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PCSK9 encodes a proprotein convertase belonging to the proteinase K subfamily of the secretory subtilase family. 再加上，我们可以发PCSK9 试剂盒 (74) 和 PCSK9 蛋白 (64)和数多这个蛋白质的别的产品。
Showing 10 out of 160 products:
Human Polyclonal PCSK9 Primary Antibody for ChIP, IHC (p) - ABIN268772
Cohen, Pertsemlidis, Kotowski, Graham, Garcia, Hobbs: Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in PCSK9. in Nature genetics 2005
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Human Polyclonal PCSK9 Primary Antibody for EIA, WB - ABIN453778
McNutt, Kwon, Chen, Chen, Horton, Lagace: Antagonism of secreted PCSK9 increases low density lipoprotein receptor expression in HepG2 cells. in The Journal of biological chemistry 2009
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Human Polyclonal PCSK9 Primary Antibody for IHC, ELISA - ABIN185371
Lalanne, Lambert, Amar, Chétiveaux, Zaïr, Jarnoux, Ouguerram, Friburg, Seidah, Brewer, Krempf, Costet: Wild-type PCSK9 inhibits LDL clearance but does not affect apoB-containing lipoprotein production in mouse and cultured cells. in Journal of lipid research 2005
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Human Polyclonal PCSK9 Primary Antibody for FACS, IHC (p) - ABIN391505
Shioji, Mannami, Kokubo, Inamoto, Takagi, Goto, Nonogi, Iwai: Genetic variants in PCSK9 affect the cholesterol level in Japanese. in Journal of human genetics 2004
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Human Polyclonal PCSK9 Primary Antibody for FACS, IHC (p) - ABIN652320
Abifadel, Varret, Rabès, Allard, Ouguerram, Devillers, Cruaud, Benjannet, Wickham, Erlich, Derré, Villéger, Farnier, Beucler, Bruckert, Chambaz, Chanu, Lecerf, Luc, Moulin, Weissenbach, Prat, Krempf et al.: Mutations in PCSK9 cause autosomal dominant hypercholesterolemia. ... in Nature genetics 2003
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Human Polyclonal PCSK9 Primary Antibody for IF (p), IHC (p) - ABIN761831
Jia, Song, Yang, Ma, Li, Lu, Cao, Zhang, Zhu, Wang, Leng, Cao, Du, Xu: Effects of Tanshinone IIA on the modulation of miR‑33a and the SREBP‑2/Pcsk9 signaling pathway in hyperlipidemic rats. in Molecular medicine reports 2016
Human Polyclonal PCSK9 Primary Antibody for EIA, WB - ABIN569616
Kwon, Lagace, McNutt, Horton, Deisenhofer: Molecular basis for LDL receptor recognition by PCSK9. in Proceedings of the National Academy of Sciences of the United States of America 2008
PCSK9 inhibits lipoprotein(a) clearance through the LDLR (显示 LDLR 抗体).
PCSK9 variants reduced fasting LDL-C as well as fasting triglycerides.
Proprotein convertase subtilisin/kexin 9 V4I variant with LDLR (显示 LDLR 抗体) mutations modifies the phenotype of familial hypercholesterolemia
PCSK9 associated with Familial Hypercholesterolemia and Polygenic Hypercholesterolemia in patients with Acute Coronary Syndrome , age =65 years, and LDL-C levels >/=160 mg/dl.
Results clearly that PCSK9 serum concentrations were associated to liver function and mortality, pointed to the disturbance of steroid regulation in patients with end-stage liver disease and an association of such disturbance with mortality. Further studies are required to acquire a more detailed understanding of the role of PCSK9 in liver-related mortality.
Use Crispr-Cas (显示 CSE1L 抗体) system to introduce nonsense variants into PCSK9 to lower blood cholesterol levels.
PCSK9 decreased in youth participating in an intensive dietary intervention. Change in HOMA-IR was associated with change in PCSK9, independent of weight loss, suggesting an important relationship with insulin (显示 INS 抗体) sensitivity.
these studies support that reductions in Lp(a (显示 APOA 抗体)) with PCSK9 inhibition are partly due to increased LDLR (显示 LDLR 抗体)-mediated uptake. In most situations, Lp(a (显示 APOA 抗体)) appears to compete poorly with LDL for LDLR (显示 LDLR 抗体) binding and internalization, but when LDLR (显示 LDLR 抗体) expression is increased with evolocumab, particularly in the setting of low circulating LDL, Lp(a (显示 APOA 抗体)) is reduced.
Plasma levels of proprotein convertase subtilisin/kexin type 9 (PCSK9), apolipoprotein C-III (apoC3 (显示 APOC3 抗体)) and small dense low density lipoprotein cholesterol (sdLDL-C) showed significant interactions with current dyslipidemias, and were predictive in the screening.
Some loss of function variants in PCSK9 are associated with enhanced LDL cholesterol lowering response to statin therapy.
Use Crispr-Cas (显示 CTNND1 抗体) system to introduce nonsense variants into PCSK9 to lower blood cholesterol levels.
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.
These observations suggest positive feedback interplay between SMC (显示 DYM 抗体)-derived PCSK9 and mtDNA damage in the proinflammatory milieu involving mtROS. This interaction results in cellular injury, characterized by apoptosis-a hallmark of atherosclerosis.
AdipoR activation by agonists regulated PCSK9 expression and inhibits atherosclerosis in apoE (显示 APOE 抗体)(-/-) mice.
Adeno (显示 ADORA2A 抗体)-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.
conditions that cause ER stress regardless of their ability to dysregulate ER Ca(2 (显示 CA2 抗体)+) inhibit PCSK9 secretion, thereby reducing PCSK9-mediated LDLR (显示 LDLR 抗体) degradation and promoting LDLR (显示 LDLR 抗体)-dependent hepatic cholesterol uptake.
Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) Single Domain Antibodies Are Potent Inhibitors of Low Density Lipoprotein Receptor (显示 LDLR 抗体) Degradation.
PCSK9 increases hepatic lipid and lipoprotein production via apoE (显示 APOE 抗体)- and LDLR (显示 LDLR 抗体)-dependent mechanisms
Podocyte damage triggers marked inductions in plasma PCSK9, and knockout of Pcsk9 ameliorates dyslipidemia in a mouse model of nephrotic syndrome.
This gene encodes a proprotein convertase belonging to the proteinase K subfamily of the secretory subtilase family. The encoded protein is synthesized as a soluble zymogen that undergoes autocatalytic intramolecular processing in the endoplasmic reticulum. The protein may function as a proprotein convertase. This protein plays a role in cholesterol homeostasis and may have a role in the differentiation of cortical neurons. Mutations in this gene have been associated with a third form of autosomal dominant familial hypercholesterolemia (HCHOLA3).
proprotein convertase subtilisin/kexin type 9
, convertase subtilisin/kexin type 9 preproprotein
, neural apoptosis regulated convertase 1
, subtilisin/kexin-like protease PC9
, convertase subtilisin
, neural apoptosis-regulated convertase 1
, proprotein convertase 9
, proprotein convertase PC9
, proprotein convertase subtilisin/kexin type 9 preproprotein
, Proprotein convertase 9
, Subtilisin/kexin-like protease PC9