LDLR / LDL Receptor Antibody ( FITC )

LDLR / LDL Receptor Antibody Datasheet

LDLR / LDL Receptor Antibody Product Information

• Immunogen: Recombinant Mouse LDLR / LDL Receptor protein (Catalog#50305-M08H)
• Reagents: FITC-conjugated rabbit monoclonal antibody
• Clone ID: 032
• Ig Type: Rabbit IgG
• Concentration: 10 μl/Test, 0.1 mg/ml
• Formulation: Aqueous solution containing 0.5% BSA and 0.09% sodium azide
• Preparation: This antibody was obtained from a rabbit immunized with purified, recombinant Mouse LDLR / LDL Receptor (rM LDLR / LDL Receptor; Catalog#50305-M08H; NP_034830.2; Met 1-Arg 790) and conjugated with FITC under optimum conditions, the unreacted FITC was removed.

LDLR / LDL Receptor Antibody Usage Guide

• Specificity: Mouse LDLR / LDL Receptor
• Flow Cytometry:
  

  Profile of anti-LDLR reactivity on Raw264.7 cells analyzed by flow cytometry. Cells should be Fc-blocked by treatment with Mouse BD Fc Block™ purified anti-CD16/CD32 mAb 2.4G2 (Cat. No. 553141) prior to staining, washed, then stained with FITC Rabbit anti-LDLR.

  Flow cytometry was performed on a BD FACSCalibur flow cytometry system

  Please refer to www.sinobiological.com/Flow-Cytometry-FACS-Protocols-a-750.html for technical protocols.

• Storage: This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !
  Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.

LDLR / LDL Receptor Antibody Background

Low-density lipoprotein (LDL) is a type of lipoprotein that transports cholesterol and triglycerides from the liver to peripheral tissues, and enables fats and cholesterol to move within the water-based solution of the blood stream. The Low-Density Lipoprotein Receptor (LDLR) is the prototype member of the LDLR family of scavenger receptors which is involved in receptor-mediated endocytosis of specific ligands. In order to be internalized, the receptor-ligand complexes must first cluster into clathrin-coated pits. LDLR recognizes the apoprotein B100 which is embedded in the phospholipid outer layer of LDL particles, as well as the apoE protein found in chylomicron remnants and VLDL remnants (IDL). After taken into the cell ending up in lysosomes, LDL is degraded and the cholesterol is made available for repression of microsomal enzyme HMG CoA reductase, the rate-limiting step in cholesterol synthesis. As a mosaic protein, the extracellular region of LDLR consists of seven N-terminal complement-like cysteinerich repeats followed by three EGF like repeats with a β-propeller YWTD containing motif, and a membrane proximal Ser/Thr rich region. Furthermore, it is reported that in case of HIV-1 infection, LDLR functions as a receptor for extracellular Tat (HIV-1 transactivator) into neurons, mediating its internalization in uninfected cells. Mutations in LDLR gene cause the autosomal dominant disorder, familial hypercholesterolemia.

References

1. Suedhof, T.C. et al., 1985, Science. 228: 815-822.
2. Hobbs, H.H. et al., 1993, Hum. Mutat. 1: 445-466.
3. Barrett, P.H. and Watts, G.F. 2002, Atherosclerosis. Supplements. 2: 1-4.
4. Liu, Y. et al., 2000, Nat. Med. 6: 1380-1387.
5. Nomura, S. et al., 2004, Gene. Therapy. 11: 1540-1548.