CKIP-1 recruits nuclear ATM partially to the plasma membrane through interaction with ATM

Lingqiang Zhang; Yi Tie; Chunyan Tian; Guichun Xing; Yi Song; Yunping Zhu; Zhixian Sun; Fuchu He

doi:10.1016/j.cellsig.2005.10.017

CKIP-1 recruits nuclear ATM partially to the plasma membrane through interaction with ATM

Cell Signal. 2006 Sep;18(9):1386-95. doi: 10.1016/j.cellsig.2005.10.017. Epub 2005 Dec 1.

Authors

Lingqiang Zhang¹, Yi Tie, Chunyan Tian, Guichun Xing, Yi Song, Yunping Zhu, Zhixian Sun, Fuchu He

Affiliation

¹ Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine, Beijing Proteome Reseacrh Center, Beijing 100850, P.R. China. [email protected]

PMID: 16325375
DOI: 10.1016/j.cellsig.2005.10.017

Abstract

CKIP-1 (casein kinase-2 interacting protein-1) is implicated in muscle differentiation, regulation of cell morphology and actin cytoskeleton. More recently, we showed that CKIP-1 regulated AP-1 activity and promoted apoptosis via caspase-3-dependent cleavage and translocation. Here, we report that overexpression of CKIP-1 in SK-BR-3 breast cancer cells prevents p53 degradation induced by cycloheximide treatment through increase of p53 N-terminal Ser-15 phosphorylation level. CKIP-1 could interact with ATM, which is an upstream kinase of p53, thereby enhance the stability of p53. Interestingly, CKIP-1 is localized both at the plasma membrane and in the nucleus dependent on the cell types, and only the plasma membrane-localized CKIP-1 could form a complex with ATM. Importantly, CKIP-1 recruits nuclear ATM proteins partially to the plasma membrane. Our data provide the first evidence that ATM, a predominantly nuclear kinase, could be relocalized to the plasma membrane by CKIP-1 and shed new light on the multi-functional CKIP-1.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Ataxia Telangiectasia Mutated Proteins
Carrier Proteins / genetics
Carrier Proteins / metabolism*
Cell Cycle Proteins / genetics
Cell Cycle Proteins / metabolism*
Cell Line, Tumor
Cell Membrane / metabolism*
Cell Nucleus / metabolism*
Cycloheximide / metabolism
DNA-Binding Proteins / genetics
DNA-Binding Proteins / metabolism*
Humans
Intracellular Signaling Peptides and Proteins
Protein Binding
Protein Serine-Threonine Kinases / genetics
Protein Serine-Threonine Kinases / metabolism*
Protein Synthesis Inhibitors / metabolism
Tumor Suppressor Protein p53 / genetics
Tumor Suppressor Protein p53 / metabolism
Tumor Suppressor Proteins / genetics
Tumor Suppressor Proteins / metabolism*

Substances

Carrier Proteins
Cell Cycle Proteins
DNA-Binding Proteins
Intracellular Signaling Peptides and Proteins
PLEKHO1 protein, human
Protein Synthesis Inhibitors
Tumor Suppressor Protein p53
Tumor Suppressor Proteins
Cycloheximide
ATM protein, human
Ataxia Telangiectasia Mutated Proteins
Protein Serine-Threonine Kinases