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anti-Human HMGCR Antibodies:
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Human Polyclonal HMGCR Primary Antibody for IF (p), IHC (p) - ABIN709196
Wu, He, Wang, Xue, Ning, Zou, Ye, Li, Wang, Pang: The antihypercholesterolemic effect of jatrorrhizine isolated from Rhizoma Coptidis. in Phytomedicine : international journal of phytotherapy and phytopharmacology 2014
Show all 4 Pubmed References
Human Polyclonal HMGCR Primary Antibody for ICC, IF - ABIN4319308
Bjarnadottir, Romero, Bendahl, Jirström, Rydén, Loman, Uhlén, Johannesson, Rose, Grabau, Borgquist: Targeting HMG-CoA reductase with statins in a window-of-opportunity breast cancer trial. in Breast cancer research and treatment 2013
Show all 4 Pubmed References
Human Polyclonal HMGCR Primary Antibody for IF (p), IHC (p) - ABIN753283
Zanoni, Aiello, Arnoldi, Lammi: Hempseed Peptides Exert Hypocholesterolemic Effects with a Statin-Like Mechanism. in Journal of agricultural and food chemistry 2017
Human Polyclonal HMGCR Primary Antibody for ELISA - ABIN450058
Hanai, Cao, Tanksale, Imamura, Koshimizu, Zhao, Kishi, Yamashita, Phillips, Sukhatme, Lecker: The muscle-specific ubiquitin ligase atrogin-1/MAFbx mediates statin-induced muscle toxicity. in The Journal of clinical investigation 2007
The specificity and evolutionary conservation of the HMGCoAr pathway for germ cells suggest that an attractant common to invertebrates and vertebrates guides germ cells in early embryos.
HMGCR genetic variation is associated with Alzheimer's disease.
our study demonstrates A allele of HMGCR rs3846662 acts as a protective factor for late-onset Alzheimer's disease in northern Han Chinese
UBXD8 (show FAF2 Antibodies) is necessary for sterol-stimulated dislocation of ubiquitylated HMGCR from the endoplasmic reticulum membrane en route to proteasomal degradation, a function dependent on its UBX domain.
The docking studies indicate rutin as the best compound that can inhibit HMG-CoA reductase as it had strong binding affinity to the enzyme.
Both HMGCR and SQLE (show SQLE Antibodies) promoters have two SREs that may act as a homing region to attract a single SREBP-2 (show SREBF2 Antibodies) homodimer.
To estimate the association between changes in levels of LDL-C (and other lipoproteins) and the risk of cardiovascular events related to variants in the CETP (show CETP Antibodies) gene, both alone and in combination with variants in the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene.
Low LDL cholesterol levels due to PCSK9 (show PCSK9 Antibodies) and HMGCR variants had no causal effect on high risk of Alzheimer's disease, vascular dementia, any dementia, or Parkinson's disease; however, low LDL cholesterol levels may have a causal effect in reducing the risk of Alzheimer's disease.
These results indicate that HIF-mediated induction of Insig-2 (show INSIG2 Antibodies) and degradation of HMGCR are physiologically relevant events that guard against wasteful oxygen consumption and inappropriate cell growth during hypoxia.
TGF-beta1 (show TGFB1 Antibodies) induces cholesterol synthesis by increasing HMG-CoA reductase mRNA expression in keratinocytes.
Gene expression profile and the biological functions of HMGCR in gastric cancer were studied. It was found that the expression of HMGCR was increased in gastric cancer tissues. Over-expression of HMGCR promoted the growth and migration of gastric cancer cells, while knocking down the expression of HMGCR inhibited the growth, migration and tumorigenesis of gastric cancer cells.
HMGCR inhibits the early stage of PCV2 infection, while PKC enhances the infection at the late stage.
The relative expression level of HMGR was high in liver, heart, kidney, bladder and subcutaneous fat, medium in lung, uterus and large intestine, and low in cerebrum, spleen, spinal cord, stomach, ovary, longissimus muscle, and small intestine.
Deletion of HMGCR expression in T cells led to a severe decrease in their numbers with the remaining cells displaying an activated phenotype, with an increased proportion of regulatory T cells (Tregs) in particular.
these studies designate sterol-accelerated degradation of HMGCR as a potential therapeutic target for prevention of atherosclerosis and associated cardiovascular disease.
To eludicate the mechanisms underlying statin myotoxicity and HMGCR function in skeletal muscle, we developed the skeletal muscle-specific (show EIF3K Antibodies) HMGCR knockout mice.
High-dose simvastatin inhibits HMGCoA reductase and prevents experimental hyperinflation lung injury by angioprotective and anti-inflammatory effects.
TSH can regulate the phosphorylation of HMGCR via AMPK (show PRKAA1 Antibodies).
HMGCR proteasomal-degradation by IFN strictly requires the synthesis of endogenous 25-Hydroxycholesterol.
Increased cholesterol synthesis mediated by HMGCoA (show HMGCS2 Antibodies)-R under inflammatory stress may be one of the mechanisms for intracellular lipid accumulation and statin resistance.
we consistently observe involvement of gp78 (show AMFR Antibodies) in Insig-1 (show INSIG1 Antibodies) degradation, we find no substantive evidence to support roles for either gp78 (show AMFR Antibodies) or TRC8 (show RNF139 Antibodies) in the robust sterol-accelerated degradation of HMG-CoA reductase.
Hepatocyte HMGCR is essential for the survival of mice, and its abrogation elicits hepatic steatosis with jaundice and hypoglycemia.
HMG-CoA reductase is the rate-limiting enzyme for cholesterol synthesis and is regulated via a negative feedback mechanism mediated by sterols and non-sterol metabolites derived from mevalonate, the product of the reaction catalyzed by reductase. Normally in mammalian cells this enzyme is suppressed by cholesterol derived from the internalization and degradation of low density lipoprotein (LDL) via the LDL receptor. Competitive inhibitors of the reductase induce the expression of LDL receptors in the liver, which in turn increases the catabolism of plasma LDL and lowers the plasma concentration of cholesterol, an important determinant of atherosclerosis. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
3-Hydroxy-3-Methylglutaryl CoA reductase
, 3-hydroxy-3-methylglutaryl coenzyme A reductase
, HMG coenzyme A reductase
, HMG-CoA reductase
, HMGCo-A reductase
, HMGCoA reductase
, lethal (3) 04684
, 3-hydroxy-3-methylglutaryl CoA reductase (NADPH)
, 3-hydroxy-3-methylglutaryl-Coenzyme A reductase
, hydroxymethylglutaryl-CoA reductase
, 3-hydroxy-3-methylglutaryl coenzyme A reductase/HMG-CoA reductase
, 3-hydroxy-3-methylglutaryl-coenzyme A reductase
, 3-hydroxy-3-methylglutaryl CoA reductase
, 3-hydroxy-3-methylglutaryl-CoA reductase