ArticleActa biochimica et biophysica Sinica2023
E3 ligase Deltex2 accelerates myoblast proliferation and inhibits myoblast differentiation by targeting Pax7 and MyoD, respectively.
Article in Acta biochimica et biophysica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 1 citations in OpenAlex.
- The expanding landscape of Deltex: signaling crosstalk and clinical implications.Cellular and molecular life sciences : CMLS · 2026Review
- RNF126 writes a non-canonical ubiquitin code on midnolin to tune protein stability.Acta biochimica et biophysica Sinica · 2026Article
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8 authors.
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Abstract
E3 ubiquitin ligases are closely related to cell division, differentiation, and survival in all eukaryotes and play crucial regulatory roles in multiple biological processes and diseases. While Deltex2, as a member of the DELTEX family ubiquitin ligases, is characterized by a RING domain followed by a C-terminal domain (DTC), its functions and underlying mechanisms in myogenesis have not been fully elucidated. Here, we report that Deltex2, which is highly expressed in muscles, positively regulates myoblast proliferation via mediating the expression of Pax7. Meanwhile, we find that Deltex2 is translocated from the nucleus into the cytoplasm during myogenic differentiation, and further disclose that Deltex2 inhibits myoblast differentiation and interacts with MyoD, resulting in the ubiquitination and degradation of MyoD. Altogether, our findings reveal the physiological function of Deltex2 in orchestrating myogenesis and delineate the novel role of Deltex2 as a negative regulator of MyoD protein stability.
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