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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
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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
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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
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.
High HMGR expression is associated with breast cancer metastasis.
High HMGCR expression is associated with hypercholesterolemia.
The presence of rs17244841 ve rs17238540 mutations in HMGCR causes a significant reduction in total cholesterol and LDL-c levels.
A positive relationship emerged between HMG-CoAR, hormone receptors and TAZ/YAP, suggesting a connection between the mevalonate pathway, the hormonal milieu and Hippo in Male breast cancer. Moreover, HMG-CoAR expression may be a favorable prognostic indicator.
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 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 promoters have two SREs that may act as a homing region to attract a single SREBP-2 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 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 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 and degradation of HMGCR are physiologically relevant events that guard against wasteful oxygen consumption and inappropriate cell growth during hypoxia.
TGF-beta1 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.
In this study, variants in PCSK9 had approximately the same effect as variants in HMGCR on the risk of cardiovascular events and diabetes per unit decrease in the LDL cholesterol level. The effects of these variants were independent and additive.
Data show that simvastatin significantly inhibited cellular proliferation, induced cell cycle G1 arrest and apoptosis, and caused cellular stress via reduction in the enzymatic activity of 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR).
no associations found between HMGCR rs3846662, HMRCR alternative splicing and Alzheimer's disease pathology pathology.
results indicate that abnormal lipid metabolism may exist in spontaneous preterm delivery (SPTD) women and the premature fetus and the HMGCR gene may be a susceptible gene for SPTD
Report the mechanism of polyphenol binding to and activity regulation of HMGR using molecular docking.
the results of the present study showed that luteolin modulates HMGCR transcription by decreasing the expression and nuclear translocation of SREBP-2.
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 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.
HMGCR proteasomal-degradation by IFN strictly requires the synthesis of endogenous 25-Hydroxycholesterol.
Increased cholesterol synthesis mediated by HMGCoA-R under inflammatory stress may be one of the mechanisms for intracellular lipid accumulation and statin resistance.
we consistently observe involvement of gp78 in Insig-1 degradation, we find no substantive evidence to support roles for either gp78 or TRC8 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.
Linalool reduces the expression of 3-hydroxy-3-methylglutaryl CoA reductase via sterol regulatory element binding protein-2- and ubiquitin-dependent mechanisms.
Although gene expressions of HMG-CoAR and CYP7A1 in diabetic buckwheat sprout-fed groups were higher than in the diabetic control group, the elevation of mRNA level of CYP7A1 was greater than that of HMG-CoAR.
mechanistic basis for the differential Hmgcr expression in these mouse models of human essential hypertension and implications for better understanding the role of this gene in regulation of blood pressure
HMG-CoA reductase is crucial for early development of the mouse embryos
Hepatic neutral cytosolic cholesteryl ester hydrolase decreased mRNAs for cholesterol 7alpha-hydroxylase, sterol 27-hydroxylase, and HMG-CoA reductase on day 7 after transfection, coinciding with peak hepatic free cholesterol concentrations
Docosahexaenoic acid may enhance brain HMG-CoA reductase activity in aged mice.
macrophages from diabetic mice demonstrate increased oxidative stress and increased expression HMG-CoA reductase
simvastatin-mediated inhibition of HMGR activity in acutely regenerating tissue of wounded mice was paralleled by a marked loss of VEGF protein expression and disturbances of normal proliferation processes in wound margin keratinocytes during skin repair.
Data show that in vitro down regulation of NRIF expression decreased the mRNA for two main cholesterogenic enzymes, 3-hydroxy-3-methylglutaryl-coenzyme A reductase and 7-dehydrocholesterol reductase.
renal ischemia/reperfusion activates the HMGCR gene via multiple stress-activated transcriptional and epigenetic pathways, contributing to renal cholesterol loading.
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.
Study identified a mutation in the 3-hydroxy-3-methylglutaryl-Coenzyme A reductase 1b (hmgcr1b) gene that affects myocardial migration to the midline and subsequent heart-tube morphogenesis.
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-Coenzyme A reductase
, 3-hydroxy-3-methylglutaryl coenzyme A reductase/HMG-CoA reductase
, 3-hydroxy-3-methylglutaryl-coenzyme A reductase
, 3-hydroxy-3-methylglutaryl CoA reductase (NADPH)
, HMG-CoA reductase
, hydroxymethylglutaryl-CoA reductase
, 3-hydroxy-3-methylglutaryl CoA reductase
, 3-hydroxy-3-methylglutaryl-CoA reductase
, 3-Hydroxy-3-Methylglutaryl CoA reductase
, 3-hydroxy-3-methylglutaryl coenzyme A reductase
, HMG coenzyme A reductase
, HMGCo-A reductase
, HMGCoA reductase
, lethal (3) 04684
, 3-alpha-hydroxy-3-methylglutaryl-CoA reductase
, 3-hydroxy-3-methylglutaryl-CoA reductase b
, 3-hydroxy-3-methylglutaryl-Coenzyme A reductase b