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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.
Both HMGCR and SQLE (show SQLE Proteins) promoters have two SREs that may act as a homing region to attract a single SREBP-2 (show SREBF2 Proteins) 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 Proteins) 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 Proteins) 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 Proteins) and degradation of HMGCR are physiologically relevant events that guard against wasteful oxygen consumption and inappropriate cell growth during hypoxia.
TGF-beta1 (show TGFB1 Proteins) 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 (show PCSK9 Proteins) 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
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.
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 Proteins) 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 Proteins).
HMGCR proteasomal-degradation by IFN strictly requires the synthesis of endogenous 25-Hydroxycholesterol.
Increased cholesterol synthesis mediated by HMGCoA (show HMGCS2 Proteins)-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 Proteins) in Insig-1 degradation, we find no substantive evidence to support roles for either gp78 (show AMFR Proteins) or TRC8 (show RNF139 Proteins) 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.
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