|Datasheet||Specific References||Reviews||Related Products||Protocols|
|19A, CS1, 19A24, CRACC, 4930560D03Rik, Slamf7|
|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.
SLAM family member 7 (SLAMF7), also known as CRACC, CD319, CD2-like receptor-activating cytotoxic cells, and CS1, is a single-pass type I membrane protein and a member of the CD2 family of cell surface receptors. SLAMF7 is expressed in NK cells, activated B-cells, NK-cell line but not in promyelocytic, B-cell lines, or T-cell lines. Although the cytoplasmic domain of CS1 contains immunoreceptor tyrosine-based switch motifs (ITSM), which enables to recruite signaling lymphocyte activation molecule (SLAM)-associated protein (SAP/SH2D1A), it activates NK cells in the absence of a functional SAP. CS1 is a self ligand and homophilic interaction of CS1 regulates NK cell cytolytic activity. CRACC positively regulated natural killer cell functions by a mechanism dependent on the adaptor EAT-2 but not the related adaptor SAP. However, in the absence of EAT-2, CRACC potently inhibited natural killer cell function. It was also inhibitory in T cells, which are typically devoid of EAT-2. Thus, CRACC can exert activating or inhibitory influences on cells of the immune system depending on cellular context and the availability of effector proteins.