hydroxymethylglutaryl-CoA reductase

ヒドロキシメチルグルタリルCoA還元酵素

WordNet

1. the 3rd letter of the Roman alphabet (同)c
2. (music) the keynote of the scale of C major
3. a general-purpose programing language closely associated with the UNIX operating system
4. an enzyme that catalyses the biochemical reduction of some specified substance

PrepTutorEJDIC

1. carbonの化学記号
2. cobaltの化学記号

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2018/04/27 21:59:50」(JST)

wiki en

[Wiki en表示]

Hydroxymethylglutaryl-CoA reductase
Identifiers
EC number	1.1.1.88
CAS number	37250-24-1
Databases
IntEnz	IntEnz view
BRENDA	BRENDA entry
ExPASy	NiceZyme view
KEGG	KEGG entry
MetaCyc	metabolic pathway
PRIAM	profile
PDB structures	RCSB PDB PDBe PDBsum
Search PMC articles PubMed articles NCBI proteins

In enzymology, a Hydroxymethylglutaryl-CoA reductase (EC 1.1.1.88) is an enzyme that catalyzes the chemical reaction

(R)-mevalonate + CoA + 2 NAD⁺ $\rightleftharpoons$ 3-hydroxy-3-methylglutaryl-CoA + 2 NADH + 2 H⁺

The 3 substrates of this enzyme are (R)-mevalonate, CoA, and NAD⁺, whereas its 3 products are 3-hydroxy-3-methylglutaryl-CoA, NADH, and H⁺.

This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD⁺ or NADP⁺ as acceptor. The systematic name of this enzyme class is (R)-mevalonate:NAD⁺ oxidoreductase (CoA-acylating). Other names in common use include beta-hydroxy-beta-methylglutaryl coenzyme A reductase, beta-hydroxy-beta-methylglutaryl CoA-reductase, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and hydroxymethylglutaryl coenzyme A reductase.

External links

• Hydroxymethylglutaryl-CoA reductase at the US National Library of Medicine Medical Subject Headings (MeSH)

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

• 1. スタチン：作用、副作用、および投与statins actions side effects and administration [show details]
  …competitive inhibitors of hydroxymethylglutaryl (HMG) CoA reductase, the rate-limiting step in cholesterol biosynthesis They occupy a portion of the binding site of HMG CoA, blocking access of this substrate …
• 2. 高IgD症候群：病態生理hyperimmunoglobulin d syndrome pathophysiology [show details]
  … and ubiquinone 10 . MVK is one enzyme downstream of the highly regulated hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase enzyme Compound heterozygous MVK mutations in HIDS patients usually consist …
• 3. 慢性閉塞性肺疾患（COPD）：危険因子およびリスク低減chronic obstructive pulmonary disease risk factors and risk reduction [show details]
  …has been extensively studied and is discussed separately. Statins – Statins (hydroxymethylglutaryl [HMG] CoA reductase inhibitors) are generally used for their lipid lowering characteristics, but also…
• 4. 筋系に生じるスタチン系薬剤の副作用statin muscle related adverse events [show details]
  …statin-associated autoimmune myopathy that results from autoantibodies that recognize hydroxymethylglutaryl (HMG)-CoA reductase (HMGCR). These antibodies may have a direct effect on muscle tissue expressing HMGCR …
• 5. 心血管疾患の二次予防としての低比重リポタンパク（LDL-C）高値の管理management of elevated low density lipoprotein cholesterol ldl c in primary prevention of cardiovascular disease [show details]
  …prescribe fluvastatin or pitavastatin in patients intolerant to other members of the hydroxymethylglutaryl CoA reductase inhibitor class. However, these drugs are not commonly prescribed by non-specialists…

English Journal

• The impact of anti-inflammatory agents on the outcome of patients with colorectal cancer.

• Park JH, McMillan DC, Horgan PG, Roxburgh CS.Author information Academic Unit of Surgery, University of Glasgow, Glasgow Royal Infirmary, Glasgow G4 0SF, United Kingdom. Electronic address: james.park@glasgow.ac.uk.AbstractAlthough there is increasing appreciation of the role of the host inflammatory response in determining outcome in patients in colorectal cancer, there has been little concerted effort to favourably manipulate cancer-associated inflammation, either alone or in combination with current oncological treatment. Epidemiological and cardiovascular disease studies have identified aspirin, other nonsteroidal anti-inflammatory drugs and statins as potential chemotherapeutic agents which may manipulate the host inflammatory response to the benefit of the patient with cancer. Similarly, evidence of a chemotherapeutic effect of histamine-2 receptor antagonists, again mediated by an immunomodulatory effect, has previously led to increased interest in their use in gastrointestinal cancer. Extensive pre-clinical data and a limited number of clinical investigations have proposed a direct effect of these agents on tumour biology, with an anti-tumour effect on several of the hallmarks of cancer, including proliferative capacity, evasion from apoptosis and cell cycle regulation, and invasive capability of tumour cells. Furthermore, clinical evidence has suggested a pertinent role in down-regulating the systemic inflammatory response whilst favourably influencing the local inflammatory response within the tumour microenvironment. Despite such compelling results, the clinical applicability of nonsteroidal anti-inflammatory drugs, statins and histamine-2 receptor antagonists has not been fully realised, particularly in patients identified at high risk on the basis of inflammatory parameters. In the present review, we examine the potential role that these agents may play in improving survival and reducing recurrence in patients with potentially curative colorectal cancer, and in particular focus on their effects on the local and systemic inflammatory response.
• Cancer treatment reviews.Cancer Treat Rev.2014 Feb;40(1):68-77. doi: 10.1016/j.ctrv.2013.05.006. Epub 2013 Jun 14.
• Although there is increasing appreciation of the role of the host inflammatory response in determining outcome in patients in colorectal cancer, there has been little concerted effort to favourably manipulate cancer-associated inflammation, either alone or in combination with current oncological tre
• PMID 23773805

• NLRP3 inflammasome activation in coronary artery disease: results from prospective and randomized study of treatment with atorvastatin or rosuvastatin.

• Satoh M, Tabuchi T, Itoh T, Nakamura M.Author information *Division of Cardioangiology, Department of Internal Medicine and Memorial Heart Center, Iwate Medical University School of Medicine, Iwate, Japan.AbstractThe NLRP-3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome has recently emerged as a pivotal regulator of chronic inflammation. The aim of the present study was to determine whether NLRP3 inflammasome is expressed in patients with CAD (coronary artery disease) and whether statins (atorvastatin or rosuvastatin) might affect NLRP3 levels. In an in vitro study, human THP-1 cells treated with statins were analysed for NLRP3 inflammasome levels. The present study included 60 patients with CAD and 30 subjects without CAD (non-CAD). Patients with CAD randomly received either 8 months of treatment with atorvastatin or rosuvastatin. PBMCs (peripheral blood mononuclear cells) were obtained from peripheral blood at baseline and after 8 months of statin therapy. Levels of NLRP3 inflammasome, IL (interleukin)-1β and IL-18 were measured by real-time RT-PCR (reverse transcription-PCR) and FACS. Levels of NLRP3 inflammasome were higher in the CAD group than in the non-CAD group. There was a positive correlation between NLRP3 inflammasome and cytokines (IL-1β and IL-18) levels. A randomized clinical study has shown that atorvastatin markedly diminished NLRP3 inflammasome levels, whereas rosuvastatin had no impact on these levels. Levels of NLRP3 inflammasome decreased in THP-1 cells treated with statins compared with those treated with vehicle, and the fold changes in NLRP3 inflammasome were higher in THP-1 cells treated with atorvastatin compared with those treated with rosuvastatin. The present study suggests that atorvastatin down-regulates NLRP3 inflammasome expression in CAD, possibly contributing to the inhibitory effects of atorvastatin on chronic inflammation and atherogenic progression in this disorder.
• Clinical science (London, England : 1979).Clin Sci (Lond).2014 Feb;126(3):233-41. doi: 10.1042/CS20130043.
• The NLRP-3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome has recently emerged as a pivotal regulator of chronic inflammation. The aim of the present study was to determine whether NLRP3 inflammasome is expressed in patients with CAD (coronary art
• PMID 23944632

• Toxin-induced hepatic injury.

• Lopez AM, Hendrickson RG.Author information Department of Emergency Medicine, Oregon Health and Science University, 3181 South West, Sam Jackson Park Road, CSB-550, Portland, OR 97239, USA; Medical Toxicology, Oregon Health and Science University, 3181 South West Sam Jackson Park Road, CSB-550, Portland, OR 97239, USA. Electronic address: lopezan@ohsu.edu.AbstractToxins such as pharmaceuticals, herbals, foods, and supplements may lead to hepatic damage. This damage may range from nonspecific symptoms in the setting of liver test abnormalities to acute hepatic failure. The majority of severe cases of toxin-induced hepatic injury are caused by acetaminophen and ethanol. The most important step in the patient evaluation is to gather an extensive history that includes toxin exposure and exclude common causes of liver dysfunction. Patients whose hepatic dysfunction progresses to acute liver failure may benefit from transfer to a transplant service for further management. Currently, the mainstay in management for most exposures is discontinuing the offending agent. This manuscript will review the incidence, pathophysiology, diagnosis and management of the different forms of toxin-induced hepatic injury and exam in-depth the most common hepatic toxins.
• Emergency medicine clinics of North America.Emerg Med Clin North Am.2014 Feb;32(1):103-25. doi: 10.1016/j.emc.2013.09.005.
• Toxins such as pharmaceuticals, herbals, foods, and supplements may lead to hepatic damage. This damage may range from nonspecific symptoms in the setting of liver test abnormalities to acute hepatic failure. The majority of severe cases of toxin-induced hepatic injury are caused by acetaminophen an
• PMID 24275171

Japanese Journal

• Rationale and Design of the Standard Versus Intensive Statin Therapy for Hypercholesterolemic Patients with Diabetic Retinopathy (EMPATHY) Study: a Randomized Controlled Trial

• Journal of Atherosclerosis and Thrombosis advpub(0), 2016
• NAID 130005131899

• Biochemical effects, hypolipidemic and anti-inflammatory activities of <i>Artemisia vulgaris</i> extract in hypercholesterolemic rats

• Journal of Clinical Biochemistry and Nutrition 57(1), 33-38, 2015
• NAID 130005085267

• Biochemical effects, hypolipidemic and anti-inflammatory activities of <i>Artemisia vulgaris</i> extract in hypercholesterolemic rats

• Journal of Clinical Biochemistry and Nutrition advpub(0), 2015
• NAID 130005065118

Related Links

• Hydroxymethylglutaryl-CoA Reductase - ScienceDirect.com ...

HMG-CoA reductase catalyzes the following four reactions: Effectors, Products The enzyme is inactivated by [Hydroxymethylglutaryl–CoA reductase (NADPH)] kinase; reductase kinase ( E. C. 2.7.1.109) and reactivated by ...

• hydroxymethylglutaryl-CoA-reductase - definition of ...

hydroxymethylglutaryl-CoA a regulatory enzyme involved in the maintenance of the level of cholesterol in cells; key intermediate in synthesis of cholesterol in cytosol; also produced in mitochondria during ketogenesis.

---

★リンクテーブル★

リンク元	「ヒドロキシメチルグルタリルCoA還元酵素」
拡張検索	「NADP-dependent hydroxymethylglutaryl-CoA-reductase」「NAD-dependent hydroxymethylglutaryl-CoA reductase」「hydroxymethylglutaryl-CoA reductase inhibitor」
関連記事	「C」「reductase」「CoA」「hydroxymethylglutaryl」「COA」

「ヒドロキシメチルグルタリルCoA還元酵素」

　　[★]

英

hydroxymethylglutaryl-CoA reductase

同

ヒドロキシメチルグルタリルCoAレダクターゼ、HMG-CoA還元酵素 HMG-CoA reductase

3-ヒドロキシ-3-メチルグルタリルCoA還元酵素 3-hydroxy-3-methylglutaryl-CoA reductase 3-hydroxy-3-methylglutaryl CoA reductase

関

「NADP-dependent hydroxymethylglutaryl-CoA-reductase」

　　[★]

• NADP依存性ヒドロキシメチルグルタリルCoA還元酵素

「NAD-dependent hydroxymethylglutaryl-CoA reductase」

　　[★]

• NAD依存性ヒドロキシメチルグルタリルCoA還元酵素

「hydroxymethylglutaryl-CoA reductase inhibitor」

　　[★] HMG-CoA還元酵素阻害薬

「C」

　　[★]

• 炭素 carbon
• シトシン cytosine
• システイン cysteine
• シチジン
• セルシウス度 摂氏 degrees Celsius degree C
• 産婦人科領域で「子宮外頚 子宮外頚部 exocervix」を表現するための略語

　 　 　 　

「reductase」

　　[★]

• n.

(酵素)還元酵素、レダクターゼ、リダクターゼ

関

dehydrogenase、oxidase、oxidoreductase、reducing enzyme

　

「CoA」

　　[★]

• 大動脈縮窄症 coactation of the aorta
• 補酵素A coenzyme A

「hydroxymethylglutaryl」

　　[★]

ヒドロキシメチルグルタリル

「COA」

　　[★] 補酵素A coenzyme A CoA