3 edition of Manipulation of apoptosis using the HMG-CoA reductase inhibitor--lovastatin found in the catalog.
Manipulation of apoptosis using the HMG-CoA reductase inhibitor--lovastatin
Thesis (M.Sc.) -- University of Toronto, 2000.
|Series||Canadian theses = -- Thèses canadiennes|
|The Physical Object|
|Pagination||3 microfiches : negative. --|
In the HMG-CoA reductase gene promoter region the cis element responsible for cholesterol-regulated transcription is called ___ SRE (sterol regulatory element or sterol responsive element) The SRE sequence in the HMG-CoA reductase gene . Apomine, a 1,1-bisphosphonate-ester with antitumor activity, has previously been reported to strongly down-regulate 3-hydroxymethylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate-limiting enzyme in the mevalonate pathway responsible for the prenylation of proteins. Here, we show that although apomine down-regulated HMG-CoA reductase protein Cited by: 6.
In vitro and in vivo biotransformation of simvastatin, an inhibitor of HMG CoA reductase. S Vickers, C A Duncan, K P Vyas, P H Kari, B Arison, S R Prakash, H G Ramjit, S M Pitzenberger, G Stokker and D E DugganCited by: STATIN-INDUCED APOPTOSIS. It has been shown that statins can induce apoptosis in a variety of cell types, such as rheumatoid synovial cells, pericytes, smooth muscle cells, cardiac myocytes, and several types of cancer cells (3–5, 8, 12–14, 17, 27, 33, 49).It is thought that apoptosis of these above-mentioned cell types in diseased tissue may contribute to the Cited by:
Statins are 3-hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors that may play an important role in the evolution of cancers, due to their effects on cancer cell metabolism. Statins affect several potential pathways, including cell proliferation, angiogenesis, apoptosis Author: Meysam Gachpazan, Hoda Kashani, Majid Khazaei, Seyed Mahdi Hassanian, Majid Rezayi, Fereshteh Asghar. Lovastatin is a lactone metabolite isolated from the fungus Aspergillus terreus with cholesterol-lowering and potential antineoplastic atin is hydrolyzed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxylmethylgutarylcoenzyme A reductase, an enzyme involved in cholesterol addition, this agent may induce tumor cell apoptosis .
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The results of this study revealed that HMG-CoA reductase inhibitor, lovastatin, effectively inhibited the growth of DLA cell line induced ascites tumor in mice. The doses of lovastatin, 4 and 16 mg/kg body weight, in mice were calculated from the standard (20 mg/day) and maximum (80 mg/day) doses used to reduce cholesterol in an average human by: if the HMG CoA reductase inhibitor, lovastatin, is combined with nicotinic acid or a fibric-acid deriv-ative.1,9 Small-framed, older patients with renal impairment are particularly prone to combination statin and fibrate-induced myopathy Patients with low hepatic levels of cytochrome P3A4 (CYP3A4) expression may also be at increased risk Original Article from The New England Journal of Medicine — Influence of Pravastatin, a Specific Inhibitor of HMG-CoA Reductase, on Hepatic Metabolism of Cholesterol logo logoCited by: Statins, 3-hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, which are approved for cholesterol reduction, may also be beneficial in.
HMG‐CoA reductase is the committed and therefore the regulatory step in cholesterol biosynthesis. If HMG‐CoA is reduced to mevalonate, cholesterol is the only product that can result. The reduction is a two‐step reaction, which releases the Coenzyme A cofactor and converts the thiol‐bound carboxylic group of HMG‐CoA to a free alcohol.
HMG-CoA Reductase Inhibitor, Atorvastatin, Induces Apoptosis in Human Lung Adenocarcinoma Cells (A) By Pritika Ramharack B. Med. (Hons) (UKZN) in the Discipline of Medical Biochemistry and Chemical Pathology School of Laboratory Medicine and Medical Sciences College of Health Sciences University of KwaZulu-Natal Durban Differentiation therapy may provide a new therapeutic approach to increasing the survival rate in such patients.
3-Hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are reported to promote cellular apoptosis and differentiation in many cancer cells; these effects are unrelated to lipid reduction.
HMG-CoA reductase inhibitors (statins) are commonly prescribed for lipid lowering to treat hypercholesterolemia.
Although they are well tolerated, their pharmacokinetic interactions with other drugs can lead to some adverse clinical consequences.
The avenue of interaction has been asserted to be CYP3A4 because most (or all) Cited by: Black DM, Bakker-Arkema RG, Nawrocki JW. An overview of the clinical safety profile of atorvastatin (Lipitor), a new HMG-CoA reductase inhibitor. Arch Intern Med ; (6): Google ScholarCited by: Of the following drug characteristic, what contributes significantly to the difference in the HMG CoA reductase inhibitors (the statins) potencies.
a) Route of elimination b) Bio-availability and half-life c) Effect on hepatic function d) Pharmacodynamics. Lovastatin is an inhibitor of hydroxymethyl glutaryl (HMG)-CoA reductase, the rate-limiting enzyme in cholesterol synthesis.
Previously, we reported that lovastatin can be used to arrest cultured cells in the G 1 phase of the cell cycle, resulting in the stabilization of the cyclin-dependent kinase inhibitors (CKIs) p21 and p It is a type of HMG-CoA reductase inhibitor and a type of statin.
Definition (CSP) a synthetic lipid-lowering agent; an inhibitor of 3-hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase that catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis. Definition (PDQ). Lovastatin and beyond: the history of the HMG-CoA reductase inhibitors Jonathan A.
Tobert 1 Nature Reviews Drug Discovery volume 2, Cited by: Hyperlipidemia (treatment)—3-Hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are indicated as adjuncts to diet in the treatment of primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (type IIa and IIb hyperlipoproteinemia) caused by elevated low-density lipoprotein cholesterol (LDL-C) concentrations in patients with a significant risk of coronary artery disease.
Previous reports have suggested that statins can induce apoptosis per se. Under our experimental conditions (i.e., at low dose and after short time of exposure) lovastatin does not induce apoptotic death (Figs.
5A and B), but exerts protective effects against UV-C-driven apoptosis. Only upon treatment of CHO cells with high dose of lovastatin for a long period Cited by: HMG CoA is acted upon by HMG CoA reductase (the target enzyme of statins) to produce mevalonic acid When HMG CoA reductase is inhibited it could lead to acetyl-CoA accumulation in the cells.
When HMG CoA reductase is inhibited it could lead to acetyl-CoA accumulation in the by: HMG-CoA Reductase Assay Kit Catalog Number CS Storage Temperature –70 °C TECHNICAL BULLETIN Product Description 3-hydroxymethylglutaryl-CoA reductase (HMGR) is a transmembrane glycoprotein, located on the endoplasmic reticulum.1 This enzyme catalyzes the four-electron reduction of HMG-CoA to coenzyme A.
Rosuvastatin: A High-Potency HMG-CoA Reductase Inhibitor Larry M. Lopez ABSTRACT Objective: To summarize the relevant pharmacologic, clinical, and safety data regarding rosuvastatin (Crestor—AstraZeneca), the most recently market-ed 3-hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor approved for the treatment of dyslipidemia.
HMG-CoA (3-hydroxymethylglutaryl—coenzyme A) reductase (HMGR) cat-alyzes the committed step in cholesterol biosynthesis. Statins are HMGR in-hibitors with inhibition constant values in the nanomolar range that effectively lower serum cholesterol levels and are widely prescribed in the treatment of.
Rosuvastatin (Crestor) is a member of the drug class of statins, used to treat high cholesterol and related conditions, and to prevent cardiovascular disease. Rosuvastatin is a competitive inhibitor of the enzyme HMG-CoA reductase, having a mechanism of action similar to that of other statins.
The objective of this study was to evaluate the cardiac toxicity of the HMG-CoA reductase inhibitors by testing the hypothesis that lovastatin induces apoptotic Author: Simon Rabkin. PowerPoint Presentation: Historical Overview and Development The development and use of HMGRIs began in with the discovery of mevastatin by Endo et al.
Originally named compactin, this fungal metabolite was isolated from Penicillium citrinum and demonstrated potent, competitive inhibition of HMG-CoA reductase.Several modalities that upregulate eNOS expression and/or activity have recently been identified, including HMG-CoA reductase inhibitors (statins), steroid hormones, nutrients and physical activity.
Treatment with an HMG-CoA reductase inhibitor led to an overall risk reduction of 31% (odds ratio, ; 95% confidence interval, to ).