Rabbit anti Human Proprotein convertase subtilisin/kexin type 9 (PCSK9), LDLR-binding epitope blocking

• Background:

  This anitbody is made to an epitope that is reported to block the PCSK9-LDLR (low density lipoprotein receptor) interaction. PCSK9 binds to the EGF-A domain of the LDLR and signals LDLR degradation. Reduced LDLR levels result in decreased LDL (low density lipid) metabolism leading to hypercholesterolemia. _x000B__x000B_Additioanlly, PCSK9 may be implicated in the differentiation of cortical neurons and may also play a role in cholesterol homeostasis. Defects in PCSK9 gene are the cause of familial hypercholesterolemia 3 (FH3). The protein is thought to play a central role in cholesterol homeostais

• Synonyms:

  ProProtein convertase PC9, Subtilisin/kexin-like protease PC9, Neural apoptosis-regulated convertase 1

• UniProt:

  Q8NBP7

• Host:

  Rabbit

• Species Reactivity:

  Human

• Isotype:

  IgG

• Conjugation:

  Affinity Purified

• Type:

  Antigen Immunoaffinity Purified Polyclonal

• Applications:

  WB, ELISA

• Field of Research:

  Lipid Mediators

• Purification Method:

  Antigen Immunoaffiinity Purification

• Assay Principle:

  Antibody can be used for Western blotting (1:400 dilution) and immunocytochemisty (2 µg/mL). Optimal concentration should be evaluated by serial dilutions.

• Stability:

  See expiration date on vial

• Concentration:

  See vial for Concentration

• Form:

  Provided as solution in phosphate buffered saline with 0,08% sodium azide

• Precautions:

  This product is intended FOR RESEARCH USE ONLY, and FOR TESTS IN VITRO, not for use in diagnostic or therapeutic procedures involving Humans or animals.

• References & Citations:

  1. Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):928-33. Epub 2003 Jan 27. The secretory proprotein convertase neural apoptosis-regulated convertase 1 (NARC-1): liver regeneration and neuronal differentiation. Seidah NG, et al 2. Nat Genet. 2003 Jun;34(2):154-6. Mutations in PCSK9 cause autosomal dominant hypercholesterolemia. Abifadel et al 3. Hum Mutat. 2005 Nov;26(5):497. Novel mutations of the PCSK9 gene cause variable phenotype of autosomal dominant hypercholesterolemia. Allard D et al 4. Am J Hum Genet. 2006 Mar;78(3):410-22. Epub 2006 Jan 20. A spectrum of PCSK9 alleles contributes to plasma levels of low-density lipoprotein cholesterol. Kotowski IK, et al 5. Clin Genet. 2004 May;65(5):419-22. Mutations in the PCSK9 gene in Norwegian subjects with autosomal dominant hypercholesterolemia. Leren TP. 6. PLoS One. 2007 Oct 31;2(10):e1098. Evidence for positive selection in the C-terminal domain of the cholesterol metabolism gene PCSK9 based on phylogenetic analysis in 14 primate species. Ding K, McDonough SJ, Kullo IJ. 7. J Hum Genet. 2004;49(2):109-14. Epub 2004 Jan 15. Genetic variants in PCSK9 affect the cholesterol level in Japanese. Shioji K, et al 8. Atherosclerosis. 2005 Oct;182(2):331-40. Genetic screening protocol for familial hypercholesterolemia which includes splicing defects gives an improved mutation detection rate. Graham CA et al 9. Cell. 2006 Nov 3;127(3):635-48. Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. Olsen J V et al 10. J Am Coll Cardiol. 2005 May 17;45(10):1611-9. Epub 2005 Apr 21. A common PCSK9 haplotype, encompassing the E670G coding single nucleotide polymorphism, is a novel genetic marker for plasma low-density lipoprotein cholesterol levels and severity of coronary atherosclerosis. Chen SN et al

• Shipping Conditions:

  Ambient Temperature, freeze upon arrival

• Storage Conditions:

  Product should be stored at -20ºC; Aliquot to avoid freeze/thaw cycles

• Functional Analysis:

  WB

• CAS Number:

  9007-83-4