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p21H-ras诱导的形态转化及c-myc表达增加与功能性蛋白激酶C无关。

p21H-ras-induced morphological transformation and increases in c-myc expression are independent of functional protein kinase C.

作者信息

Lloyd A C, Paterson H F, Morris J D, Hall A, Marshall C J

机构信息

Institute of Cancer Research, Chester Beatty Laboratories, London, UK.

出版信息

EMBO J. 1989 Apr;8(4):1099-104. doi: 10.1002/j.1460-2075.1989.tb03479.x.

Abstract

It has previously been demonstrated that efficient DNA synthesis by oncogenic p21H-ras only occurs in the presence of insulin and is absolutely dependent on functional protein kinase C. Here we show that morphological transformation induced by oncogenic p21H-ras does not require functional protein kinase C. The early phases of protein kinase C-independent morphological transformation do not require de novo protein synthesis. We have also demonstrated that the introduction of p21H-ras into quiescent Swiss 3T3 cells by scrape-loading leads to increased levels of c-myc mRNA similar to those seen following serum stimulation. The increases in c-myc mRNA levels induced by p21H-ras are also independent of functional protein kinase C. Both morphological transformation and the elevation of c-myc mRNA levels do not require insulin. These results demonstrate that p21H-ras is generating protein kinase C-dependent and -independent signals.

摘要

先前已经证明,致癌性p21H-ras的有效DNA合成仅在胰岛素存在的情况下发生,并且绝对依赖于功能性蛋白激酶C。在此我们表明,致癌性p21H-ras诱导的形态转化不需要功能性蛋白激酶C。不依赖蛋白激酶C的形态转化的早期阶段不需要从头合成蛋白质。我们还证明,通过刮擦加载将p21H-ras导入静止的瑞士3T3细胞会导致c-myc mRNA水平升高,类似于血清刺激后所见的水平。p21H-ras诱导的c-myc mRNA水平升高也不依赖于功能性蛋白激酶C。形态转化和c-myc mRNA水平升高均不需要胰岛素。这些结果表明,p21H-ras正在产生依赖蛋白激酶C和不依赖蛋白激酶C的信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6954/400920/2915bfd476e9/emboj00128-0106-a.jpg

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