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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/05/30 08:50:47」(JST)
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- 1. グルコース-6-リン酸脱水素酵素欠損症の診断および治療 diagnosis and treatment of glucose 6 phosphate dehydrogenase deficiency
- 2. ヘキソースリン酸側路およびグルタチオン代謝関連疾患 related disorders of the hexose monophosphate shunt and glutathione metabolism
- 3. メトヘモグロビン血症の遺伝学および病因 genetics and pathogenesis of methemoglobinemia
- 4. グルコース-6-リン酸脱水素酵素欠損症の臨床症状 clinical manifestations of glucose 6 phosphate dehydrogenase deficiency
- 5. 先天性副腎過形成の稀な原因 uncommon causes of congenital adrenal hyperplasia
English Journal
- Design and discovery of novel quinazolinedione-based redox modulators as therapies for pancreatic cancer.
- Pathania D, Sechi M, Palomba M, Sanna V, Berrettini F, Sias A, Taheri L, Neamati N.Author information Department of Pharmacology and Pharmaceutical Sciences, University of Southern California, School of Pharmacy, 1985 Zonal Avenue, Los Angeles, CA, USA.AbstractBACKGROUND: Altered cellular bioenergetics and oxidative stress are emerging hallmarks of most cancers including pancreatic cancer. Elevated levels of intrinsic reactive oxygen species (ROS) in tumors make them more susceptible to exogenously induced oxidative stress. Excessive oxidative insults overwhelm their adaptive antioxidant capacity and trigger ROS-mediated cell death. Recently, we have discovered a novel class of quinazolinediones that exert their cytotoxic effects by modulating ROS-mediated signaling.
- Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jan;1840(1):332-43. doi: 10.1016/j.bbagen.2013.08.005. Epub 2013 Aug 15.
- BACKGROUND: Altered cellular bioenergetics and oxidative stress are emerging hallmarks of most cancers including pancreatic cancer. Elevated levels of intrinsic reactive oxygen species (ROS) in tumors make them more susceptible to exogenously induced oxidative stress. Excessive oxidative insults ove
- PMID 23954204
- Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis.
- Sun X1, Chen RC1, Yang ZH1, Sun GB1, Wang M1, Ma XJ1, Yang LJ2, Sun XB3.Author information 1Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.2Medical Functional Laboratory, Basic Medical Department, Beihua University, Jilin, China.3Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China. Electronic address: sunxiaobosubmit@163.com.AbstractDiabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy. The objective of this study was to investigate the potential protective effects and mechanisms of taxifolin on cardiac function of streptozotocin-induced diabetic mice and on hyperglycemia-induced apoptosis of H9c2 cardiac myoblasts. In vivo study revealed that taxifolin improved diastolic dysfunction, ameliorated myocardium structure abnormality, inhibited myocyte apoptosis and enhanced endogenous antioxidant enzymes activities. Interestingly, taxifolin reduced angiotensin II level in myocardium, inhibited NADPH oxidase activity, and increased JAK/STAT3 activation. In vitro investigation demonstrated that taxifolin inhibited 33mM glucoseinduced H9c2 cells apoptosis by decreasing intracellular ROS level. It also inhibited caspase-3 and caspase-9 activation, restored mitochondrial membrane potential, and regulated the expression of proteins related to the intrinsic pathway of apoptosis, thus inhibiting the release of cytochrome c from mitochondria into the cytoplasm. In conclusion, taxifolin exerted cardioprotective effects against diabetic cardiomyopathy by inhibiting oxidative stress and cardiac myocyte apoptosis and might be a potential agent in the treatment of diabetic cardiomyopathy.
- Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association.Food Chem Toxicol.2014 Jan;63:221-32. doi: 10.1016/j.fct.2013.11.013. Epub 2013 Nov 20.
- Diabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy. The objective of this study was to investigate the potential prot
- PMID 24269735
- Activation of NF-κB and respiratory burst following Aspergillus fumigatus stimulation of macrophages.
- Sun H, Xu XY, Tian XL, Shao HT, Wu XD, Wang Q, Su X, Shi Y.Author information Department of Respiratory and Critical Care Medicine, Jinling Hospital, Clinical School of Nanjing, Second Military Medical University, Nanjing 210002, China.AbstractDectin-2, a C-type lectin receptor (CLR), plays an essential role in mediating nuclear factor-kappa B (NF-κB) activation and anti-fungal immunity in response to Candida albicans infection. However, the molecular mechanisms and function of Dectin-2 signaling in response to infection by the pathogenic fungus Aspergillus fumigatus have not been characterized. In order to characterize Dectin-2 signaling in response to A. fumigatus infection, activation of Dectin-2 was analyzed at both transcriptional and translational levels. Spleen tyrosine kinase (Syk) phosphorylation, NF-κB activation and cytokine production downstream of Dectin-2 activation were also investigated. In addition, Dectin-2-Syk function and its ability to mediate reactive oxygen species (ROS) production and elimination of A. fumigatus conidia was examined. We demonstrate that Syk is involved in Dectin-2-induced IκBα (inhibitor of kappa B protein) phosphorylation and NF-κB activation following A. fumigatus stimulation in a time dependent manner. Silencing of Dectin-2 and Syk as well as Syk inhibition blocks NF-κB activation and cytokine secretion. Furthermore, the killing of A. fumigatus conidia and ROS production are significantly affected by Dectin-2 or Syk silencing as well as Syk inhibition. Swelling and germination of the fungus followed by hyphae formation and not the resting and heat-inactivated form of A. fumigatus mediate the activation of Dectin-2 signaling. In conclusion, Syk plays an essential role in IκBα kinase phosphorylation, NF-κB activation, and ROS production mediated by Dectin-2 activation in response to A. fumigatus infection.
- Immunobiology.Immunobiology.2014 Jan;219(1):25-36. doi: 10.1016/j.imbio.2013.06.013. Epub 2013 Jul 4.
- Dectin-2, a C-type lectin receptor (CLR), plays an essential role in mediating nuclear factor-kappa B (NF-κB) activation and anti-fungal immunity in response to Candida albicans infection. However, the molecular mechanisms and function of Dectin-2 signaling in response to infection by the pathogeni
- PMID 23886693
Japanese Journal
- Mechanism of repression of 11β-hydroxysteroid dehydrogenase type 1 by growth hormone in 3T3-L1 adipocytes
- Muraoka Toko,Hizuka Naomi,Fukuda Izumi,Ishikawa Yukiko,Ichihara Atsuhiro
- Endocrine Journal 61(7), 675-682, 2014
- … 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is an NADPH-dependent reductase that converts cortisone to cortisol in adipose tissue. … Hexose-6-phosphate dehydrogenase (H6PDH) is involved in the production of NADPH, which is a coenzyme for 11β-HSD1. …
- NAID 130004443977
- 2P-068 改変型亜リン酸デヒドロゲナーゼを用いたNADPH再生系と不斉還元バイオプロセスへの応用(酵素学,酵素工学,一般講演)
- 児玉 洋輔,廣田 隆一,池田 丈,黒田 章夫
- 日本生物工学会大会講演要旨集 65, 120, 2013-08-25
- NAID 110009737734
- Light Driven CO2 Fixation by Using Cyanobacterial Photosystem I and NADPH-Dependent Formate Dehydrogenase
- Ihara Masaki,Kawano Yusuke,Urano Miho,Okabe Ayako
- PLOS ONE 8(8), e71581, 2013-08-06
- … Formate, a chemical hydrogen carrier and important industrial material, can be produced from CO2 by using the reducing power and the catalytic function of formate dehydrogenase (FDH). … We created a bacterial FDH mutant that experimentally switched the cofactor specificity from NADH to NADPH, and combined it with an in vitro-reconstituted cyanobacterial light-driven NADPH production system consisting of PS I, ferredoxin (Fd), and ferredoxin-NADP(+)-reductase (FNR). …
- NAID 120005462742
Related Links
- NADPHデヒドロゲナーゼ（NADPH dehydrogenase）は、次の化学反応を触媒する 酸化還元酵素である。 NADPH + H+ + 受容体 \ ... NADP+ + 還元型受容体. 反応式の 通り、この酵素の基質はNADPHと受容体、生成物はNADP+と還元型受容体である。
- In enzymology, a NADPH dehydrogenase (EC 1.6.99.1) is an enzyme that catalyzes the chemical reaction. NADPH + ... The 3 substrates of this enzyme are NADPH, H, and acceptor, whereas its two products are NADP and reduced acceptor.
Related Pictures
★リンクテーブル★
| リンク元 | 「NADPHデヒドロゲナーゼ」「NADPH diaphorase」「NADPH脱水素酵素」 |
| 関連記事 | 「NADPH」「NAD」「NADP」「dehydrogenase」「dehydrogenases」 |
「NADPHデヒドロゲナーゼ」
「NADPH diaphorase」
「NADPH脱水素酵素」
「NADPH」
- グルタチオンの還元に必要。
- 足らなくなると、フリーラジカルや過酸化物を無毒化できなくなる。
- 赤血球の場合でNADPHが足らないと、fava beans, sulfonamides, primaquineおよび抗結核薬などの酸化剤によって溶血性貧血を起こす。
「NAD」
「NADP」
[★] ニコチンアミドアデニンジヌクレオチドリン酸 nicotinamide adenine dinucleotide phosphate