|Tested species reactivity||Bovine, Hamster, Human, Mink, Mouse, Rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||A peptide containing residues from mouse SR-BII (between residues 450-510) plus an N-terminal cysteine was coupled to KLH|
|Storage buffer||whole serum|
|Contains||0.1% sodium azide|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||Assay-Dependent|
|Immunohistochemistry (Paraffin) (IHC (P))||1:25|
|Western Blot (WB)||1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
High density lipoproteins (HDLs) play a critical role in cholesterol metabolism and their plasma concentrations are inversely correlated with risk for atherosclerosis. SR-BI and SR-BII (previously known as SR-BI.2) are the alternatively spliced products of a single gene. SR-BII differs from SR-BI in that the encoded c-terminal cytoplasmic domain is almost completely different. SR-BII binds HDLs and mediates selective uptake of HDL cholesteryl ester, but with an approximately 4-fold lower efficiency than SR-BI. Nuclease protection assays show SR-BII to be abundant in mouse tissues expressing SR-BI, with SR-BII expression found in liver, adrenal glands, and testes. Although the role of SR-BII is not completely clear, research suggests that it may be a functional HDL receptor. In addition, SR-BII mRNA results from the alternative splicing of SR-BI precursor transcripts with the SR-BII isoform mediating selective transfer of lipid between HDL and cells. The relative expression and functional activities of these two isoforms create a potential means of regulating selective lipid transfer between HDL and cells.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.