scholarly journals Cell Invasion by Neisseria meningitidis Requires a Functional Interplay between the Focal Adhesion Kinase, Src and Cortactin

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e39613 ◽  
Author(s):  
Heiko Slanina ◽  
Sabrina Hebling ◽  
Christoph R. Hauck ◽  
Alexandra Schubert-Unkmeir
2005 ◽  
Vol 43 (4) ◽  
pp. 207-214 ◽  
Author(s):  
Jenq-Chang Lee ◽  
Ming-Chei Maa ◽  
Hsiu-Shan Yu ◽  
Jung-Hui Wang ◽  
Chia-Kuang Yen ◽  
...  

2019 ◽  
Vol 31 (6) ◽  
pp. 1057 ◽  
Author(s):  
Zhihui Dai ◽  
Fei Sheng ◽  
Ningxia Sun ◽  
Yixuan Ji ◽  
Qiuying Liao ◽  
...  

Normal implantation and placental development depend on the appropriate differentiation and invasion of trophoblast cells. Inadequate trophoblast cell invasion results in pregnancy-related disorders, which endanger both mother and fetus; however, the mechanism of early placental development has not been fully explained. In this study we conducted gene expression profile analysis using mouse placental tissues at different developmental stages (embryonic day (E)7.5, E14.5 and E19.5) using series tests of cluster (STC) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway analyses. Focal adhesion kinase (FAK) signalling pathway-related gene expression levels were verified using quantitative reverse transcription polymerase chain reaction and western blot. The results showed that caveolin-1 (Cav1) was downregulated in the placenta of unexplained spontaneous abortion subjects compared with that of induced abortion. Furthermore, by modulating CAV1 expression levels, CAV1 was shown to promote human trophoblast cell proliferation, migration and invasion by activating the FAK signalling pathway. These results indicate that CAV1 and the FAK signalling pathway are crucial for early placental development, which sheds new light on our understanding of the mechanisms of human trophoblast cell invasion and early development of the placenta.


Cancer ◽  
2002 ◽  
Vol 95 (12) ◽  
pp. 2508-2515 ◽  
Author(s):  
Galen B. Schneider ◽  
Zoya Kurago ◽  
Rebecca Zaharias ◽  
Lynn M. Gruman ◽  
Michael D. Schaller ◽  
...  

2006 ◽  
Vol 26 (13) ◽  
pp. 5155-5167 ◽  
Author(s):  
Shu-Yi Chen ◽  
Hong-Chen Chen

ABSTRACT Focal adhesion kinase (FAK) has been implicated to be a point of convergence of integrin and growth factor signaling pathways. Here we report that FAK directly interacts with the hepatocyte growth factor receptor c-Met. Phosphorylation of c-Met at Tyr-1349 and, to a lesser extent, Tyr-1356 is required for its interaction with the band 4.1 and ezrin/radixin/moesin homology domain (FERM domain) of FAK. The F2 subdomain of the FAK FERM domain alone is sufficient for Met binding, in which a patch of basic residues (216KAKTLRK222) are critical for the interaction. Met-FAK interaction leads to FAK activation and subsequent contribution to hepatocyte growth factor-induced cell motility and cell invasion. Our results provide evidence that constitutive Met-FAK interaction may be a critical determinant for tumor cells to acquire invasive potential.


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