A novel protein MAJN binds to Jak3 and inhibits apoptosis induced by IL-2 deprival

被引：4

作者：

Ji, HB ^{[1
]}

Zhai, QW ^{[1
]}

Zhu, JF ^{[1
]}

Yan, MD ^{[1
]}

Sun, LY ^{[1
]}

Liu, XY ^{[1
]}

Zheng, ZC ^{[1
]}

机构：

[1] Chinese Acad Sci, Shanghai Inst Biochem, Shanghai 200031, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2000年 / 270卷 / 01期

关键词：

two-hybrid system; tyrosine-phosphorylation-modified two-hybrid system; interleukin-2 (IL-2); Jak3 N-terminal (JN); molecule associated with Jak3 N-terminal (MAJN); apoptosis;

D O I：

10.1006/bbrc.2000.2413

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：

To find a possible signal interacting with the Jak3 N-terminal, we screened the human peripheral blood cDNA library through both a two-hybrid system and a tyrosine-phosphorylation-modified two-hybrid system using: the N-terminal of Jak3 as bait. Results showed that one new homologue of myosin heavy chain, designated MAJN (molecule associated with Jak3 N-terminal), could bind to Jak3 in a tyrosine-phosphorylation-independent manner. The interaction between Jak3 and MAJN was further confirmed by immunoprecipitation in BAF-B03 beta cells. To investigate the function of MAJN, we have constructed the BAF-B03 beta/MAJN cell line that stably expresses MAJN and found that overexpression of MAJN can partially inhibit the apoptosis induced by interleukin-2 deprival. Further studies are needed to elucidate how MAJN executes its function to antagonize BAF-B03 beta cell death in the absence of IL-2. (C) 2000 Academic Press.

引用

页码：267 / 271

页数：5

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