Human Proprotein Convertase 9/PCSK9 DuoSet ELISA, 15 Plate

• Reactivity: Hu
• Applications: ELISA
• Conjugate: Biotin

Human Proprotein Convertase 9/PCSK9 DuoSet ELISA, 15 Plate Summary

• Source: N/A
• Assay Type: Solid Phase Sandwich ELISA
• Inter-Assay: See PDF Datasheet for details
• Intra-Assay: See PDF Datasheet for details
• Spike Recovery: See PDF Datasheet for details
• Sample Volume: See PDF Datasheet for details
• Gene: PCSK9

Applications/Dilutions

• Dilutions:
  • ELISA
• Application Notes: No significant interference observed with available related molecules.

Packaging, Storage & Formulations

• Storage: Store the unopened product at 2 - 8 °C. Do not use past expiration date.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Human Proprotein Convertase 9/PCSK9 DuoSet ELISA, 15 Plate

• EC 3.4.21
• EC 3.4.21.111
• FH3
• FH3neural apoptosis regulated convertase 1
• FHCL3
• HCHOLA3
• hypercholesterolemia, autosomal dominant 3
• LDLCQ1
• NARC1
• NARC-1
• NARC-1convertase subtilisin/kexin type 9 preproprotein
• NARC1EC 3.4.21.-
• Neural apoptosis-regulated convertase 1
• PC9
• PCSK9
• Proprotein Convertase 9
• proprotein convertase subtilisin/kexin type 9
• Subtilisin/kexin-like protease PC9

Background

Proprotein convertase subtilisin kexin 9 (PCSK9), also named neural apoptosis-regulated convertase 1 (NARC-1), is a member of the proteinase K subfamily of subtilisin-related serine endoproteases. The full-length protein has 692 amino acids, including a signal peptide, a pro- domain, and a catalytic domain. PCSK9 is highly expressed in the liver, intestine, and kidney. It is initially synthesized as a soluble 74 kDa precursor protein. In the endoplasmic reticulum, it undergoes autocatalytic intramolecular cleavage to generate a 14 kDa pro- domain and a 60 kDa catalytic domain. These two domains remain associated when PCSK9 is secreted outside the cells (1-3). The primary physiologic function of PCSK9 is to mediate the degradation of low density lipoprotein receptor (LDL R). Early observations indicated that gain-of-function missense mutations in the PCSK9 gene can cause an autosomal dominant form of hypercholesterolemia (4, 5). The expression of PCSK9 was observed to be up-regulated by the sterol regulatory element binding proteins (SREBPs), a family of transcription factors that are responsible for the upregulation of genes involved in cholesterol and fatty acid metabolism, such as the LDL R gene (6, 7). Further experimental evidence revealed that in mice, when the PCSK9 gene was knocked out, the number of LDL R in hepatocytes increased, whereas when PCSK9 was over-expressed, the amount of LDL R protein was reduced in the liver (8, 9). In humans, genetic analyses have shown that individuals who have nonsense or loss-of-function mutations in the PCSK9 gene have significantly lower plasma LDL cholesterol levels (10, 11). These investigations clearly indicated that PCSK9 plays a key role in reducing the hepatic LDL R levels. Recently, the underlying mechanism has been uncovered: under normal physiologic conditions, the LDL R is internalized on the cell surface and directed to the endosomes in order to be recycled back to the cell surface. PCSK9 binds to the EGF domain of the LDL R and prevents LDL R from being sorted to the endosomes. Instead, the PCSK9/LDL R complex is redistributed to the lysosomes for degradation (12-14). As such, PCSK9 regulates the amount of LDL R in the circulation and modulates cholesterol levels. Serum PCSK9 concentrations have been found to be directly associated with cholesterol levels (15, 16). Since individuals with loss-of-function PCSK9 mutations have strikingly reduced risk of coronary heart diseases, PCSK9 has become an attractive drug target in recent years (17, 18). One approach is to generate small molecules that are able to interfere with PCSK9 autoactivation and its interaction with LDL R. Other approaches aiming to reduce the amounts of PCSK9 in the circulation, such as small interfering RNAs (siRNAs), have also shown promise (19, 20).

Publications for Proprotein Convertase 9/PCSK9 (DY3888)(8)

Publications using DY3888

• Jin, W;Yu, J;Su, Y;Lin, H;Liu, T;Chen, J;Ge, C;Zhao, F;Geng, Q;Mao, L;Jiang, S;Cui, Y;Chen, T;Jiang, G;Li, J;Miao, C;Xiao, X;Li, H; Drug Repurposing Flubendazole to Suppress Tumorigenicity via PCSK9-dependent Inhibition and Potentiate Lenvatinib Therapy for Hepatocellular Carcinoma International journal of biological sciences 2023-04-23 [PMID: 37151886] (Human)
• R Chen, H Zhao, J Zhou, Y Wang, J Li, X Zhao, N Li, C Liu, P Zhou, Y Chen, L Song, H Yan Prognostic Impacts of LL-37 in Relation to Lipid Profiles of Patients with Myocardial Infarction: A Prospective Cohort Study Biomolecules, 2022-10-14;12(10):. 2022-10-14 [PMID: 36291690] (Human)
• L Song, X Zhao, R Chen, J Li, J Zhou, C Liu, P Zhou, Y Wang, Y Chen, H Zhao, H Yan Association of PCSK9 with inflammation and platelet activation markers and recurrent cardiovascular risks in STEMI patients undergoing primary PCI with or without diabetes Cardiovascular Diabetology, 2022-05-20;21(1):80. 2022-05-20 [PMID: 35596184] (Human)
• C Ayoub, Y Azar, Y Abou-Khali, Y Ghaleb, S Elbitar, G Halaby, S Jambart, MH Gannagé-Ya, C Yaghi, C Saade Riac, R El Khoury, JP Rabès, M Varret, C Boileau, P El Khoury, M Abifadel Identification of a Variant in APOB Gene as a Major Cause of Hypobetalipoproteinemia in Lebanese Families Metabolites, 2021-08-24;11(9):. 2021-08-24 [PMID: 34564380] (Human)
• J Grimm, G Peschel, M Müller, D Schacherer, R Wiest, K Weigand, C Buechler Rapid Decline of Serum Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) in Non-Cirrhotic Patients with Chronic Hepatitis C Infection Receiving Direct-Acting Antiviral Therapy Journal of Clinical Medicine, 2021-04-11;10(8):. 2021-04-11 [PMID: 33920491] (Human)
• A Alabi, XD Xia, HM Gu, F Wang, SJ Deng, N Yang, A Adijiang, DN Douglas, NM Kneteman, Y Xue, L Chen, S Qin, G Wang, DW Zhang Membrane type 1 matrix metalloproteinase promotes LDL receptor shedding and accelerates the development of atherosclerosis Nature Communications, 2021-03-25;12(1):1889. 2021-03-25 [PMID: 33767172] (Human)
• J Frostegård, S Ahmed, I Hafström, S Ajeganova, M Rahman Low levels of PCSK9 are associated with remission in patients with rheumatoid arthritis treated with anti-TNF-&alpha: potential underlying mechanisms Arthritis Research & Therapy, 2021-01-19;23(1):32. 2021-01-19 [PMID: 33461620] (Human)
• J Shi, W Zhang, Y Niu, N Lin, X Li, H Zhang, R Hu, G Ning, J Fan, L Qin, Q Su, Z Yang Association of circulating proprotein convertase subtilisin/kexin type 9 levels and the risk of incident type 2 diabetes in subjects with prediabetes: a population-based cohort study Cardiovascular Diabetology, 2020-12-10;19(1):209. 2020-12-10 [PMID: 33302966] (Human)

FAQs for Proprotein Convertase 9/PCSK9 (DY3888). (Showing 1 - 1 of 1 FAQs).

1. wondering what the difference is between your quantikine and duo set elisas?
   • Usually the duosets do not have the entire kit such as plates and buffers, whereas the other kits are complete.

Bioinformatics

• Gene Symbol: PCSK9