Study record

MOTS-c modulates skeletal muscle function by directly binding and activating CK2

Kumagai H, Kim SJ, Miller B et al. · iScience · 2024

Human obs.SeveralEvidence tier BAlso: Animal study (in vivo)Also: Cell study (in vitro)

What this study reported

Reported that MOTS-c binds and activates CK2 in cell-free systems, and that in mice administered MOTS-c was associated with less skeletal muscle atrophy and greater muscle glucose uptake, effects blunted when CK2 activity was suppressed. In human carriers, the K14Q variant was associated with higher sarcopenia and type 2 diabetes risk in men in an age- and physical-activity-dependent way, and with an age-specific lower type 2 diabetes risk in women.

Limitations

The human analysis is observational with no sample size reported in the abstract; animal work does not state sex or group sizes; tissue-specific conclusions are inferred from a single kinase target.

Study record

Annotated fields for this study
Study modelHuman observational
Substance studiedSeveralMore than one of these is central to the paper (common for reviews).
Specieshuman, mouse
System studiedCell-free CK2 assays, mice given MOTS-c, and human carriers of the K14Q MOTS-c variant
Populationhuman carriers and non-carriers of the K14Q MOTS-c variant
DesignMechanistic cell and animal experiments with a human genetic association analysis
Sample size as reportedNot reported
Control groupnon-carriers of the variant; untreated mice and cell-free systems
Route (data field only)Not reported
Endpoints measuredCK2 binding and activity; skeletal muscle atrophy; muscle glucose uptake; sarcopenia risk; type 2 diabetes risk
Pathways measuredInsulin & glucose handling · Other
Research areasSkeletal muscle · Metabolic · Aging
Evidence tierB — Other human study
Publication typesJournal Article

Appraisal

Each dimension is recorded separately and never combined into a single score. A study can be well controlled and still tell you little about people.

Relevance to MOTS-c
Direct
Model applicability
Human
Sample size
Not reported
Controls
Appropriate
Outcome validity
Surrogate
Support for its own conclusion
Moderate

Provenance

  • Bibliographic fields retrieved from PubMed E-utilities efetch (title, journal, date, authors, DOI) on 2026-11-11.
  • Annotated from the published abstract.
  • Editorial review: approved (2026-11-11).
  • Classification follows the site methodology; the record describes the study, not what MOTS-c does in people.