The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress.
Kim KH, Son JM, Benayoun BA et al. · Cell metabolism · PMID 29983246
Study summary
Main finding
MOTS-c moved to the nucleus in an AMPK-dependent response to metabolic stress. The authors linked it to changes in stress-response genes and interactions with NRF2-associated regulatory pathways.
Cell experiments examined movement of MOTS-c from mitochondria-related signaling into the nucleus during metabolic stress and glucose restriction.
What the researchers measured
Nuclear localization, AMPK dependence, gene-expression changes, and interactions with stress-responsive transcription factors were measured.
How to read this evidence
Researchers studied cells, isolated tissue, or animals. These experiments can help explain a mechanism, but do not establish benefits or safety in people. Human cells grown in a laboratory also belong in this category.
Results in context
The results describe communication inside cells. A change in stress-response genes is not a measurement of human metabolic health or longevity.
What this does not establish
Mechanistic cell experiments do not demonstrate therapeutic effects, exercise benefits, or safety from administering MOTS-c to people.
Publication & source
Why this paper is included
The compound is a named subject of the publication title.
Publication indexing
Journal Article · Research Support, N.I.H., Extramural · Research Support, Non-U.S. Gov't
Indexed subjects
AMP-Activated Protein Kinases · Animals · Antioxidant Response Elements · Cell Line · Cell Nucleus · Gene Expression · Gene Expression Regulation · Glucose · HEK293 Cells · Hep G2 Cells · Homeostasis · Humans · Mitochondria · Mitochondrial Proteins · NF-E2-Related Factor 2 · Signal Transduction · Stress, Physiological
Source checked
October 4, 2026. Years follow journal issues; online-first dates may differ.