SRC-RELATED PROTEIN-TYROSINE KINASES AND THEIR SURFACE-RECEPTORS

被引:88
作者
RUDD, CE [1 ]
JANSSEN, O [1 ]
PRASAD, KVS [1 ]
RAAB, M [1 ]
DASILVA, A [1 ]
TELFER, JC [1 ]
YAMAMOTO, M [1 ]
机构
[1] HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA
关键词
D O I
10.1016/0304-419X(93)90007-Y
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
The CD4-p56lck and CD8-p56lck complexes have served as a paradym for an expanding number of interactions between src-family members (p56lck, p59fyn, p56lyn, p55blk) and surface receptors. These interactions implicate src-related kinapses in the regulation of a variety of intracellular events, from lymphokine production and cytotoxicity to the expression of specific nuclear binding proteins. Different molecular mechanisms appear to have evolved to facilitate the receptor-kinase interactions, including the use of N-terminal regions, SH2 regions and kinase domains. Variations exists in stoichiometry, affinity and the nature of signals generated by these complexes in cells. The CD4-p56lck complex differs from receptor-tyrosine kinases in a number of important ways, including mechanisms of kinase domain regulation of recruitment of substrates such as PI 3-kinase. Furthermore, they may have a special affinity for receptor-substrates such as the TcRζ, MB1/B29 or CD5 receptors, and act to recruit other SH2-carrying proteins, such as ZAP-70 to the receptor complexes. Receptor-sr kinase interactions represent the first step in a cascade of intracellular events within the protein-tyrosine kinase/phosphatase cascade. © 1993.
引用
收藏
页码:239 / 266
页数:28
相关论文
共 338 条
[1]   THYMIC TUMORIGENESIS INDUCED BY OVEREXPRESSION OF P56LCK [J].
ABRAHAM, KM ;
LEVIN, SD ;
MARTH, JD ;
FORBUSH, KA ;
PERLMUTTER, RM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (09) :3977-3981
[2]   DELAYED THYMOCYTE DEVELOPMENT INDUCED BY AUGMENTED EXPRESSION OF P56LCK [J].
ABRAHAM, KM ;
LEVIN, SD ;
MARTH, JD ;
FORBUSH, KA ;
PERLMUTTER, RM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 173 (06) :1421-1432
[3]   ENHANCEMENT OF T-CELL RESPONSIVENESS BY THE LYMPHOCYTE-SPECIFIC TYROSINE PROTEIN-KINASE P56LCK [J].
ABRAHAM, N ;
MICELI, MC ;
PARNES, JR ;
VEILLETTE, A .
NATURE, 1991, 350 (6313) :62-66
[4]  
ADAMS JM, 1992, ONCOGENE, V7, P611
[5]   RAS GTPASE-ACTIVATING PROTEIN - A SUBSTRATE AND A POTENTIAL BINDING-PROTEIN OF THE PROTEIN-TYROSINE KINASE P56LCK [J].
AMREIN, KE ;
FLINT, N ;
PANHOLZER, B ;
BURN, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (08) :3343-3346
[6]   BINDING OF SH2 DOMAINS OF PHOSPHOLIPASE-C-GAMMA-1, GAP, AND SRC TO ACTIVATED GROWTH-FACTOR RECEPTORS [J].
ANDERSON, D ;
KOCH, CA ;
GREY, L ;
ELLIS, C ;
MORAN, MF ;
PAWSON, T .
SCIENCE, 1990, 250 (4983) :979-982
[7]  
ANDERSON P, 1988, J IMMUNOL, V140, P1732
[8]  
ANDERSON P, 1987, IMMUNOLOGY, V1439, P678
[9]   DEFECTIVE T-CELL RECEPTOR SIGNALING IN MICE LACKING THE THYMIC ISOFORM OF P59(FYN) [J].
APPLEBY, MW ;
GROSS, JA ;
COOKE, MP ;
LEVIN, SD ;
QIAN, X ;
PERLMUTTER, RM .
CELL, 1992, 70 (05) :751-763
[10]   INTERLEUKIN-2 AND POLYOMAVIRUS MIDDLE T-ANTIGEN-INDUCED MODIFICATION OF PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY IN ACTIVATED LYMPHOCYTES-T [J].
AUGUSTINE, JA ;
SUTOR, SL ;
ABRAHAM, RT .
MOLECULAR AND CELLULAR BIOLOGY, 1991, 11 (09) :4431-4440