|Datasheet||Specific References||Reviews||Related Products||Protocols|
|LCK, YT16, p56lck, pp58lck|
|Verified forward and reverse primers for analyzing the quantitative expression of gene|
|The primer mix has been verified to generate satisfactory qPCR data on Roche LightCycler480|
|1 vial of lyophilized qPCR primer mix (1 nmol each primer, sufficient for 200 numbers of 25 μl reactions) is shipped at ambiente temperatura.|
|The lyophilized product is stable for one year from date of receipt when stored at -20℃.|
The suspended product is stable for six months from date of receipt when stored at -20℃.
Sino biological qEASY qPCR primer pairs are used for SYBR Green-based real-time RT-PCR, The primers are designed by using SBI's proprietary primer design algorithm. Our primer collection covers the entire human genomes. It can be widely applied in the quantitative analysis of gene expression.
To avoid genomic DNA amplification, at least one primer is designed crosses the junction of exons according to the conserved region of a specific gene with all variants.
Confirmed in positive organizations; screened the primer with high specificity and high sensitivity.
Protein kinases are critically involved in signaling pathways that regulate cell growth, differentiation, activation, and survival. Initially identified as a T-cell specific member of the Src family of protein tyrosine kinases, Lck has become the object of intensive investigations which have revealed a key role for this kinase in the central processes controlling T-cell development, activation, proliferation and survival. Lck is expressed specifically in lymphoid cells. It contains one protein kinase domain, one SH2 domain, and one SH3 domain. It is associated with a variety of cell surface receptors and is critical for signal transduction from the T-cell antigen receptor (TCR). Consequently, Lck is targeted by regulatory proteins of T-lymphotropic viruses, especially by the Herpesvirus saimiri (HVS) tyrosine kinase interacting protein (Tip). This oncoprotein physically interacts with Lck in HVS transformed T cells and has an impact on its catalytic activity. Together with the identification of defects in the regulation of Lck expression or activity in T-cell leukemias, suggests that dysregulation of Lck might play a role in neoplastic transformation. However, under certain conditions Lck is also involved in the induction of apoptosis. This chemosensitizing effect of Lck is independent of T-cell receptor signaling and does not require the kinase activity of Lck. The findings demonstrate that Lck might be part of two independent signaling pathways leading to either cell proliferation or apoptosis.