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Deficiency of a STE20/PAK family kinase LOK leads to the acceleration of LFA‐1 clustering and cell adhesion of activated lymphocytes
Author(s) -
Endo Junji,
Toyama-Sorimachi Noriko,
Taya Choji,
Kuramochi-Miyagawa Satomi,
Nagata Kisaburo,
Kuida Keisuke,
Takashi Tohru,
Yonekawa Hiromichi,
Yoshizawa Yasuyuki,
Miyasaka Nobuyuki,
Karasuyama Hajime
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01219-9
Subject(s) - lymphocyte , lymphocyte function associated antigen 1 , microbiology and biotechnology , mitogen activated protein kinase , cell adhesion , adhesion , chemistry , kinase , intracellular , biology , cell , intercellular adhesion molecule 1 , immunology , biochemistry , organic chemistry
Lymphocyte‐oriented kinase (LOK) is a member of the STE20/p21‐activated kinase (PAK) family and expressed predominantly in lymphoid organs. Generation of LOK‐deficient mice revealed that the leukocyte‐function‐associated antigen (LFA‐1)/intercellular adhesion molecules (ICAM)‐mediated aggregation of mitogen‐stimulated T cells was greatly enhanced in the absence of LOK. Though levels of total LFA‐1 and ICAMs as well as the active form of LFA‐1 on T cell blasts were comparable in the presence and absence of LOK, clustering of active LFA‐1 detected by binding of soluble ICAM‐1 was accelerated in the absence of LOK. These results suggest that LOK is potentially involved in the regulation of LFA‐1‐mediated lymphocyte adhesion.