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CART启动子CRE位点结合磷酸化的CREB。

CART promoter CRE site binds phosphorylated CREB.

作者信息

Lakatos A, Dominguez G, Kuhar M J

机构信息

Yerkes Regional Primate Research Center of Emory University, Division of Neuroscience, 954 Gatewood Rd. NE, Atlanta, GA 30329, USA.

出版信息

Brain Res Mol Brain Res. 2002 Jul 15;104(1):81-5. doi: 10.1016/s0169-328x(02)00321-2.

Abstract

It has been shown previously that: CART (cocaine- and amphetamine-regulated transcript) mRNA is tightly regulated in brain; protein kinase A (PKA) is involved in CART expression in GH3 cells; and a cyclic AMP-responsive element (CRE) site is present in the proximal promoter region of the CART gene. Thus, the goal of this study was to test if CRE binding protein (CREB) can bind to the consensus CRE site and if phosphorylation of CREB occurs in GH3 cells under conditions of enhanced CART gene expression. Electromobility shift assays showed that a 27-bp oligonucleotide containing the CART CRE site was indeed bound by nuclear factors. Western blotting showed that incubation of GH3 cells with forskolin, which enhances CART mRNA expression, caused an increase in phosphorylated CREB (P-CREB) levels. Supershift analyses indicated that the CART CRE oligo/protein complex interacted with a P-CREB antibody. Taken together, these data indicate that P-CREB is a likely regulator of CART expression in GH3 cells.

摘要

先前的研究表明

可卡因和苯丙胺调节转录物(CART)mRNA在大脑中受到严格调控;蛋白激酶A(PKA)参与GH3细胞中CART的表达;并且在CART基因的近端启动子区域存在一个环磷酸腺苷反应元件(CRE)位点。因此,本研究的目的是测试CRE结合蛋白(CREB)是否能结合到共有CRE位点,以及在CART基因表达增强的条件下,GH3细胞中CREB是否会发生磷酸化。电泳迁移率变动分析表明,含有CART CRE位点的27个碱基对的寡核苷酸确实被核因子结合。蛋白质印迹法表明,用福司可林处理GH3细胞可增强CART mRNA表达,导致磷酸化CREB(P-CREB)水平升高。超迁移分析表明,CART CRE寡核苷酸/蛋白质复合物与P-CREB抗体相互作用。综上所述,这些数据表明P-CREB可能是GH3细胞中CART表达的调节因子。

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