The diverse roles and multiple forms of focal adhesion kinase in brain

被引:24
作者
Armendariz, Beatriz G. [1 ,2 ,3 ]
del Mar Masdeu, Maria [1 ,2 ,3 ]
Soriano, Eduardo [1 ,2 ,3 ]
Urena, Jesus M. [1 ,2 ,3 ]
Burgaya, Ferran [1 ,2 ,3 ]
机构
[1] Univ Barcelona, Fac Biol, Dept Cellular Biol, E-08028 Barcelona, Spain
[2] Parc Cient Barcelona, Barcelona, Spain
[3] Ctr Invest Biomed Red Enfermedades Neurodegenerat, Madrid, Spain
关键词
gene transcription; guidance; kinases; neuritogenesis; synaptogenesis; PROTEIN-TYROSINE KINASE; SRC-FAMILY KINASES; CENTRAL-NERVOUS-SYSTEM; CHONDROITIN SULFATE PROTEOGLYCANS; OLIGODENDROCYTE PRECURSOR CELLS; NEURONAL GROWTH CONES; AXON GUIDANCE; RAT-BRAIN; EXTRACELLULAR-MATRIX; SIGNAL-TRANSDUCTION;
D O I
10.1111/ejn.12737
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Although it was originally characterized as a constituent of focal adhesions in fibroblasts, focal adhesion kinase (FAK) is now considered to be not only a mediator of adhesion processes but also a crucial regulator of guidance and a modulator of gene expression. FAK is the main transducer of the integrin signaling required to stabilize the actin cytoskeleton. However, additional activities have been described over the years. In the brain, FAK deserves particular attention as it is found in various alternatively spliced forms - these distributed in multiple subcellular compartments or bound to multiple partners. Moreover, its signaling involves not only phosphorylation but also ubiquitination and proteolysis. Several experimental cell models demonstrate that FAK increases or decreases migration, participates in differentiation and contributes to plasticity events. In addition, this kinase is linked to cell survival in cancer and apoptosis. This review focuses on the diversity of events involving brain-located forms of FAK.
引用
收藏
页码:3573 / 3590
页数:18
相关论文
共 194 条
[1]   EXPRESSION OF AN N-TERMINALLY TRUNCATED FORM OF HUMAN FOCAL ADHESION KINASE IN BRAIN [J].
ANDRE, E ;
BECKERANDRE, M .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1993, 190 (01) :140-147
[2]   Slit-Robo interactions during cortical development [J].
Andrews, William D. ;
Barber, Melissa ;
Parnavelas, John G. .
JOURNAL OF ANATOMY, 2007, 211 (02) :188-198
[3]  
ARREGUI CO, 1994, J NEUROSCI, V14, P6967
[4]   Tuberin, the tuberous sclerosis complex 2 tumor suppressor gene product, regulates Rho activation, cell adhesion and migration [J].
Astrinidis, A ;
Cash, TP ;
Hunter, DS ;
Walker, CL ;
Chernoff, J ;
Henske, EP .
ONCOGENE, 2002, 21 (55) :8470-8476
[5]   Aggregation of integrins and RhoA activation are required for Thy-1-induced morphological changes in astrocytes [J].
Avalos, AM ;
Arthur, WT ;
Schneider, P ;
Quest, AFG ;
Burridge, K ;
Leyton, L .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (37) :39139-39145
[6]  
Battye R, 1999, DEVELOPMENT, V126, P2475
[7]   FAK-MAPK-dependent adhesion disassembly downstream of L1 contributes to semaphorin3A-induced collapse [J].
Bechara, Ahmad ;
Nawabi, Homaira ;
Moret, Frederic ;
Yaron, Avraham ;
Weaver, Eli ;
Bozon, Muriel ;
Abouzid, Karima ;
Guan, Jun-Lin ;
Tessier-Lavigne, Marc ;
Lemmon, Vance ;
Castellani, Valerie .
EMBO JOURNAL, 2008, 27 (11) :1549-1562
[8]   Reelin and cyclin-dependent kinase 5-dependent signals cooperate in regulating neuronal migration and synaptic transmission [J].
Beffert, U ;
Weeber, EJ ;
Morfini, G ;
Ko, J ;
Brady, ST ;
Tsai, LH ;
Sweatt, JD ;
Herz, J .
JOURNAL OF NEUROSCIENCE, 2004, 24 (08) :1897-1906
[9]   FAK deficiency in cells contributing to the basal lamina results in cortical abnormalities resembling congenital muscular dystrophies [J].
Beggs, HE ;
Schahin-Reed, D ;
Zang, KL ;
Goebbels, S ;
Nave, KA ;
Gorski, J ;
Jones, KR ;
Sretavan, D ;
Reichardt, LF .
NEURON, 2003, 40 (03) :501-514
[10]   NCAM140 interacts with the focal adhesion kinase p125(fak) and the SRC-related tyrosine kinase p59(fyn) [J].
Beggs, HE ;
Baragona, SC ;
Hemperly, JJ ;
Maness, PF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (13) :8310-8319