ArticleNucleic acids research2004
VITO-1 is an essential cofactor of TEF1-dependent muscle-specific gene regulation.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 68 citations in OpenAlex.
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- Kinetin stimulates differentiation of C2C12 myoblasts.PloS one · 2021Article
- TEAD2 as a novel prognostic factor for hepatocellular carcinoma.Oncology reports · 2020Article
- The Transcriptional Cofactor VGLL1 Drives Transcription of Human Papillomavirus Early Genes via TEAD1.Journal of virology · 2020Article
- Mechanosensitive transcriptional coactivators MRTF-A and YAP/TAZ regulate nucleus pulposus cell phenotype through cell shape.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- VGLL3 operates via TEAD1, TEAD3 and TEAD4 to influence myogenesis in skeletal muscle.Journal of cell science · 2019Article
- Deficiency ofFrontiers in sports and active living · 2019Article
- VGLL4 is a transcriptional cofactor acting as a novel tumor suppressor via interacting with TEADs.American journal of cancer research · 2018Review
- Regulation of the Hippo Pathway Transcription Factor TEAD.Trends in biochemical sciences · 2017Review
- Vestigial-like 3 is a novel Ets1 interacting partner and regulates trigeminal nerve formation and cranial neural crest migration.Biology open · 2017Article
- Vestigial-like 2 contributes to normal muscle fiber type distribution in mice.Scientific reports · 2017Article
- Review
- From vestigial to vestigial-like: the Drosophila gene that has taken wing.Development genes and evolution · 2016Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of several muscle-specific genes is partially or completely regulated by MCAT elements, which bind members of the TEF family of transcription factors. TEF1 itself is unable to activate reporter plasmids bearing TEF1-binding sites, suggesting that additional bridging or co-activating factors are necessary to allow interaction of TEF1 with the transcriptional machinery. In addition, none of the known TEF genes are exclusively expressed in the cardiac or skeletal muscle lineage to account for the muscle-specific expression of MCAT-dependent genes. Here we describe that VITO-1, a new SID (scalloped interaction domain)-containing protein, binds to TEF1 in vitro and strongly stimulates transcription of a MCAT reporter plasmid together with TEF-1. Since VITO-1 is predominantly expressed in the skeletal muscle lineage, it might serve as an essential transcriptional intermediary factor to promote muscle-specific expression via MCAT cis-regulatory elements. Although VITO-1 alone is not sufficient to initiate myogenic conversion of 10T1/2 fibroblastic cells, it enhanced MyoD-mediated myogenic conversion. In addition, interference with VITO-1 expression by siRNA attenuated differentiation of C2C12 muscle cells and MyoD-dependent myogenesis in 10T1/2 cells. We conclude that VITO-1 is a crucial new cofactor of the muscle regulatory programme.
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