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Western blot analysis of Lck on jurkat lysate. Lane 1: 1:5000, lane 2: 1:10000, lane 3: 1:20000 dilution of Lck.
Jurkat
BD Transduction Laboratories™ Purified Mouse Anti-Lck
BD Transduction Laboratories™ Purified Mouse Anti-Lck
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- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- Please refer to www.bdbiosciences.com/us/s/resources for technical protocols.
- Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
- Source of all serum proteins is from USDA inspected abattoirs located in the United States.
The p56[lck] protein kinase is a member of the src family of cytoplasmic protein-tyrosine kinases (PTKs). Members of this family have several common features: 1) unique N-terminal domains, 2) attachment to cellular membranes through a myristylated N-terminus, and 3) homologous SH2, SH3, and catalytic domains. Within the src family of PTKs, lck, fyn, and Yes are expressed in T cells. The unique N-terminal domain of p56[lck] interacts with the cytoplasmic tails of the CD4 and CD8 cell surface glycoproteins. CD4 and CD8 bind to surface major histocompatibility complex (MHC) class II and class I molecules, respectively. These complexes interact with the T cell antigen receptor (TCR) in the early stages of T cell activation. In addition, an activated lck kinase increases responsiveness of some T cell hybridomas to antigen. The phosphorylation status and, therefore, the activity of p56[lck] kinase is regulated by the CD45 tyrosine protein phosphatase. Several studies suggest that lck has many functions critical to T cell development and activation. Mice lacking a functional lck gene are drastically impaired in the production of T lymphocytes. Variants of the human Jurkat T cell line that do not express p56[lck] exhibit a diminished response to stimulation of the T cell receptor. Evidence suggests that lck is directly upstream from PI3-kinase in the signal transduction cascade in T cell activation.
개발 참고 자료 (5)
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Horak ID, Gress RE, Lucas PJ, Horak EM, Waldmann TA, Bolen JB. T-lymphocyte interleukin 2-dependent tyrosine protein kinase signal transduction involves the activation of p56lck. Proc Natl Acad Sci U S A. 1991; 88(5):1996-2000. (Biology). 참조 보기
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Maccalli C, Pisarra P, Vegetti C, Sensi M, Parmiani G, Anichini A. Differential loss of T cell signaling molecules in metastatic melanoma patients' T lymphocyte subsets expressing distinct TCR variable regions. J Immunol. 1999; 163(12):6912-6923. (Clone-specific: Flow cytometry). 참조 보기
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Xu H, Littman DR. A kinase-independent function of Lck in potentiating antigen-specific T cell activation. Cell. 1993; 74(4):633-643. (Biology). 참조 보기
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Zeyda M, Staffler G, Horejsi V, Waldhausl W, Stulnig TM. LAT displacement from lipid rafts as a molecular mechanism for the inhibition of T cell signaling by polyunsaturated fatty acids. J Biol Chem. 2002; 277(32):28418-28423. (Clone-specific: In vitro kinase assay, Western blot). 참조 보기
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Zhou YJ, Magnuson KS, Cheng TP, et al. Hierarchy of protein tyrosine kinases in interleukin-2 (IL-2) signaling: activation of syk depends on Jak3; however, neither Syk nor Lck is required for IL-2-mediated STAT activation. Mol Cell Biol. 2000; 20(12):4371-4380. (Clone-specific: Immunoprecipitation, Western blot). 참조 보기
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