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丝裂原活化蛋白激酶p42mapk和p44mapk是成纤维细胞增殖所必需的。

Mitogen-activated protein kinases p42mapk and p44mapk are required for fibroblast proliferation.

作者信息

Pagès G, Lenormand P, L'Allemain G, Chambard J C, Meloche S, Pouysségur J

机构信息

Centre de Biochimie, Centre National de la Recherche Scientifique, Université de Nice, France.

出版信息

Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8319-23. doi: 10.1073/pnas.90.18.8319.

DOI:10.1073/pnas.90.18.8319
PMID:8397401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC47347/
Abstract

The mitogen-activated protein kinases (MAP kinases) p42mapk and p44mapk are serine/threonine kinases rapidly activated in cells stimulated with various extracellular signals by dual phosphorylation of tyrosine and threonine residues. They are thought to play a pivotal role in integrating and transmitting transmembrane signals required for growth and differentiation. Here we demonstrate that activation of these ubiquitously expressed MAP kinases is essential for growth. To specifically suppress MAP kinase activation in fibroblasts, we transiently expressed either the entire p44mapk antisense RNA or p44mapk kinase-deficient mutants (T192A or Y194F). As expected, and through independent mechanisms, both approaches strongly inhibited MAP kinase activation. The antisense reduced the expression of endogenous p42mapk and p44mapk by 90%, whereas overexpression of the T192A mutant inhibited growth factor activation of both endogenous MAP kinases by up to 70%. As a consequence, we found that the antisense as well as the T192A mutant of p44mapk inhibited growth factor-stimulated gene transcription (collagenase promoter assay with chloramphenicol acetyltransferase reporter) and cell growth. These effects were proportional to the extent of MAP kinase inhibition and reversed by coexpression of the wild-type p44mapk. Therefore we conclude that growth factor activation of p42mapk and p44mapk is an absolute requirement for triggering the proliferative response.

摘要

丝裂原活化蛋白激酶(MAP激酶)p42mapk和p44mapk是丝氨酸/苏氨酸激酶,在受到各种细胞外信号刺激的细胞中,通过酪氨酸和苏氨酸残基的双重磷酸化而迅速被激活。它们被认为在整合和传递生长与分化所需的跨膜信号中起关键作用。在此我们证明,这些普遍表达的MAP激酶的激活对生长至关重要。为了特异性抑制成纤维细胞中的MAP激酶激活,我们瞬时表达了完整的p44mapk反义RNA或p44mapk激酶缺陷型突变体(T192A或Y194F)。正如预期的那样,并且通过独立的机制,这两种方法都强烈抑制了MAP激酶的激活。反义RNA使内源性p42mapk和p44mapk的表达降低了90%,而T192A突变体的过表达使内源性两种MAP激酶的生长因子激活受到高达70%的抑制。结果,我们发现p44mapk的反义RNA以及T192A突变体均抑制了生长因子刺激的基因转录(用氯霉素乙酰转移酶报告基因进行胶原酶启动子分析)和细胞生长。这些效应与MAP激酶的抑制程度成正比,并可通过共表达野生型p44mapk而逆转。因此我们得出结论,p42mapk和p44mapk的生长因子激活是触发增殖反应的绝对必要条件。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/660a26d22d39/pnas01475-0026-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/36c2b4004ab2/pnas01475-0024-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/f810908b2011/pnas01475-0025-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/73d52d6e339e/pnas01475-0025-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/660a26d22d39/pnas01475-0026-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/36c2b4004ab2/pnas01475-0024-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/f810908b2011/pnas01475-0025-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/73d52d6e339e/pnas01475-0025-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d5/47347/660a26d22d39/pnas01475-0026-a.jpg

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