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肌细胞生成素独立于其他肌肉特异性基因产物诱导肌细胞特异性增强子结合因子MEF-2。

Myogenin induces the myocyte-specific enhancer binding factor MEF-2 independently of other muscle-specific gene products.

作者信息

Cserjesi P, Olson E N

机构信息

Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030.

出版信息

Mol Cell Biol. 1991 Oct;11(10):4854-62. doi: 10.1128/mcb.11.10.4854-4862.1991.

Abstract

The myocyte-specific enhancer-binding factor MEF-2 is a nuclear factor that interacts with a conserved element in the muscle creatine kinase and myosin light-chain 1/3 enhancers (L. A. Gossett, D. J. Kelvin, E. A. Sternberg, and E. N. Olson, Mol. Cell. Biol. 9:5022-5033, 1989). We show in this study that MEF-2 is regulated by the myogenic regulatory factor myogenin and that mitogenic signals block this regulatory interaction. Induction of MEF-2 by myogenin occurs in transfected 10T1/2 cells that have been converted to myoblasts by myogenin, as well as in CV-1 kidney cells that do not activate the myogenic program in response to myogenin. Through mutagenesis of the MEF-2 site, we further defined the binding site requirements for MEF-2 and identified potential MEF-2 sites within numerous muscle-specific regulatory regions. The MEF-2 site was also found to bind a ubiquitous nuclear factor whose binding specificity was similar to but distinct from that of MEF-2. Our results reveal that MEF-2 is controlled, either directly or indirectly, by a myogenin-dependent regulatory pathway and suggest that growth factor signals suppress MEF-2 expression through repression of myogenin expression or activity. The ability of myogenin to induce MEF-2 activity in CV-1 cells, which do not activate downstream genes associated with terminal differentiation, also demonstrates that myogenin retains limited function within cell types that are nonpermissive for myogenesis and suggests that MEF-2 is regulated independently of other muscle-specific genes.

摘要

肌细胞特异性增强子结合因子MEF-2是一种核因子,它与肌肉肌酸激酶和肌球蛋白轻链1/3增强子中的保守元件相互作用(L.A.戈塞特、D.J.凯尔文、E.A.斯特恩伯格和E.N.奥尔森,《分子细胞生物学》9:5022 - 5033,1989年)。我们在本研究中表明,MEF-2受生肌调节因子肌细胞生成素调控,且有丝分裂信号会阻断这种调节相互作用。肌细胞生成素诱导MEF-2在已被肌细胞生成素转化为成肌细胞的转染10T1/2细胞中发生,也在对肌细胞生成素无反应而不激活生肌程序的CV-1肾细胞中发生。通过对MEF-2位点进行诱变,我们进一步确定了MEF-2的结合位点要求,并在众多肌肉特异性调节区域内鉴定出潜在的MEF-2位点。还发现MEF-2位点结合一种普遍存在的核因子,其结合特异性与MEF-2相似但不同。我们的结果表明,MEF-2直接或间接受肌细胞生成素依赖性调节途径控制,并提示生长因子信号通过抑制肌细胞生成素的表达或活性来抑制MEF-2的表达。肌细胞生成素在不激活与终末分化相关的下游基因的CV-1细胞中诱导MEF-2活性的能力,也表明肌细胞生成素在不允许发生肌生成的细胞类型中保留有限功能,并提示MEF-2的调节独立于其他肌肉特异性基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9774/361454/8397a817de22/molcellb00034-0061-a.jpg

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