ArticleMolecular biology reports2014
SOCS2 inhibited mitochondria biogenesis via inhibiting p38 MAPK/ATF2 pathway in C2C12 cells.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Mitochondrial oxidative stress in skeletal muscle alters metabolic signaling responses to acute muscle contraction.Free radical biology & medicine · 2026Article
- Commitment to Myogenic Differentiation Significantly Aggravates the RNA Phenotype in Myotonic Dystrophy Type 1.Neuropathology and applied neurobiology · 2026Article
- Cytosine base editor-mediated SOCS2 knockout promotes C2C12 cell differentiation via the PI3K/AKT/mTOR signaling pathway.Functional & integrative genomics · 2025Article
- Amyloid-β impairs mitochondrial dynamics and autophagy in Alzheimer's disease experimental models.Scientific reports · 2022Article
- SOCS2 Inhibits Mitochondrial Fatty Acid Oxidation via Suppressing LepR/JAK2/AMPK Signaling Pathway in Mouse Adipocytes.Oxidative medicine and cellular longevity · 2020Article
- KIAA0317 regulates pulmonary inflammation through SOCS2 degradation.JCI insight · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
In order to investigate the mechanism of suppressor of cytokine signaling 2 (SOCS2) on mitochondrial biogenesis, RNA interference and over-expression plasmid vectors of SOCS2 were used to transfect murine skeletal muscle C2C12 cells. Results demonstrated that over-expression of SOCS2 inhibited the differentiation of C2C12 cells, and reduced the expression of MyHC, MyoD and MyoG while elevated the protein expression of MSTN. Meanwhile the expression of PGC-1α, MDH, CPT-1 were significantly elevated in the RNA interference of SOCS2 group which were decreased in SOCS2 overexpression group. However, there was no change on the expression of UCP1 in both two groups. JC-1 dyeing showed overexpression of SOCS2 decreased the mitochondrial membrane potential and results of immunofluorescence, real-time PCR and western blotting indicated the increase expression of Cyt c, while interference SOCS2 had the opposite effects in C2C12 cells. Moreover, interference of SOCS2 elevated the p38 phosphorylation level then further increased the phosphorylation of ATF2, whereas overexpression of SOCS2 alleviated this phenomenon. Taken together, our observations indicated that SOCS2 could suppress myotube formation, act as an anti-regulator of mitochondria biogenesis via inhibiting p38 MAPK signal pathway.
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