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在CHO细胞中导致丝裂原活化蛋白激酶激活的蛋白激酶C亚型。

The protein kinase C isoforms leading to MAP-kinase activation in CHO cells.

作者信息

Yamaguchi K, Ogita K, Nakamura S, Nishizuka Y

机构信息

Department of Biochemistry, Kobe University School of Medicine, Japan.

出版信息

Biochem Biophys Res Commun. 1995 May 25;210(3):639-47. doi: 10.1006/bbrc.1995.1708.

DOI:10.1006/bbrc.1995.1708
PMID:7539255
Abstract

Stimulation of CHO cells with phorbol ester caused transient activation of mitogen-activated protein kinase (MAP-kinases with 42 and 44 kDa). A similar treatment of CHO cells which overexpress a massive amount of the alpha- or delta-isoform of protein kinase C (PKC) resulted in the prolonged activation of MAP-kinase and eventually in the appearance of mostly dikaryotic, sometimes tetrakaryotic cells. The results suggest that the delta-isoform, as well as the alpha-isoform, has a potential to cause MAP kinase activation. Unusual activation of the PKC/MAP-kinase pathway, however, may lead to abnormal cytokinesis.

摘要

用佛波酯刺激CHO细胞会导致丝裂原活化蛋白激酶(42 kDa和44 kDa的MAP激酶)的瞬时激活。对过量表达大量蛋白激酶C(PKC)α或δ亚型的CHO细胞进行类似处理,会导致MAP激酶的持续激活,并最终出现大多为双核、有时为四核的细胞。结果表明,δ亚型以及α亚型都有可能导致MAP激酶激活。然而,PKC/MAP激酶途径的异常激活可能会导致异常的胞质分裂。

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