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Specific decrease in the level of Hic‐5, a focal adhesion protein, during immortalization of mouse embryonic fibroblasts, and its association with focal adhesion kinase
Author(s) -
Ishino Keiko,
Kaneyama Joori Kim,
Shibanuma Motoko,
Nose Kiyoshi
Publication year - 2000
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(20000301)76:3<411::aid-jcb9>3.0.co;2-j
Subject(s) - focal adhesion , paxillin , vinculin , ptk2 , microbiology and biotechnology , cytoskeleton , lim domain , cell adhesion , biology , adhesion , chemistry , kinase , cell , signal transduction , protein kinase a , biochemistry , mitogen activated protein kinase kinase , organic chemistry , gene , zinc finger , transcription factor
Hic‐5 is a paxillin homologue with four LIM domains in its C‐terminal region, localized mainly in focal adhesions in normal fibroblasts. Hic‐5 is also known to associate with focal adhesion kinase (FAK) or the related CAKβ, and with vinculin. In the present study, we examined changes in Hic‐5 and paxillin protein levels in primary mouse embryo fibroblasts (MEF) during mortal and immortal stages. The Hic‐5 level was markedly decreased when cells became immortalized, whereas that of paxillin was increased. The vinculin level was not changed significantly. Hic‐5 was mainly localized in focal adhesion plaques of mortal MEF but was localized in the nuclear periphery in the immortalized MEF; the number of focal adhesion plaques was decreased in these cells. Mouse Hic‐5 contains three LD domains in its N‐terminal half, and the first LD domain (LD1) appears to be involved in interaction with FAK. However, this interaction was not essential for recruitment of Hic‐5 to focal adhesions, since its subcellular localization was similar in FAK −/− cells. Forced expression of Hic‐5 decreased colony forming ability of MEF from FAK +/+ mice, but not of FAK −/− cells. These observations suggested the involvement of Hic‐5 in determination of cellular proliferative capacity in collaboration with other cytoskeletal components. J. Cell. Biochem. 76:411–419, 2000. © 2000 Wiley‐Liss, Inc.