Recombinant Mouse Proprotein convertase subtilisin/kexin type 9(Pcsk9)

Code CSB-YP017647MO
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Source Yeast
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Code CSB-EP017647MO
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Source E.coli
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Code CSB-EP017647MO-B
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP017647MO
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Source Baculovirus
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Code CSB-MP017647MO
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Source Mammalian cell
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Product Details

Purity >85% (SDS-PAGE)
Target Names Pcsk9
Uniprot No. Q80W65
Alternative Names Pcsk9; Narc1; Proprotein convertase subtilisin/kexin type 9; EC 3.4.21.-; Neural apoptosis-regulated convertase 1; NARC-1; Proprotein convertase 9; PC9; Subtilisin/kexin-like protease PC9
Species Mus musculus (Mouse)
Expression Region 156-694
Target Protein Sequence SIPWN LERIIPAWHQ TEEDRSPDGS SQVEVYLLDT SIQGAHREIE GRVTITDFNS VPEEDGTRFH RQASKCDSHG THLAGVVSGR DAGVAKGTSL HSLRVLNCQG KGTVSGTLIG LEFIRKSQLI QPSGPLVVLL PLAGGYSRIL NAACRHLART GVVLVAAAGN FRDDACLYSP ASAPEVITVG ATNAQDQPVT LGTLGTNFGR CVDLFAPGKD IIGASSDCST CFMSQSGTSQ AAAHVAGIVA RMLSREPTLT LAELRQRLIH FSTKDVINMA WFPEDQQVLT PNLVATLPPS THETGGQLLC RTVWSAHSGP TRTATATARC APEEELLSCS SFSRSGRRRG DWIEAIGGQQ VCKALNAFGG EGVYAVARCC LVPRANCSIH NTPAARAGLE THVHCHQKDH VLTGCSFHWE VEDLSVRRQP ALRSRRQPGQ CVGHQAASVY ASCCHAPGLE CKIKEHGISG PSEQVTVACE AGWTLTGCNV LPGASLTLGA YSVDNLCVAR VHDTARADRT SGEATVAAAI CCRSRPSAKA SWVQ
Protein Length Full Length of Mature Protein
Tag Info The following tags are available.
N-terminal His-tagged
Tag-Free
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Form Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer before Lyophilization Tris/PBS-based buffer, 6% Trehalose, pH 8.0
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting
and FAQs
Protein FAQs
Storage Condition Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet Please contact us to get it.

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Target Background

Function
Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.
Gene References into Functions
  1. The data of the present study demonstrated that the PCSK9 shRNAmediated antiapoptotic effect induced by MCAO in hyperlipidemic mice is associated with ApoER2 downregulation, which may be a potential new therapy for stroke treatment in patients with hyperlipidemia. PMID: 30066942
  2. It was concluded that quercetin inhibits oxLDLinduced lipid droplets in RAW264.7 cells by upregulation of ABCAl, ABCG1, LXRalpha and downregulation of PCSK9, p53, p21 and p16. PMID: 29845234
  3. PCSK9 overexpression in the aorta may promote acute aortic dissection. PMID: 29197601
  4. Genetically determined PCSK9 deficiency might be associated with ectopic fat accumulation. PMID: 28758421
  5. The present study aimed to explore the direct toxicity of proprotein convertase subtilisin/kexin type 9 (PCSK9) to atherosclerosis (AS) and its association with apoptotic endothelial cells. PMID: 28656218
  6. present anti-PCSK9 vaccine induced long-lasting anti-PCSK9 antibody production and improved lipoprotein profiles. Thus, anti-PCSK9 vaccine could become a new option for the treatment of dyslipidemia as a long-acting therapy in future PMID: 29438441
  7. PCSK9 may act as an inflammatory mediator in the pathogenesis of atherosclerosis via TLR4/NF-kappaB signaling pathway. PMID: 28535426
  8. PCSK9, by sustaining smooth muscle cell synthetic phenotype, proliferation, and migration, may play a pro-atherogenic role in the arterial wall PMID: 27477186
  9. PCSK9 inhibits lipoprotein(a) clearance through the LDLR. PMID: 28750079
  10. Use Crispr-Cas system to introduce nonsense variants into PCSK9 to lower blood cholesterol levels. PMID: 28751571
  11. Studied the combination model of a single AAV-PCSK9 injection, high-fat diet, and partial carotid ligation which induces robust atherosclerosis in the flow-disturbed carotid artery within 3 weeks in C57 mice, and results suggest this is a quick and convenient model to study atherosclerosis and mechanisms using any knockout or transgenic mice without having to generate double knockouts. PMID: 28504688
  12. These observations suggest positive feedback interplay between SMC-derived PCSK9 and mtDNA damage in the proinflammatory milieu involving mtROS. This interaction results in cellular injury, characterized by apoptosis-a hallmark of atherosclerosis. PMID: 27197615
  13. AdipoR activation by agonists regulated PCSK9 expression and inhibits atherosclerosis in apoE(-/-) mice. PMID: 28546220
  14. Adeno-associated virus mediated infection with a mouse PCSK9 gain-of-function mutation is a rapid, easy, and efficient approach for inducing hypercholesterolemia and promoting abdominal aortic aneurysms in C57BL/6 mice infused with angiotensin II. PMID: 27470509
  15. conditions that cause ER stress regardless of their ability to dysregulate ER Ca(2+) inhibit PCSK9 secretion, thereby reducing PCSK9-mediated LDLR degradation and promoting LDLR-dependent hepatic cholesterol uptake. PMID: 27909053
  16. Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) Single Domain Antibodies Are Potent Inhibitors of Low Density Lipoprotein Receptor Degradation. PMID: 27284008
  17. PCSK9 increases hepatic lipid and lipoprotein production via apoE- and LDLR-dependent mechanisms PMID: 26980204
  18. Podocyte damage triggers marked inductions in plasma PCSK9, and knockout of Pcsk9 ameliorates dyslipidemia in a mouse model of nephrotic syndrome. PMID: 27358438
  19. polydatin ameliorates lipid and glucose metabolism in type 2 diabetes mellitus by downregulating PCSK9. PMID: 26833058
  20. binding of PCSK9 to GRP94 protects LDLR from degradation likely by preventing early binding of PCSK9 to LDLR PMID: 26628375
  21. The absence of PCSK9 results in a sex- and tissue-specific subcellular distribution of the LDLR and VLDLR, which is determined by estradiol levels. PMID: 26323289
  22. that ox-LDL receptor-1 and PCSK9 positively influence each other's expression, especially during an inflammatory reaction PMID: 26092101
  23. Data show that leptin treatment suppresses proprotein convertase subtilisin/kexin type 9 (PCSK9) in male, but fails to suppress PCSK9 in female. PMID: 26824363
  24. The Liver Clock Controls Cholesterol Homeostasis through Trib1 Protein-mediated Regulation of PCSK9/Low Density Lipoprotein Receptor (LDLR) Axis. PMID: 26547624
  25. PCSK9(-/-) mice display normal sodium balance and blood pressure regulation despite an increase of cleaved alphaENaC under basal condition PMID: 25621930
  26. PCSK9-mediated CD36 degradation may serve to limit fatty acid uptake and triglyceride accumulation in tissues, such as the liver and adipose tissue. PMID: 26494228
  27. HNF1alpha, but not HNF1beta, is the primary positive regulator of PCSK9 transcription in mouse liver PMID: 25652089
  28. high fructose consumption inversely modulates LDL-C and PCSK9 serum levels in mice without a significant impact on liver LDLR protein levels PMID: 25682035
  29. PCSK9-reactive oxygen species interaction may be important in the development of atherosclerosis in arterial channels with low shear stress. PMID: 25490141
  30. reduced PCSK9 function is associated with increased pathogen lipid clearance. PMID: 25320235
  31. Genome editing with the CRISPR-CRISPR-associated 9 system disrupts the Pcsk9 gene in vivo with high efficiency and reduces blood cholesterol levels in mice. PMID: 24916110
  32. MMP-2 overexpression may protect the LDLR from PCSK-9-induced degradation. PMID: 25613181
  33. PCSK9 markedly increases intestinal triglyceride-rich apoB production through mechanisms mediated in part by transcriptional effects on apoB. PMID: 25070550
  34. data revealed a plausible new role of AnxA2 in the reduction of PCSK9 protein levels via a translational mechanism. PMID: 24808179
  35. A vicious cycle in LDLR degradation might be generated by PCSK9 induced by hepatic Idol overexpression via dual mechanisms: sterol regulatory element-binding protein 2/LDLR. PMID: 24675665
  36. Pcsk9 inactivation decreases the HDL cholesterol concentration and cholesterol efflux capacity in serum, but does not increase atherosclerotic fatty streak volume. PMID: 23883163
  37. Low-density lipoprotein receptor (LDLR) is the main route of elimination of proprotein convertase subtilisin/kexin type 9 (PCSK9) and reciprocal regulation between these 2 proteins controls serum PCSK9 levels, hepatic LDLR expression, and serum LDL level. PMID: 23690465
  38. Data indicate that FoxO3 and Sirt6 suppress the PCSK9 gene expression and reduce LDL-cholesterol. PMID: 23974119
  39. Studies indicate that PCSK9 knockout (KO) (Pcsk9-/-) mice exhibit higher levels of LDLR protein in the liver and less circulating total cholesterol. PMID: 23775089
  40. PCSK9 deficiency caused a decrease in several cholesteryl esters (CE) and short fatty acid chain containing sphingolipid species. PMID: 23623011
  41. Transintestinal cholesterol excretion is regulated by PCSK9/ABCB1/statins. PMID: 23559630
  42. Furin-cleaved proprotein convertase subtilisin/kexin type 9 (PCSK9) is active and modulates low density lipoprotein receptor and serum cholesterol levels. PMID: 23135270
  43. AnxA2 acts as an endogenous regulator of PCSK9-induced LDLR degradation PMID: 22848640
  44. immunization with human-PCSK9 in mice is able to raise antibodies that cross-react and neutralize circulating mouse-PCSK9 protein thus resulting in increased liver LDL receptor levels and plasma cholesterol uptake PMID: 22611251
  45. Results indicate that although PPARgamma activation increased PCSK9 expression, PPARgamma activation induced LDLR and CYP7A1 expression that enhanced LDL cholesterol metabolism. PMID: 22593575
  46. propose a new role for PCSK9 that involves shuttling between apoB and low-density lipoprotein receptor PMID: 22580899
  47. PCSK9 potentiates neuronal apoptosis via modulation of ApoER2 levels and related anti-apoptotic signaling pathways. PMID: 22481440
  48. Increased PCSK9 might be responsible for the reduction in LDLR that results from decreased insulin signaling. The mTORC1 inhibitor rapamycin caused increased expression of PCSK9. PMID: 22426206
  49. PCSK9 overexpression is proatherogenic. PMID: 22261195
  50. PCSK9 downregulates LDLR levels during brain development and following transient ischemic stroke in adult mice PMID: 21518694

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Subcellular Location Cytoplasm. Secreted. Endosome. Lysosome. Cell surface. Endoplasmic reticulum. Golgi apparatus.
Protein Families Peptidase S8 family
Tissue Specificity Hepatocytes, kidney mesenchymal cells, intestinal ileum, colon epithelia and embryonic brain telencephalon neurons.
Database Links

KEGG: mmu:100102

STRING: 10090.ENSMUSP00000055757

UniGene: Mm.133268

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