Cellular-biology research
MOTS-c
Lyophilized mitochondrial and cellular-signaling research material
MOTS-c is a mitochondrial-derived peptide studied in metabolic stress, AMPK-adjacent signaling, glucose metabolism, and cellular adaptation literature.
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Get catalog updatesSolo per ricerca di laboratorio. Non per uso umano o veterinario. Non destinato a diagnosticare, trattare, curare, mitigare o prevenire malattie.
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Contesto di ricerca
Profilo di ricerca MOTS-c
MOTS-c is a mitochondrial-derived peptide encoded within mitochondrial 12S rRNA and studied as a signal connecting mitochondrial status with cellular metabolism. Research examines metabolic stress, AMPK-adjacent signaling, glucose handling, mitochondrial-to-nuclear communication, gene expression, exercise-related models, and aging-associated markers. It differs from SS-31, which is studied primarily for interaction with the inner mitochondrial membrane and cardiolipin. MOTS-c is selected when a project focuses on signaling and metabolic adaptation rather than direct membrane stabilization. Most mechanistic evidence is preclinical, while human literature includes biomarker and observational work; neither establishes the performance of a specific catalog batch.
Meccanismo proposto
A mitochondrial-derived peptide proposed to act as a metabolic stress signal. Reported pathways include AMPK activation, altered folate and purine metabolism, GLUT4-related glucose uptake, and stress-dependent movement to the nucleus where it may influence gene expression.
Effetti riportati negli studi
- Cell studies report AMPK-related signaling, improved glucose uptake, stress resistance, and changes in metabolic gene expression.
- Mouse studies report improved insulin sensitivity, exercise capacity, metabolic homeostasis, and resistance to diet- or age-related metabolic stress.
- Human studies are mainly observational or biomarker based and do not establish the effects of administered MOTS-c.
Endpoint di ricerca comuni
AMPK phosphorylation, glucose uptake, insulin sensitivity, mitochondrial and nuclear gene expression, exercise capacity, body composition, metabolic stress, and circulating MOTS-c levels.
Evidenze e limiti
Mechanistic and animal evidence is promising, but interventional human evidence is limited and pharmacology remains incompletely defined.
External reading
Literature for context—not product proof.
Third-party sources describe their own research materials and methods. They do not validate a specific Azure catalog batch.
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