MOTS-c peptide binding protein
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1064922 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description: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
2025-09-11 | GSE305383 | GEO
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
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.
2015-03-07 | GSE65068 | GEO
Project description:This clinical trial studies the side effects of 18F-alphavbeta6-binding-peptide and how well it works in imaging patients with primary or cancer that has spread to the breast, colorectal, lung, or pancreatic. Radiotracers, such as 18F-alphavbeta6-binding-peptide, may improve the ability to locate cancer in the body.
| 2245248 | ecrin-mdr-crc
Project description:Engineered Peptide Barcodes for In-Depth Analyses of Binding Protein Ensembles
| PRJEB25673 | ENA
Project description:Peptide binding to human IgE antibody
| PRJEB87853 | ENA
Project description:BACKGROUND: Atrial fibrillation (AF) is the most common clinical arrhythmia associated with mitochondrial dysfunction, oxidative stress, and atrial fibrosis. Mitochondrial-derived peptides (MDPs) including humanin (HN) and MOTS-c, demonstrated potent cytoprotective effects, but their role in AF remains elusive. METHODS: Public GEO database, immunohistochemistry and immunofluorescence were applied to determine their expressions in atrial tissues. Plasma peptide levels were measured in a clinical cohort. Murine AF models and primary rat cardiomyocytes and fibroblasts models were established by administration of angiotensin II (Ang II) and treated with (Gly14)-Humanin (HNG, an HN analogue) or MOTS-c. RESULTS: Both HN and MOTS-c gene expressions were significantly downregulated in human AF atrial tissue and negatively correlated with the extent of fibrosis. Plasma MOTS-c level decreased in AF patients and showed an inverse correlation with NT-proBNP. In vivo, administration of HNG or MOTS-c significantly reduced AF inducibility, attenuated atrial fibrosis and hypertrophy induced by Ang II. Furthermore, HNG or MOTS-c treatment improved mitochondrial ultrastructure, as well as downregulated the expressions of mitochondrial fission proteins (Drp1 and Fis1) and pro-inflammatory cytokines (IL-1β and IL-6) of atrial tissue in murine AF models. In primary cardiomyocytes, both peptides mitigated Ang II-induced oxidative stress. In addition, they directly inhibited Ang II-induced fibroblast activation, proliferation, and migration in vitro. Further RNA sequencing results suggested that HNG mainly affects cell adhesion pathways and MOTS-c acts on metabolic process of cardiac fibroblasts. CONCLUSIONS: The downregulation of HN and MOTS-c in human AF is associated with AF severity. Administration of HNG or MOTS-c effectively suppressing atrial fibrosis and mitochondrial dysfunction and prevents AF in murine models. Therefore, mitochondrial-derived peptides represent as the underappreciated contributor to AF therapy and potential biomarkers.
2026-06-03 | GSE322635 | GEO
Project description:Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes
| PRJNA1305433 | ENA
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