S ribosomal RNA type-c (MOTS-c), 16S rRNA (humanin and short humanin like peptide 1-6 [SHLP1-6]), or small human mitochondrial open reading frame over serine tRNA (SHMOOSE) are associated with regulation of cellular metabolism and insulin action in age-related diseases, such as type 2 diabetes mellitus. This review focuses mainly on recent advances in MOTS-c research with regards to diabetes, including both type 1 and type 2. The emerging understanding of MOTS-c in diabetes may provide insight into the development of new therapies for diabetes and other age or senescence-related diseases.

| S-EPMC10244198 | biostudies-literature

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