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anti-Human CSK Antibodies:
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Human Monoclonal CSK Primary Antibody for ICC, FACS - ABIN969069
Levy, Ehret, Rice, Verwoert, Launer, Dehghan, Glazer, Morrison, Johnson, Aspelund, Aulchenko, Lumley, Köttgen, Vasan, Rivadeneira, Eiriksdottir, Guo, Arking, Mitchell, Mattace-Raso, Smith, Taylor et al.: Genome-wide association study of blood pressure and hypertension. ... in Nature genetics 2010
Show all 3 Pubmed References
Human Polyclonal CSK Primary Antibody for ELISA, WB - ABIN1531264
Trepanier, Lei, Xie, MacDonald: Group II metabotropic glutamate receptors modify N-methyl-D-aspartate receptors via Src kinase. in Scientific reports 2013
Human Polyclonal CSK Primary Antibody for IHC (p), IHC - ABIN256941
Holtrich, Bräuninger, Strebhardt, Rübsamen-Waigmann: Two additional protein-tyrosine kinases expressed in human lung: fourth member of the fibroblast growth factor receptor family and an intracellular protein-tyrosine kinase. in Proceedings of the National Academy of Sciences of the United States of America 1992
Human Polyclonal CSK Primary Antibody for ICC, IF - ABIN4300691
Gallagher, Rambow, Kumasaka, Champeval, Bellacosa, Delmas, Larue: Beta-catenin inhibits melanocyte migration but induces melanoma metastasis. in Oncogene 2013
CSK is down-regulated in patients with rheumatoid arthritis.
Meta-analysis shows that C-allele of CSK (rs1378942) associates with higher systolic and diastolic blood pressure in East Asian populations.
It was discovered that pseudo-kinase pragmin uses the tyrosine kinase CSK to induce protein tyrosine phosphorylation in human cells.
Study indicated that MTHFR rs1801133, FGF5 rs16998073 and CSK rs1378942 were associated with increased the risk of obesity in the Chinese children.
These results identified a novel role for Csk as a host tyrosine kinase involved in dengue virus replication.
Domain interactions of C-terminal Src Kinase determined through NMR spectroscopy with segmental isotope labeling
Data suggest that myristoylation of Src kinase is essential to facilitate Src-induced and high-fat diet-accelerated prostatic tumor progression; targeting Src kinase myristoylation, which is required for Src kinase association at cellular membrane, blocks dietary fat-accelerated tumorigenesis.
Linear mixed-effect regressions showed significant association between rs1378942 in CSK and systolic blood pressure (beta = 0.98+/-0.46, P = 3.4x10-2). The child genotype scores for diastolic and systolic blood pressure were not associated in children.
H2O2-induced Csk translocation to the plasma membrane leads to phosphorylation of Src at the tyrosine 530 residue resulting in a reduction of ERK1/2 phosphorylation.
Data suggest that as a natural inhibitor of c-Src kinase, naringin could be an effective candidate for the treatment of melanoma.
deregulation of the Pragmin-Csk axis may induce aberrant cell migration that contributes to tumor invasion and metastasis
Our results do not support association between PTPN22/CSK and Henoch-Schonlein purpura
Results identify CSK downregulation as a principal driver of SRC activation and castration resistance.
Variant rs1378942 near CSK was nominally associated with systolic blood pressure in a Chinese population.
CSK is the kinase responsible for C-terminal phosphorylation of SRC, but not BRK.
Data indicate that the potent c-Src inhibitors pyrazolo[3,4-d]pyrimidines showed in vivo activity in neuroblastoma xenograft model.
Haemophilus ducreyi LspA1 protein inhibits phagocytosis by activation of host CSK.
In Chinese children, no association of CSK rs1378942, MTHFR rs1801133, CYP17A1 rs1004467, STK39 rs3754777 and FGF5 rs16998073 with BP/risk of hypertension.
the activity of SIRT2 is regulated by c-Src through post-translational modifications.
Data indicate that the accumulation of the cleaved C-terminal small fragment of eukaryotic elongation factor 2 (eEF2) in the nucleus, and C-terminal Src kinase (Csk) could enhance the proteolytic cleavage of eEF2.
These data suggest that inhibition of GABAergic inhibitory postsynaptic currents by morphine involves a beta-arr2/c-Src mediated mechanism.
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.
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.
N1-Src was implicated in L1-CAM signalling as PDN1 inhibited L1-CAM dependent neurite elongation in cerebellar granule neurons (CGNs).
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.
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.
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.
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
Csk plays an important role, not only in basal signaling, but also in setting the T cell antigen receptor signaling threshold and affinity recognition.
SHIP1 and Csk are part of the PSTPIP2-dependent inhibitory network that prevents the development of autoinflammatory disease.
If Cbp enhances the interaction between c-Src and FAK, Cbp could promote c-Src function when lipid rafts are disrupted.
Suggest critical role of Cav1 in modulating cSrc activation, gap junction remodeling, and ventricular arrhythmias.
Differentiation of embryonic stem cells is driven by c-Src is antagonized by c-Yes.
critical role in preventing TCR signaling
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.
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.
The Csk pathway appears to be a critical signaling cascade regulating social learning and memory
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.
Data show that the phosphoprotein associated with glycosphigolipid-enriched microdomains (PAG)/Csk binding protein (Cbp) modulates SFK activity in the brain.
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.
Dok-4 has a role as an anchoring molecule for the tyrosine kinase c-Src, and in turn as a regulator of TNF-alpha-mediated ROS production and NF-kappaB activation
Src family tyrosine kinases play a central role of arginase and inducible nitric oxide synthase in pulmonary artery endothelium.
Glucose 6-phosphate dehydrogenase is regulated through c-Src-mediated tyrosine phosphorylation in endothelial cells.
Non-receptor tyrosine-protein kinase that plays an important role in the regulation of cell growth, differentiation, migration and immune response. Phosphorylates tyrosine residues located in the C-terminal tails of Src-family kinases (SFKs) including LCK, SRC, HCK, FYN, LYN or YES1. Upon tail phosphorylation, Src-family members engage in intramolecular interactions between the phosphotyrosine tail and the SH2 domain that result in an inactive conformation. To inhibit SFKs, CSK is recruited to the plasma membrane via binding to transmembrane proteins or adapter proteins located near the plasma membrane. Suppresses signaling by various surface receptors, including T- cell receptor (TCR) and B-cell receptor (BCR) by phosphorylating and maintaining inactive several positive effectors such as FYN or LCK (By similarity).
, protein-tyrosine kinase CYL
, tyrosine-protein kinase CSK
, protein-tyrosine kinase MPK-2
, C-SRC kinase
, protein-tyrosine kinase (CSK)
, protein kinase
, src kinase