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锌指转录因子 ZNF24 对血小板衍生生长因子受体-β的转录抑制作用。

The transcriptional repression of platelet-derived growth factor receptor-beta by the zinc finger transcription factor ZNF24.

机构信息

Department of Biochemical Pharmacy, Second Military Medical University, Shanghai, China.

出版信息

Biochem Biophys Res Commun. 2010 Jun 25;397(2):318-22. doi: 10.1016/j.bbrc.2010.05.110. Epub 2010 May 26.

DOI:10.1016/j.bbrc.2010.05.110
PMID:20510677
Abstract

The zinc finger transcription factor ZNF24 is a relatively uncharacterized Krüppel-like transcription factor, displaying a suppressive effect on the transcription. ZNF24 is involved in negative regulation of vascular endothelial growth factor (VEGF) and may represent a novel repressor of VEGF transcription. In a previous study, our analysis reveals that ZNF24 is a pleiotropic factor that has a role in hematopoiesis, brain development and cancers. Activation of PDGFR-beta is critically involved into various cell functions including recruitment of stromal cells and VEGF induction in tumor and perivascular cells. Here, overexpression of ZNF24 resulted in a significant down-regulation of PDGFR-beta, whereas silencing of ZNF24 with small interfering RNA led to increased PDGFR-beta expression. Overexpression of ZNF24 resulted in a significant decrease in PDGFR-beta promoter activity. These data suggest that ZNF24 is involved in negative regulation of PDGFR-beta and may represent a novel repressor of PDGFR-beta transcription.

摘要

锌指转录因子 ZNF24 是一种相对不为人知的 Krüppel 样转录因子,对转录具有抑制作用。ZNF24 参与血管内皮生长因子 (VEGF) 的负调控,可能代表 VEGF 转录的新型抑制剂。在之前的一项研究中,我们的分析表明 ZNF24 是一种多效性因子,在造血、大脑发育和癌症中发挥作用。PDGFR-β 的激活对各种细胞功能至关重要,包括招募基质细胞和肿瘤及血管周围细胞中 VEGF 的诱导。在此,ZNF24 的过表达导致 PDGFR-β 的显著下调,而用小干扰 RNA 沉默 ZNF24 则导致 PDGFR-β 表达增加。ZNF24 的过表达导致 PDGFR-β 启动子活性显著降低。这些数据表明 ZNF24 参与 PDGFR-β 的负调控,可能代表 PDGFR-β 转录的新型抑制剂。

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