|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.
UL16-binding proteins (ULBP) or retinoic acid early transcripts-1 (RAET1) are ligands to the activating receptor, NKG2D. Ten members of the human ULBP/RAET1 gene family have been identified to encode for potentially functional proteins, and have tissue-specific expressions. ULBP1, also known as RAET1I and NKG2DL1, together with at least ULBP 2 and 3, are well-known ligands for NKG2D, and activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. ULBP1 is expressed in T-cells, B-cells, erythroleukemia cell lines and in a wide range of tissues including heart, brain, lung, liver and bone marrow, as well as some tumor cells. As an unconventional member of the MHC class I family, ULBP1 function in immune responses, especially in cancer and infectious diseases. Unlike other ULBP members, ULBP1 is able to interact with soluble CMV glycoprotein UL16 in CMV infected cells. The interaction with UL16 blocked the interaction with the NKG2D receptor, and thus might escape the immune surveillance. Furthermore, UL16 also causes ULBP1 to be retained in the ER and cis-Golgi apparatus so that it does not reach the cell surface. The ULBP1 regulation may have implications for development of new therapeutic strategies against cancer cells.
1. Rölle, A. et al., 2003, J Immunol. 171(2): 902-908.
2. López-Soto, A. et al., 2006, J Biol Chem. 281(41): 30419-30430.
3. Song, H. et al., 2006, Cell Immunol. 239(1): 22-30.
4. Eisele, G. et al., 2006, Brain. 129 (9): 2416-2425.
5. Romphruk, AV. et al., 2009, Immunogenetics. 61(9): 611-617.
6. Sutherland, C.L. et. al., 2002, J. Immunol. 168: 671-679.