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一种增强子核心元件在心肌细胞肥大过程中介导α1-肾上腺素能激动剂和活化的β-蛋白激酶C对大鼠β-肌球蛋白重链启动子的刺激作用。

An enhancer core element mediates stimulation of the rat beta-myosin heavy chain promoter by an alpha 1-adrenergic agonist and activated beta-protein kinase C in hypertrophy of cardiac myocytes.

作者信息

Kariya K, Karns L R, Simpson P C

机构信息

Division of Cardiology, Veterans Affairs Medical Center, San Francisco, California 94121.

出版信息

J Biol Chem. 1994 Feb 4;269(5):3775-82.

PMID:8106422
Abstract

In hypertrophy of cultured rat cardiac myocytes, alpha 1-adrenergic agonists activate protein kinase C (PKC) and up-regulate beta-myosin heavy chain (MHC). The 3300-base pair (bp) rat beta-MHC promoter is stimulated by both an alpha 1-agonist and a constitutively activated mutant of beta-PKC (Kariya, K., Karns, L. R., Simpson, P. C. (1991) J. Biol. Chem. 266, 10023-10026). Here, we report the convergence of alpha 1-adrenergic and beta-PKC signaling on the same element of the beta-MHC promoter. A 20-bp sequence in the beta-MHC promoter (-215/-196) was required for induction by both alpha 1-adrenergic stimulation and beta-PKC and conferred induction on a heterologous promoter. This sequence bound myocyte nuclear factor(s) through a 9-bp "enhancer core" (5'-TGTGGTATG-3'). A 3-bp mutation within the enhancer core which abolished factor binding also abolished inducibility of a 215-bp beta-MHC promoter. These results support the idea that beta-PKC is in the pathway for alpha 1-adrenergic regulation of beta-MHC transcription during cardiac myocyte hypertrophy. The enhancer core is the first PKC response element mapped by transfection of an activated PKC mutant, rather than by treatment with phorbol esters.

摘要

在培养的大鼠心肌细胞肥大过程中,α1 - 肾上腺素能激动剂激活蛋白激酶C(PKC)并上调β - 肌球蛋白重链(MHC)。3300个碱基对(bp)的大鼠β - MHC启动子受到α1 - 激动剂和β - PKC的组成型激活突变体的刺激(Kariya,K.,Karns,L. R.,Simpson,P. C.(1991)J. Biol. Chem. 266,10023 - 10026)。在此,我们报告α1 - 肾上腺素能和β - PKC信号在β - MHC启动子的同一元件上汇聚。β - MHC启动子中一个20 bp的序列(-215 / -196)是α1 - 肾上腺素能刺激和β - PKC诱导所必需的,并赋予异源启动子诱导能力。该序列通过一个9 bp的“增强子核心”(5'-TGTGGTATG-3')结合心肌细胞核因子。增强子核心内一个消除因子结合的3 bp突变也消除了215 bp β - MHC启动子的诱导性。这些结果支持β - PKC处于心肌细胞肥大过程中α1 - 肾上腺素能对β - MHC转录调控途径中的观点。该增强子核心是通过转染激活的PKC突变体而非佛波酯处理绘制的第一个PKC反应元件。

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