CAM-FGF receptor interactions: A model for axonal growth

被引:315
作者
Doherty, P
Walsh, FS
机构
[1] Department of Experimental Pathology, UMDS, Guy's Hospital, London SE1 9RT, London Bridge
关键词
D O I
10.1006/mcne.1996.0049
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A number of experimental paradigms have been used to demonstrate that NCAM, N-cadherin, and L1 stimulate axonal growth. The molecular basis of this response has been extensively studied and a range of agents that inhibit neurite outgrowth stimulated by the above CAMs, but not integrins, have now been identified. These studies pointed to the activation of a tyrosine kinase-PLC gamma cascade as being important for the neurite outgrowth responses stimulated by all three CAMs, and this was substantiated by the identification of agents that could activate the cascade and mimic the growth response. In this review we will suggest that the neurite growth response stimulated by these CAMs is mediated by activation of the fibroblast growth factor receptor (FGFR) in neurons and that this results in the recruitment and activation of PLC gamma via interactions of its SH2 domain with the activated receptor. In this context the key events downstream from activation of PLC gamma required for neurite growth appear to be the conversion of diacylglycerol (DAG) to arachidonic acid (AA) via DAG lipase activity, followed by an increased influx of calcium into the neurons. The evolutionary conservation of putative binding motifs between the above CAMs and the FGFR suggests that activation of the FGFR-PLC gamma cascade by the CAMs might involve a direct CAM-FGFR interaction. The identification of the binding motifs also allows for predictions to be made concerning whether other CAMs might directly interact with the FGFR.
引用
收藏
页码:99 / 111
页数:13
相关论文
共 77 条
[1]   SEROTONIN-MEDIATED ENDOCYTOSIS OF APCAM - AN EARLY STEP OF LEARNING-RELATED SYNAPTIC GROWTH IN APLYSIA [J].
BAILEY, CH ;
CHEN, M ;
KELLER, F ;
KANDEL, ER .
SCIENCE, 1992, 256 (5057) :645-649
[2]  
Baird Andrew, 1994, Current Opinion in Neurobiology, V4, P78, DOI 10.1016/0959-4388(94)90035-3
[3]   NCAM-DEPENDENT NEURITE OUTGROWTH IS INHIBITED IN NEURONS FROM FYN-MINUS MICE [J].
BEGGS, HE ;
SORIANO, P ;
MANESS, PF .
JOURNAL OF CELL BIOLOGY, 1994, 127 (03) :825-833
[4]   PURIFIED N-CADHERIN IS A POTENT SUBSTRATE FOR THE RAPID INDUCTION OF NEURITE OUTGROWTH [J].
BIXBY, JL ;
ZHANG, R .
JOURNAL OF CELL BIOLOGY, 1990, 110 (04) :1253-1260
[5]  
BIXBY JL, 1991, ANNU REV CELL BIOL, V7, P117, DOI 10.1146/annurev.cellbio.7.1.117
[6]   NEURITE OUTGROWTH ON MUSCLE-CELL SURFACES INVOLVES EXTRACELLULAR-MATRIX RECEPTORS AS WELL AS CA-2+-DEPENDENT AND CA-2+-INDEPENDENT CELL-ADHESION MOLECULES [J].
BIXBY, JL ;
PRATT, RS ;
LILIEN, J ;
REICHARDT, LF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (08) :2555-2559
[7]   IDENTIFICATION OF A CONSERVED REGION COMMON TO CADHERINS AND INFLUENZA STRAIN A HEMAGGLUTININS [J].
BLASCHUK, OW ;
POULIOT, Y ;
HOLLAND, PC .
JOURNAL OF MOLECULAR BIOLOGY, 1990, 211 (04) :679-682
[8]   Telling axons where to grow: A role for Eph receptor tyrosine kinases in guidance [J].
Brambilla, R ;
Klein, R .
MOLECULAR AND CELLULAR NEUROSCIENCE, 1995, 6 (06) :487-495
[9]  
BRUMMENDORF T, 1995, PROTEIN PROFILE, V2, P963
[10]   FIBROBLAST GROWTH-FACTOR RECEPTORS CONTAIN A CONSERVED HAV REGION COMMON TO CADHERINS AND INFLUENZA STRAIN-A HEMAGGLUTININS - A ROLE IN PROTEIN-PROTEIN INTERACTIONS [J].
BYERS, S ;
AMAYA, E ;
MUNRO, S ;
BLASCHUK, O .
DEVELOPMENTAL BIOLOGY, 1992, 152 (02) :411-414