WordNet
- executed with proper legal authority; "a binding contract"
- the protective covering on the front, back, and spine of a book; "the book had a leather binding" (同)book binding, cover, back
- strip sewn over or along an edge for reinforcement or decoration
- the capacity to attract and hold something
- any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
- the 8th letter of the Roman alphabet (同)h
PrepTutorEJDIC
- 義務的な,拘束力ある / 〈U〉しばること;〈C〉しばる物 / 〈C〉製本,装丁 / 〈U〉縁(‘ふち')取り材料
- 蛋白(たんばく)質
- hydrogenの化学記号
- 鉛筆の硬度 / 《俗》heroin
UpToDate Contents
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- 1. HDLコレステロール：異常値の臨床的側面 hdl cholesterol clinical aspects of abnormal values
- 2. 2型糖尿病の病因 pathogenesis of type 2 diabetes mellitus
- 3. リポ蛋白の分類、代謝、およびアテローム性動脈硬化症における役割 lipoprotein classification metabolism and role in atherosclerosis
- 4. 二次予防における脂質（高コレステロール血症を含む）の治療 treatment of lipids including hypercholesterolemia in secondary prevention
- 5. エストロゲン・プロゲスチン避妊剤と関連したリスクおよび副作用 risks and side effects associated with estrogen progestin contraceptives
English Journal
- Proteasome inhibitor treatment reduced fatty acid, triacylglycerol and cholesterol synthesis.
- Oliva J, French SW, Li J, Bardag-Gorce F.AbstractIn the present study, the beneficial effects of proteasome inhibitor treatment in reducing ethanol-induced steatosis were investigated. A microarray analysis was performed on the liver of rats injected with PS-341 (Bortezomib, Velcade®), and the results showed that proteasome inhibitor treatment significantly reduced the mRNA expression of SREBP-1c, and the downstream lipogenic enzymes, such as fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), which catalyzes the carboxylation of acetyl-CoA to malonyl-CoA, the rate-limiting step in fatty acid synthesis. ELOVL6, which is responsible for fatty acids long chain elongation, was also significantly downregulated by proteasome inhibitor treatment. Moreover, PS-341 administration significantly reduced the expression of acyl-glycerol-3-phosphate acyltransferase (AGPAT), and diacylglycerol acyltransferase (DGAT), enzyme involved in triacylglycerol (TAG) synthesis. Finally, PS-341 was found to downregulate the enzyme 3-hydroxy-3-methylglutaryl-CoenzymeA synthase (HMG-CoA synthase) that is responsible for cholesterol synthesis. Proteasome inhibitor was also found to play a role in intestinal lipid adsorption because apolipoproteins A (apoA-I, apoAII, apoA-IV and ApoCIII) were downregulated by proteasome inhibitor treatment, especially ApoA-II that is known to be a marker of alcohol consumption. Proteasome inhibitor treatment also decreased apobec-1 complementation factor (ACF) leading to lower level of editing and production of ApoB protein. Moreover apolipoprotein C-III, a major component of chylomicrons was significantly downregulated. However, lipoprotein lipase (Lpl) and High density lipoprotein binding protein (Hdlbp) mRNA levels were increased by proteasome inhibitor treatment. These results suggested that proteasome inhibitor treatment could be used to reduce the alcohol-enhanced lipogenesis and alcohol-induced liver steatosis. A morphologic analysis, performed on the liver of rats fed ethanol for one month and treated with PS-341, showed that proteasome inhibitor treatment significantly decreased ethanol-induced liver steatosis. SREBP-1c, FAS and ACC were increased by ethanol feeding alone, but were significantly decreased when proteasome inhibitor was administered to rats fed ethanol. Our results also show that both mRNA and protein levels of these lipogenic enzymes, up regulated by ethanol, were then downregulated when proteasome inhibitor was administered to rats fed ethanol. It was also confirmed that alcohol feeding caused an increase in AGPAT and DGAT, which was prevented by proteasome inhibitor treatment of the animal fed ethanol. Chronic alcohol feeding did not affect the gene expression of HMG-CoA synthase. However, PS341 administration significantly reduced the HMG-CoA synthase mRNA levels, confirming the results obtained with the microarray analysis. C/EBP transcription factors alpha (CCAAT/enhancer-binding protein alpha) has been shown to positively regulate SREBP-1c mRNA expression, thus regulating lipogenesis. Proteasome inhibition caused a decrease in C/EBP alpha mRNA expression, indicating that C/EBP downregulation may be the mechanism by which proteasome inhibitor treatment reduced lipogenesis. In conclusion, our results indicate that proteasome activity is not only involved in downregulating fatty acid synthesis and triacylglycerol synthesis, but also cholesterol synthesis and intestinal lipid adsorption. Proteasome inhibitor, administrated at a non-toxic low dose, played a beneficial role in reducing lipogenesis caused by chronic ethanol feeding and these beneficial effects are obtained because of the specificity and reversibility of the proteasome inhibitor used.
- Experimental and molecular pathology.Exp Mol Pathol.2012 Aug;93(1):26-34. Epub 2012 Mar 16.
- In the present study, the beneficial effects of proteasome inhibitor treatment in reducing ethanol-induced steatosis were investigated. A microarray analysis was performed on the liver of rats injected with PS-341 (Bortezomib, Velcade®), and the results showed that proteasome inhibitor treatment si
- PMID 22445925
- Chylomicronemia mutations yield new insights into interactions between lipoprotein lipase and GPIHBP1.
- Gin P, Goulbourne CN, Adeyo O, Beigneux AP, Davies BS, Tat S, Voss CV, Bensadoun A, Fong LG, Young SG.SourceThe authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.
- Human molecular genetics.Hum Mol Genet.2012 Jul 1;21(13):2961-72. Epub 2012 Apr 6.
- Lipoprotein lipase (LPL) is a 448-amino-acid head-to-tail dimeric enzyme that hydrolyzes triglycerides within capillaries. LPL is secreted by parenchymal cells into the interstitial spaces; it then binds to GPIHBP1 (glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein 1) on
- PMID 22493000
Japanese Journal
- Novel Combined GPIHBP1 Mutations in a Patient with Hypertriglyceridemia Associated with CAD
- Journal of Atherosclerosis and Thrombosis 20(10), 777-784, 2013
- NAID 130004444648
- Regulation of synthesis and secretion of the lipoprotein by cultured eel hepatocytes (Proceedings of International Commemorative Symposium 70th Anniversary of The Japanese Society of Fisheries Science)
- Fisheries Science 68(-), 1213-1216, 2002-11
- NAID 40005648167
- Regulation of synthesis and secretion of the lipoprotein by cultured eel hepatocytes
- Fisheries science 68(sup2), 1213-1216, 2002
- NAID 130003903767
Related Links
- 1. J Biol Chem. 2003 Feb 28;278(9):7344-9. Epub 2002 Dec 20. Expression cloning and characterization of a novel glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein, GPI-HBP1. Ioka RX(1), Kang MJ ...
- Gene ID: 3069, updated on 14-Sep-2013 Summary The protein encoded by this gene binds high density lipoprotein (HDL) and may function to regulate excess cholesterol levels in cells. The encoded protein also binds ...
Related Pictures
★リンクテーブル★
| リンク元 | 「HBP」「HDL結合タンパク質」「high density lipoprotein-binding protein」 |
| 関連記事 | 「binding」「HD」「binding protein」「HDL」「H」 |
「HBP」
- HDL結合タンパク質、ヘキソサミン生合成経路、((略))(病名)高血圧
- 関
- HDL-binding protein、hexosamine biosynthesis pathway、high blood pressure、HT、hypertension、hypertensive
「HDL結合タンパク質」
「high density lipoprotein-binding protein」
- 高密度リ・タンパク質結合タンパク質
「binding」
- n.
- adj.
- 結合性の
- 関
- affinity、associate、bind、bond、bonding、combine、conjoin、conjugate、conjugation、conjunction、connect、connection、connective、connectivity、couple、dock、engage、engagement、join、ligate、linkage、symphysial、symphysic、union
「HD」
- ハンチントン病 Huntington's chorea, Huntington's disease Huntington disease
- ホジキン病 Hodgkin disease Hodgkin's disease
- 血液透析 hemodialysis
「binding protein」
「HDL」
[★] 高比重リポ蛋白 high-density lipoprotein high density lipoprotein
「H」