Coming soon
MOTS-c
20mg · Single vial · Lyophilized powder
- Dose
- 20mg
- Pack size
- Single vial
- Form
- Lyophilized powder
- Storage
- 2–8°C
In vitro laboratory research use only · Not for human or veterinary use · Batch documented · Third-party tested · Ships from Canada
§ Research
Research · MOTS-c
Overview
MOTS-c (mitochondrial open reading frame of the 12S rRNA type-c) is a 16-residue sequence encoded within the mitochondrial 12S rRNA region, Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg. It was first described in 2015 by Lee, Cohen, and colleagues at the University of Southern California. It belongs to a family of mitochondrial-derived signaling molecules and is studied as a reference compound in metabolic regulation, exercise physiology, and aging research. Unlike most signaling molecules, it is encoded by the mitochondrial rather than the nuclear genome, and its discovery broadened interest in small open reading frames within mitochondrial DNA.
Mechanism of action
Proposed to act as a mitochondria-to-nucleus signal. MOTS-c inhibits folate-dependent one-carbon metabolism and de novo purine biosynthesis, leading to accumulation of AICAR and activation of AMP-activated protein kinase (AMPK). Under metabolic stress it translocates to the nucleus, where it interacts with antioxidant response element-associated transcription factors including NRF2 to regulate nuclear gene expression. Skeletal muscle is a principal target tissue, where it enhances glucose uptake and insulin sensitivity. Recent work reports direct binding and activation of casein kinase 2 (CK2) in muscle. Circulating levels are reported to respond to exercise and metabolic state, consistent with an endocrine signaling role in addition to its intracellular actions.
Key research findings
- 01
Rodent studies characterize effects on insulin sensitivity and glucose homeostasis associated with AMPK activation in skeletal muscle.
- 02
Endogenous levels in human skeletal muscle and plasma increase following exercise, and administration in aged mice was associated with improved physical capacity endpoints.
- 03
Cell-culture studies characterize nuclear translocation under metabolic stress and regulation of NRF2-dependent gene expression.
- 04
Circulating levels decline with age in rodents and humans, prompting investigation as a marker of mitochondrial signaling.
Published references
MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis
MOTS-c modulates skeletal muscle function by directly binding and activating CK2
The information above is derived from published preclinical and clinical research. It is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment recommendations.