The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Hopx and Hdac2 Interact to Modulate Gata4 Acetylation and Embryonic Cardiac Myocyte Proliferation
Open accessAbstract
Summary Regulation of chromatin structure via histone modification has received intense recent attention. Here, we demonstrate that the chromatin modifying enzyme histone deacetylase 2 (Hdac2) functions with a small homeodomain factor, Hopx, to mediate deacetylation of Gata4, which is expressed by cardiac progenitor cells and plays critical roles in the regulation of cardiogenesis. In the absence of Hopx and Hdac2 in mouse embryos, Gata4 hyperacetylation is associated with a marked increase in cardiac myocyte proliferation, up-regulation of Gata4 target genes, and peri-natal lethality. Hdac2 physically interacts with Gata4, and this interaction is stabilized by Hopx. The ability of Gata4 to transactivate cell cycle genes is impaired by Hopx/Hdac2-mediated deacetylation and this effect is abrogated by loss of Hdac2-Gata4 interaction. These results suggest that Gata4 is a non-histone target of Hdac2-mediated deacetylation and that Hdac2, Hopx and Gata4 coordinately regulate cardiac myocyte proliferation during embryonic development.
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Self-citationMeis1 regulates postnatal cardiomyocyte cell cycle arrest
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He, X., Hui, Z., Xu, L., Bai, R., Gao, Y., Wang, Z., Xie, T., & Ye, X.-Y. (2022) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2021.113946 · Cited by 89
Metadata
- Authors
- Trivedi, C. M., Zhu, W., Wang, Q., Jia, C., Kee, H. J., Li, L., Hannenhalli, S., & Epstein, J. A.
- Venue
- Developmental Cell
- Publisher
- Elsevier BV
- Published
- 2010-09
- Volume
- 19
- Issue
- 3
- Pages
- 450-459
- ISSN
- 1534-5807 (ISSN-L)
- OpenAlex
- W2019725230
- Cited by
- 160
- References
- 6
- FWCI
- 3.90
- Type
- journal article
- Language
- en
- Open access
- bronze
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