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This study establishes Csk and CD148 as critical molecular switches controlling the thrombotic and hemostatic capacity of platelets and reveals cell-intrinsic mechanisms that prevent pathological thrombosis from occurring.
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The results suggest that Csk in Intestinal epithelial cells plays important roles in the regulation of the intestinal epithelial barrier function and protection against colitis.
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N1-Src was implicated in L1-CAM signalling as PDN1 inhibited L1-CAM dependent neurite elongation in cerebellar granule neurons (CGNs).
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identify a physiological pathway by which blood pressure is regulated, in which the insufficiency of Csk induces aldosterone production with zonal specificity in the adrenal glands, increasing sodium reabsorption and plasma volume and thus resulting in hypertension.
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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.
