RalA interacts with ZONAB in a cell density-dependent manner and regulates its transcriptional activity

被引:85
作者
Frankel, P
Aronheim, A
Kavanagh, E
Balda, MS
Matter, K
Bunney, TD
Marshall, CJ
机构
[1] Inst Canc Res, Chester Beatty Labs, Canc Res UK Ctr Cell & Mol Biol, Oncogene Team, London SW3 6JB, England
[2] Technion Israel Inst Technol, Bruce Rappaport Fac Med, Dept Mol Genet, IL-31096 Haifa, Israel
[3] UCL, Inst Ophthalmol, Div Cell Biol, London, England
[4] Inst Canc Res, Chester Beatty Labs, Canc Res UK Ctr Cell & Mol Biol, Lipid Signalling Team, London SW3 6JB, England
基金
英国医学研究理事会;
关键词
cell-cell contact; RalA; signal transduction; transcription; ZONAB;
D O I
10.1038/sj.emboj.7600497
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
Ral proteins are members of the Ras superfamily of small GTPases and are involved in signalling pathways for actin cytoskeleton remodelling, cell cycle control, cellular transformation and vesicle transport. To identify novel RalA effector proteins, we used the reverse Ras recruitment system and found that RalA interacts with a Y- box transcription factor, ZO- 1- associated nucleic acid- binding protein ( ZONAB), in a GTP- dependent manner. The amount of the RalA - ZONAB complex increases as epithelial cells become more dense and increase cell contacts. The RalA - ZONAB interaction results in a relief of transcriptional repression of a ZONAB- regulated promoter. Additionally, expression of oncogenic Ras alleviates transcriptional repression by ZONAB in a RalA- dependent manner. The data presented here implicate the RalA/ ZONAB interaction in the regulation of ZONAB function.
引用
收藏
页码:54 / 62
页数:9
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