| Literature DB >> 33778212 |
Jing Li1, Go Urabe1, Yitao Huang1, Mengxue Zhang1,2, Bowen Wang1, Lynn Marcho3, Hongtao Shen1, K Craig Kent1, Lian-Wang Guo1.
Abstract
Polo-like kinase 4 (PLK4) is canonically known for its cytoplasmic function in centriole duplication. Here we show a noncanonical PLK4 function of regulating the transcription factor SRF's nuclear activity and associated myofibroblast-like cell-type transition. In this context, we have further found that PLK4's phosphorylation and transcription are respectively regulated by PDGF receptor and epigenetic factor BRD4. Furthermore, in vivo experiments suggest PLK4 inhibition as a potential approach to mitigating vascular fibrosis.Entities:
Keywords: AA, PDGF-AA; BET, bromo/extraterminal domain–containing protein; BRD4; BRD4, bromodomain protein 4; CenB, centrinone-B; EEL, external elastic lamina; JQ1, a BET family–selective epigenetic modulator drug; MRTF-A, myocardin-related transcription factor A; PDGF receptor; PDGF, platelet-derived growth factor; PDGFR, PDGF receptor; PLK, polo-like kinase; PLK4; SRF; SRF, serum response factor; fibroblast cell-type transition; αSMA, α-smooth muscle actin
Year: 2021 PMID： 33778212 PMCID： PMC7987547 DOI： 10.1016/j.jacbts.2020.12.015
Source DB: PubMed Journal: JACC Basic Transl Sci ISSN： 2452-302X