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Our results have uncovered a previously unknown role of c-Src tyrosine kinase in regulating interneuron function in the brain and identified a novel mechanism by which TASK-1 channels are activated in neurons.
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in the absence of PAG, Csk becomes more associated with alternative partners; i.e., phosphatase PTPN22 and Dok adaptors. Combining PAG deficiency with PTPN22 or Dok adaptor deficiency further enhances effector T cell responses. Unlike PAG, Cbl ubiquitin ligases inhibit the activation of naive, but not of effector, T cells.
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Csk is a causative gene in the 15q24 locus and regulates blood pressure through Src, and these findings provide a novel therapeutic target for the treatment of hypertension
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Csk plays an important role, not only in basal signaling, but also in setting the T cell antigen receptor signaling threshold and affinity recognition.
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SHIP1 and Csk are part of the PSTPIP2-dependent inhibitory network that prevents the development of autoinflammatory disease.
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If Cbp enhances the interaction between c-Src and FAK, Cbp could promote c-Src function when lipid rafts are disrupted.
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Suggest critical role of Cav1 in modulating cSrc activation, gap junction remodeling, and ventricular arrhythmias.
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Differentiation of embryonic stem cells is driven by c-Src is antagonized by c-Yes.
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critical role in preventing TCR signaling
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It was concluded that c-Src and NADPH oxidase components are necessary for redox-mediated production of TNF-alpha following liver ischemia-reperfusion and that hepatocytes play an important role in this process.
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Data indicate that chemical rescue of c-Src provided a tool to dissect the spatiotemporal mechanism of activation of the Rap1 guanine exchange factor, C3G, one of the identified potential c-Src substrates that plays a role in focal adhesion signaling.
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The Csk pathway appears to be a critical signaling cascade regulating social learning and memory
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These data demonstrate that expression of an activated allele of c-src overcomes the block to mammary gland morphogenesis in mice arising due to the loss of the cytoplasmic C-terminal domain of Ptch1.
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Data show that the phosphoprotein associated with glycosphigolipid-enriched microdomains (PAG)/Csk binding protein (Cbp) modulates SFK activity in the brain.
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Caveolin-1 and C-terminal Src kinase binding protein are cooperative, and increases in their expression or phosphorylation favors repression of C-terminal Src kinase activity.
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expression of Cbp is downregulated during osteoclast differentiation, consequently inhibiting recruitment of Csk to lipid rafts and keeping c-Src activity high in osteoclasts. findings provide a novel paradigm that controls c-Src activity in osteoclasts.
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show that relative titration of CD45 and Csk expression reveals distinct regulation of basal and inducible T cell receptor signaling during thymic development.
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Results show that disruption of E-cadherin junctions and enhancement of cell invasion by beta-estradiol stimulation was mediated by NO-dependent activation of c-Src.
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Results identify Src-family kinase substrates involved in platelet-derived growth factor signaling.
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the absence of c-src expression indeed affects the development of selected, TCDD-induced toxic endpoints that are related to wasting syndrome
