ArticleCellular signalling2007
Differential FAK phosphorylation at Ser-910, Ser-843 and Tyr-397 induced by angiotensin II, LPA and EGF in intestinal epithelial cells.
Article in Cellular signalling, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
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- A novel role of IGFBP5 in the migration, invasion and spheroids formation induced by IGF-I and insulin in MCF-7 breast cancer cells.Breast cancer research and treatment · 2024Article
- ATX/LPA axis regulates FAK activation, cell proliferation, apoptosis, and motility in human pancreatic cancer cells.In vitro cellular & developmental biology. Animal · 2022Article
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- Metformin inhibition of colorectal cancer cell migration is associated with rebuilt adherens junctions and FAK downregulation.Journal of cellular physiology · 2020Article
- Signaling diversity enabled by Rap1-regulated plasma membrane ERK with distinct temporal dynamics.eLife · 2020Article
- Review
- Review
- PCTK3/CDK18 regulates cell migration and adhesion by negatively modulating FAK activity.Scientific reports · 2017Article
- GABAB receptor upregulates fragile X mental retardation protein expression in neurons.Scientific reports · 2015Article
- Conformational dynamics of the focal adhesion targeting domain control specific functions of focal adhesion kinase in cells.The Journal of biological chemistry · 2015Article
- Comparative analyses of downstream signal transduction targets modulated after activation of the AT1 receptor by two β-arrestin-biased agonists.Frontiers in pharmacology · 2015Article
- αν and β1 Integrins mediate Aβ-induced neurotoxicity in hippocampal neurons via the FAK signaling pathway.PloS one · 2014Article
- CRF2 signaling is a novel regulator of cellular adhesion and migration in colorectal cancer cells.PloS one · 2013Article
- Rapid protein kinase D1 signaling promotes migration of intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- MG63 osteoblast-like cells exhibit different behavior when grown on electrospun collagen matrix versus electrospun gelatin matrix.PloS one · 2012Article
- Akt directly regulates focal adhesion kinase through association and serine phosphorylation: implication for pressure-induced colon cancer metastasis.American journal of physiology. Cell physiology · 2011Article
- Protein kinase D1 mediates stimulation of DNA synthesis and proliferation in intestinal epithelial IEC-18 cells and in mouse intestinal crypts.The Journal of biological chemistry · 2011Article
- Article
- GABAB receptor activation protects neurons from apoptosis via IGF-1 receptor transactivation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A rapid increase in the tyrosine phosphorylation of the non-receptor tyrosine kinase FAK is a prominent early event in fibroblasts stimulated by a variety of signaling molecules. However, a variety of epithelial cells, including intestinal epithelial cells, show a high basal level of tyrosine phosphorylated FAK that is only slightly further increased by addition of G protein-coupled receptor (GPCR) agonists or growth factors. In this study, we determined whether these stimuli could elicit FAK phosphorylation at serine residues, including Ser-910 and Ser-843. Our results show that multiple agonists including angiotensin II (ANGII), lysophosphatidic acid (LPA), phorbol esters and EGF induced a striking stimulation of FAK phosphorylation at Ser-910 in rat intestinal epithelial IEC-18 cells via an ERK-dependent pathway. In striking contrast, none of these stimuli promoted a significant further increase in FAK phosphorylation at Tyr-397 in these cells. These results were extended using cultures of polarized human colonic epithelial T84 cells. We found that either carbachol or EGF promoted a striking ERK-dependent phosphorylation of FAK at Ser-910, but these agonists caused only slight stimulation of FAK at Tyr-397 in T84 cells. In addition, we demonstrated that GPCR agonists also induced a dramatic increase of FAK phosphorylation at Ser-843 in either IEC-18 or T84 cells. Our results indicate that Ser-910 and Ser-843, rather than Tyr-397, are prominent sites differentially phosphorylated in response to neurotransmitters, bioactive lipids, tumor promoters and growth factors in intestinal epithelial cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.