An effector peptide from glutathione-S-transferase-pi strongly and selectively blocks mitotic signaling by oncogenic ras-p21

被引：7

作者：

Chie, L

Adler, V

Friedman, FK

Chung, D

Pincus, MR ^{[1
]}

机构：

[1] New York Harbor VA Med Ctr, Dept Pathol & Lab Med, Brooklyn, NY 11209 USA

[2] Long Isl Univ, Dept Biol, Brooklyn, NY 11201 USA

[3] Long Isl Univ, Dept Chem, Brooklyn, NY 11201 USA

[4] QRNA Corp, New York, NY 10032 USA

[5] NCI, Lab Metab, Bethesda, MD 20892 USA

[6] SUNY, Downstate Med Ctr, Dept Pathol, Brooklyn, NY 11203 USA

来源：

PROTEIN JOURNAL | 2004年 / 23卷 / 03期

关键词：

glutathione-S-transferase-pi; GST-pi peptide 34-50; inhibition; jun; jun-N-terminal kinase; oncogenic ras-p21; oocyte maturation;

D O I：

10.1023/B:JOPC.0000026419.54902.bb

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Oncogenic ras-p21 directly activates jun-N-terminal kinase (JNK) and its substrate, jun as a unique step on its mitogenic signal transduction pathway. This activation is blocked by the specific JNK jun inhibitor, glutathione-S-transferase-pi (GST-pi). Four domains of GST-pi have been implicated in this regulatory function: 34-50, 99-121, 165-182, and 194-201. The 34-50 domain is unique in that it does not affect GST-pi binding to JNK jun but blocks jun phosphorylation by JNK. We now find that it completely blocks oncogenic (Val 12-) ras-p21-induced oocyte maturation but has no effect on insulin-induced oocyte maturation. Because the latter process requires activation of wild-type ras-p21, this peptide appears to be specific for inhibiting only the oncogenic form of ras-p21, suggesting its use in treating ras-induced tumors.

引用

页码：235 / 238

页数：4

共 18 条

[1]

Adler V, 2004, ANN CLIN LAB SCI, V34, P35

[2] COMPLEXES OF P21(RAS) WITH JUN N-TERMINAL KINASE AND JUN PROTEINS [J].