LCK (Lymphocyte Specific Protein Tyrosine Kinase)

LCK is the designation for the gene encoding lymphocyte protein-tyrosine kinase which has been identified in mouse, where it is coded by chromosome 4, and in man, where molecular analysis by somatic cell hybridization and in situ hybridization indicates that it is coded by the 1p35-p32 segment. (1) Rearrangement of LCK may play a role in the lymphocyte malignancy. The oncogene LCK is the protein-tyrosine kinase that regulates allelic exclusion at the T-cell receptor beta locus. (2) The T-cell antigen receptor plays a crucial role in thymocyte differentiation and T-cell activation. After antigen binding to the TCR, and in concert with engagement of other coreceptors and their associated ligands (such as CD4 (186940) and major histocompatibility complex (MHC) class II, CD28 (186760), B7 (112203), CD8 (186910), and MHC I), signal transduction cascades are activated. Data suggested that deficiency in p56(LCK) expression can produce a severe combined immunodeficiency (SCID) phenotype in humans. (3)TCR stimulation appears to directly activate STAT5, which may participate in the regulation of gene transcription and T-cell proliferation during immunologic responses. (4)
The LCK was expressed in E coli system and purified by an affinity column in combination with FPLC chromatography.
10ng of LCK is sufficient to phosphorylated 1 ug of heat-inactivated nuclear or cytoplasmic extract at 30 C for 30 mins.
The purified recombinant protein is greater than 95% homogeneous and contains no detectable protease, DNase and RNase activity
1 unit equals 1 nanogram of purified protein. 20-200ng is sufficient for an in vitro transcription assay and 100ng is sufficient for a protein-protein interaction assay.
0.5 mg/ml (in 1X dilution buffer A)
Buffer A: Tris-Cl, Glycerol, KCl, DTT and EDTA.
 
References:
1. Marth, J. D.et al, . Proc. Nat. Acad. Sci. 83: 7400-7404, 1986.
2. Anderson, S. J. et al., Nature 365: 552-554, 1993.
3. Goldman, F. D.; et al., J. Clin. Invest. 102: 421-429, 1998.
4. Welte, T.; et al., Science 283: 222-225, 1999.