Integrin-regulated FAK-Src signaling in normal and cancer cells.
By S. Mitra, D. Schlaepfer. Current Opinion in Cell Biology, 2006
1,593 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology and Allergy, Oncology
View Paper: https://www.semanticscholar.org/paper/cbb7f724c0168c469b7a669eed85df8a7852f011
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Citations in the corpus
- E-cadherin–integrin crosstalk in cancer invasion and metastasis (2013, background): “Src and FAK have key functions in the transmission of signals downstream of integrin activation (Cabodi et al., 2010; Mitra and Schlaepfer, 2006).”
- Signal transduction by focal adhesion kinase in cancer (2009, background): “This review will focus primarily on the roles of FAK signaling pathways in cancer development and progression, although it is clear that FAK also plays important roles in many other biological and disease processes [9, 10].”
- Adhesion signaling – crosstalk between integrins, Src and Rho (2009, background): “…of Cell Science 122, 1059-1069 Published by The Company of Biologists 2009 doi:10.1242/jcs.039446 Jo ur na l o f C el l S ci en ce 1060 phosphorylates other tyrosine residues in FAK and thereby maximizes its kinase activity and creates additional proteinbinding sites (Mitra and Schlaepfer, 2006).”
- Assembly of Fibronectin Extracellular Matrix (2010, background): “Paxillin phosphorylation is a consequence of Src activation (Mitra & Schlaepfer 2006) and also contributes to FN matrix formation (Wierzbicka-Patynowski et al. 2007, Zaidel-Bar et al. 2007).”
- RACK1, A multifaceted scaffolding protein: Structure and function (2011, neutral): “FAK is widely regarded as being the convergence point of growth factor and integrin signaling [176,177], yet how FAK phosphorylation is regulated within the growth factor and integrin network is not fully understood.”
- Latent bone metastasis in breast cancer tied to Src-dependent survival signals (2009, background): “The mechanism for Src activation in ER breast cancer cells remains unknown but could involve receptor tyrosine kinases, G protein-coupled receptors, integrins, and focal adhesion kinase (Bromann et al., 2004; Guo and Giancotti, 2004; Ishizawar and Parsons, 2004; Mitra and Schlaepfer, 2006).”
- Matrix Crosslinking Forces Tumor Progression by Enhancing Integrin signaling (2009, background): “Human breast tumors are often fibrotic and stiff, and breast cancer cells that exhibit high tension have elevated integrins and focal adhesions and increased integrin signaling (Madan et al., 2006; Mitra and Schlaepfer, 2006).”