ArticleMolecular pharmacology2011
Cooperative role of caveolin-1 and C-terminal Src kinase binding protein in C-terminal Src kinase-mediated negative regulation of c-Src.
Article in Molecular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- CSK-mediated signalling by integrins in cancer.Frontiers in cell and developmental biology · 2023Review
- Src: coordinating metabolism in cancer.Oncogene · 2022Review
- Sprouty2 positively regulates T cell function and airway inflammation through regulation of CSK and LCK kinases.PLoS biology · 2021Article
- Functional and Clinical Characteristics of Cell Adhesion Molecule CADM1 in Cancer.Frontiers in cell and developmental biology · 2021Review
- N-terminus-independent activation of c-Src via binding to a tetraspan(in) TM4SF5 in hepatocellular carcinoma is abolished by the TM4SF5 C-terminal peptide application.Theranostics · 2021Article
- The phospho-caveolin-1 scaffolding domain dampens force fluctuations in focal adhesions and promotes cancer cell migration.Molecular biology of the cell · 2017Article
- P-glycoprotein attenuates DNA repair activity in multidrug-resistant cells by acting through the Cbp-Csk-Src cascade.Oncotarget · 2017Article
- Repurposing cancer drugs to treat neurological diseases - Src inhibitors as examples.Neural regeneration research · 2017Article
- Src-dependent phosphorylation of caveolin-1 Tyr-14 promotes swelling and release of caveolae.Molecular biology of the cell · 2016Article
- Src Family Kinases in Brain Edema After Acute Brain Injury.Acta neurochirurgica. Supplement · 2016Article
- Clinically relevant concentrations of lidocaine and ropivacaine inhibit TNFα-induced invasion of lung adenocarcinoma cells in vitro by blocking the activation of Akt and focal adhesion kinase.British journal of anaesthesia · 2015Article
- Overexpression of Csk-binding protein decreases growth, invasion, and migration of esophageal carcinoma cells by controlling Src activation.World journal of gastroenterology · 2015Article
- PAG--a multipurpose transmembrane adaptor protein.Oncogene · 2014Review
- Caveolin-1 modulates cardiac gap junction homeostasis and arrhythmogenecity by regulating cSrc tyrosine kinase.Circulation. Arrhythmia and electrophysiology · 2014Article
- Inhibition of SRC family kinases protects hippocampal neurons and improves cognitive function after traumatic brain injury.Journal of neurotrauma · 2014Article
- Endothelial barrier protection by local anesthetics: ropivacaine and lidocaine block tumor necrosis factor-α-induced endothelial cell Src activation.Anesthesiology · 2014Article
- Nitroglycerin tolerance in caveolin-1 deficient mice.PloS one · 2014Article
- Ropivacaine attenuates endotoxin plus hyperinflation-mediated acute lung injury via inhibition of early-onset Src-dependent signaling.BMC anesthesiology · 2014Article
- SHP-2 binds to caveolin-1 and regulates Src activity via competitive inhibition of CSK in response to H2O2 in astrocytes.PloS one · 2014Article
- Nitrosation-dependent caveolin 1 phosphorylation, ubiquitination, and degradation and its association with idiopathic pulmonary arterial hypertension.Pulmonary circulation · 2013Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In the present study, we assessed the cooperative roles of C-terminal Src kinase (Csk) binding protein (Cbp) and Caveolin-1 (Cav-1) in the mechanism of Src family tyrosine kinase (SFK) inhibition by Csk. SFKs are inactivated by phosphorylation of their C-terminal tyrosine by Csk. Whereas SFKs are membrane-associated, Csk is a cytoplasmic protein and therefore requires membrane adaptors such as Cbp or Cav-1 for recruitment to the plasma membrane to mediate SFK inhibition. To determine the specific role of Cav-1 and Cbp in SFK inhibition, we measured c-Src activity in the absence of each membrane adaptor. It is noteworthy that in lungs and fibroblasts from Cav-1(-/-) mice, we observed increased expression of Cbp compared with wild-type (WT) controls. However, both c-Src activity and Csk localization at the membrane were similar between Cav-1(-/-) fibroblasts and WT cells. Likewise, Cbp depletion by small interfering RNA (siRNA) treatment of WT cells had no effect on basal c-Src activity, but it increased the phosphorylation state of Cav-1. Immunoprecipitation then confirmed increased association of Csk with phosphomimicking Cav-1. Knockdown of Cbp by siRNA in Cav-1(-/-) cells revealed increased basal c-Src activity, and re-expression of WT Cav-1 in the same cells reduced basal c-Src activity. Taken together, these results indicate that Cav-1 and Cbp cooperatively regulate c-Src activity by recruiting Csk to the membrane where it phosphorylates c-Src inhibitory tyrosine 529. Furthermore, when either Cav-1 or Cbp expression is reduced or absent, there is a compensatory increase in the phosphorylation state or expression level of the other membrane-associated Csk adaptor to maintain SFK inhibition.
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