ArticleThe Journal of biological chemistry2017
Serine/Threonine Kinase 40 (Stk40) Functions as a Novel Regulator of Skeletal Muscle Differentiation.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- STK40 inhibits profibrotic Arg1Acta pharmacologica Sinica · 2026Article
- Pseudokinase STK40 limits T cell exhaustion through COP1-dependent degradation of AP1-family transcription factors.Nature immunology · 2025Article
- STK40 inhibits trophoblast fusion by mediating COP1 ubiquitination to degrade P57Journal of translational medicine · 2024Article
- Future Perspectives in Oxidative Stress in Trisomy 13 and 18 Evaluation.Journal of clinical medicine · 2022Review
- Synthetic dysmobility screen unveils an integrated STK40-YAP-MAPK system driving cell migration.Science advances · 2021Article
- High STK40 Expression as an Independent Prognostic Biomarker and Correlated with Immune Infiltrates in Low-Grade Gliomas.International journal of general medicine · 2021Article
- Article
- RNA-Seq Reveals miRNA Role Shifts in Seven Stages of Skeletal Muscles in Goat Fetuses and Kids.Frontiers in genetics · 2020Article
- Article
- LRP5 regulates the expression of STK40, a new potential target in triple-negative breast cancers.Oncotarget · 2018Article
- Study of muscle contraction induced by electrical pulse stimulation and nitric oxide in C2C12 myotube cells.Journal of exercise nutrition & biochemistry · 2018Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle differentiation is a precisely coordinated process, and the molecular mechanism regulating the process remains incompletely understood. Here we report the identification of serine/threonine kinase 40 (Stk40) as a novel positive regulator of skeletal myoblast differentiation in culture and fetal skeletal muscle formation in vivo We show that the expression level of Stk40 increases during skeletal muscle differentiation. Down-regulation and overexpression of Stk40 significantly decreases and increases myogenic differentiation of C2C12 myoblasts, respectively. In vivo, the number of myofibers and expression levels of myogenic markers are reduced in the fetal muscle of Stk40 knockout mice, indicating impaired fetal skeletal muscle formation. Mechanistically, Stk40 controls the protein level of histone deacetylase 5 (HDAC5) to maintain transcriptional activities of myocyte enhancer factor 2 (MEF2), a family of transcription factor important for skeletal myogenesis. Silencing of HDAC5 expression rescues the reduced myogenic gene expression caused by Stk40 deficiency. Together, our study reveals that Stk40 is required for fetal skeletal muscle development and provides molecular insights into the control of the HDAC5-MEF2 axis in skeletal myogenesis.
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