MOTS-c modulates skeletal muscle function by directly binding and activating CK2.
Kumagai H, Kim SJ, Miller B et al. · iScience · PMID 39559755
Study summary
Main finding
Experiments identified CK2 binding and linked MOTS-c signaling to muscle preservation and glucose uptake; genetic associations varied with sex and age.
Biochemical assays, mouse muscle, and human genetic observations
How the study was set up
Cell-free binding assays and mouse administration experiments were combined with observational analyses of a naturally occurring human MOTS-c variant.
What the researchers measured
CK2 binding and activity, muscle atrophy, glucose uptake, tissue-specific signaling, and associations with sarcopenia and diabetes were assessed.
How to read this evidence
This paper combines observations in people with laboratory or animal experiments. Measuring a naturally occurring peptide in people is different from testing peptide administration.
Results in context
MOTS-c did not have identical signaling effects in muscle and fat. Human genetic associations differ from intervention evidence and varied with sex, age, and activity.
What this does not establish
Human genetic associations are not treatment results. Mouse and biochemical findings cannot establish clinical efficacy or safety.
Publication & source
Why this paper is included
The compound is a named subject of the publication title.
Publication indexing
Journal Article
Source checked
October 4, 2026. Years follow journal issues; online-first dates may differ.