|OSMRB, MGC75127, MGC150626, MGC150627,|
|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.
Oncostatin-M specific receptor subunit beta also known as the oncostatin M receptor (OSMR) and Interleukin-31 receptor subunit beta (IL-31RB), is one of the receptor proteins for oncostatin M. OSMR is a member of the type I cytokine receptor family. IL-31RB/OSMR heterodimerizes with interleukin 6 signal transducer to form the type II oncostatin M receptor and with interleukin 31 receptor A to form the interleukin 31 receptor, and thus transduces oncostatin M and interleukin 31 induced signaling events. Mutations in IL-31RB/OSMR have been associated with familial primary localized cutaneous amyloidosis. Defects in IL-31RB/OSMR are the cause of amyloidosis primary localized cutaneous type 1 (PLCA1), also known as familial lichen amyloidosis or familial cutaneous lichen amyloidosis. PLCA1 is a hereditary primary amyloidosis characterized by localized cutaneous amyloid deposition. This condition usually presents with itching (especially on the lower legs) and visible changes of skin hyperpigmentation and thickening (lichenification) that may be exacerbated by chronic scratching and rubbing. The amyloid deposits probably reflect a combination of degenerate keratin filaments, serum amyloid P component, and deposition of immunoglobulins.