Mouse SR-AI/MSR Antibody Summary
Trp79-Ser454
Accession # AAA39747
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: SR-AI/MSR
The scavenger receptor (SR) family comprises a group of functionally defined membrane receptors that share the common ability to bind and internalize modified forms of Low Density Lipoproteins (mLDL) (1‑3). Family members are classified alphabetically. The A class include four proteins: the three subtypes of SR-A (AI, AII, and AIII) that are generated by alternative splicing of the same gene, and a structurally similar protein named MARCO (4). All A class SRs are multidomain trimeric type II membrane proteins. SR-AI has an N-terminal cytoplasmic domain, a transmembrane domain, a spacer domain, an alpha -helical coiled coil, a collagen-like domain and a C-terminal cysteine-rich domain. SR-A is expressed by most tissue macrophages, dendritic cells and Kupffer cells. It is also highly expressed by microglia in neonatal as well as Alzheimer’ Disease brains. SR-AI binds a broad range of polyanionic ligands including modified proteins (e.g. Oxidized, acetylated or maleylated LDL, Advanced glycation end-product proteins), polyribonucleotides (polyguanosine and polyinosine), polysaccharides (dextran sulfate, fucoidan), phospholipids (phosphatidylserine), bacterial products (lipopolysaccharide and lipoteichoic acid) and selected chemical compounds (silica, crocidolite asbestos). The ligand-binding region has been localized to a positively charged region in the carboxyl end of the collagen-like domain. Based on its ligand binding characteristics, SR-AI is implicated in many physiological and pathophysiological functions. Studies using SR-A knockout mouse have also suggested roles of SR-A in atherogenesis, host defense and innate immunity, acquired immune responses, macrophage adhesion, and phagocytosis of apoptotic cells (1‑3).
- Daugherty, A. et al. (2000) Curr. Opin. Cardiovasc. Pulm. Ren. Invest. Drugs 2:223.
- Platt, N. and S. Gordon (2001) J. Clin. Invest. 108:649.
- Platt, N. and S. Gordon (1998) Chem. Biol. 5:R193.
- Elomaa, O. et al. (1995) Cell 80:603.
Product Datasheets
Citations for Mouse SR-AI/MSR Antibody
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
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CD204 suppresses large heat shock protein-facilitated priming of tumor antigen gp100-specific T cells and chaperone vaccine activity against mouse melanoma.
Authors: Qian J, Yi H, Guo C, Yu X, Zuo D, Chen X, Kane JM, Repasky EA, Subjeck JR, Wang XY
J. Immunol., 2011-08-10;187(6):2905-14.
Species: Mouse
Sample Types: Whole Cells
Applications: Flow Cytometry -
Silencing of either SR-A or CD36 reduces atherosclerosis in hyperlipidaemic mice and reveals reciprocal upregulation of these receptors.
Authors: Makinen PI, Lappalainen JP, Heinonen SE, Leppanen P, Lahteenvuo MT, Aarnio JV, Heikkila J, Turunen MP, Yla-Herttuala S
Cardiovasc. Res., 2010-07-15;88(3):530-8.
Species: Mouse
Sample Types: Whole Cells
Applications: Flow Cytometry
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