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The story is based on a study of the 3-D structure of an enzyme called pantothenate kinase, which triggers the first step in the production coenzyme A, a molecule that is indispensable to all forms of life.

整个故事基于泛酸激酶的三维结构的研究,它触发辅酶A产生过程的第一步,辅酶A对于所有生命来说都是不可缺少的。

Pantothenate is the essential precursor for phosphopantotheine, the acyl carrier found in CoA and acyl carrier protein.

泛酸是乙酰辅酶A基本前体,乙酰辅酶A在生物大分子分解代谢和三羧酸循环过程起着重要作用。

By the B vitamins pantothenic acid to be part of a coenzyme, by thiol molecules with the acid or other organic acids acyl combined into a acetyl or another acyl-carrier involved in a variety of acyl synthesis and catabolism It is an important acyl coenzyme metabolism.

由B族维生素泛酸参与组成的一种辅酶,借分子中的巯基与乙酸或其他有机酸的酰基结合,成为一种乙酰基或另一些酰基的载体,参与酰基的各种合成和分解代谢,是酰基代谢中重要的辅酶

From the femur bone density analysis of protein expression, we can see that light chain lactoferrin, annexin decreased and the expression of enolase, ATP synthase, acetyl-coenzyme A reductase, the expression of troponin, may be related to ovariectomized femoral bone density in osteoporosis-related happened; strong bone of the femoral osteoporosis Po intervention effect may be related to reduced enolase, ATP synthase, troponin, CK-MB, acetyl phosphoglycerate enzyme, the expression of myosin, and the increase in lactoferrin light chain, pyruvate kinase isoenzyme, protein expression crown.

从股骨密质骨蛋白质组表达分析可知,乳铁蛋白轻链、膜联蛋白A3的表达下降及烯醇化酶、ATP合酶、乙酰辅酶A还原酶、肌钙蛋白的表达增强,可能与去卵巢后股骨密质骨骨质疏松的发生相关;强骨宝对股骨骨质疏松的干预效应可能与下调烯醇化酶、ATP合酶、肌钙蛋白、肌酸激酶同工酶、磷酸甘油酸变味酶、肌球蛋白的表达,和上调乳铁蛋白轻链、丙酮酸激酶同工酶、冠蛋白的表达有关。

This Thesis consists of the following five pacts: Following a brief Introduction on the mechanism of reactions of coenzyme NADH models with activated ethylenic compounds is discussed. Pross-Shaik treatment is employed to analyze the results.

本论文研究了:(1)辅酶NADH模型物和活化烯烃氧化还原反应的机理,并运用Pross-Shaik构型混合模型分析了这些反应的机理;(2)用辅酶NAD~+/NADH模型物催化氧化一级和二级苄醇,还原α,β-环氧酮。

A review on the researches about co-enzyme NADH model compounds was given in the first part of this thesis. In the second part, some new synthetically useful reactions employing Hantzsch ester were discussed which are summarized as following (Scheme 1):Scheme 11 The selective reduction of the exocyclic double bond of the 4-arylmethylene- and 4-alkylidene-4H-isoxazol-5-ones and 4-arylmethylene-4H- pyrazol- 5-ones was achieved by using Hantzsch 1, 4-dihydropyridine as the reducing agent in ethanol.

论文包括两个部分:我们在第一部分对辅酶NADH模型化合物的研究作了综述,第二部分是反应研究,分为四章,我们发现和发展了辅酶NADH模型化合物—汉斯酯参与的几个具有合成价值的新反应和体系。

Esveratrol synthase is the key,exclusively necessary enzyme in the resveratrol synthetic pathway and it presents only in the plants which can synthetize resveratrol.

S催化Res的前体物质(4-香豆酰辅酶A和丙二酰辅酶A)经一步反应生成Res,而Res生物合成的前体物质普遍存在于植物中。

Bisbenzimidazolium salts were used as a tetrahydrofolate coenzyme model, and thus the biomimetic synthesis of twenty-four acyclic diketones as precursors for macrocyclic ketones was successfully accomplished by using the addition-hydrolysis reaction of the bisbenzimidazolium salts with alkyl magnesium halide, wherein six diketones have not been reported in literature.

在本文中,受四氢叶酸辅酶的一碳单元转移反应的启发,作者以双苯并咪唑盐作为四氢叶酸辅酶模型,利用格利雅试剂与双苯并咪唑盐的加成-水解反应,成功合成了二十四种作为麝香酮及类似大环酮重要前体的长链二酮,同时,提供了一种麝香酮及类似大环酮的仿生合成新方法。

Some elements of proteins,such as architectures, catalytic site of enzymes, coenzymes, cofactors, and short sequences and so on, is very conserved during evolution that can serve as molecular fossils to help infer the characters of primitive proteins on structures and functions.

蛋白质的某些性质,包括折叠类型、酶的催化位点、辅酶、辅因子以及部分短肽片段等,在进化过程中是非常保守的。

Based on the structure, those human diseases related mutation sites are mapped onto the structure accurately. As a result, it is found that these sites are all around the electron transfer prosthetic groups or ubiquinone. And these mutations will alter prosthetic groups' binding or ubiquinone's binding, causing electron leakage from the prosthetic groups in the electron transfer chain, producing reactive oxygen species and leading to tumor formation.

利用线粒体复合物 II 的结构对已知与人类疾病相关的该复合物突变位点进行了精确定位,发现这些突变位点均位于电子传递体或辅酶 Q 结合位点的周围,它们的突变或影响了电子传递体的结合,或影响了辅酶 Q 的结合,从而导致电子传递的中断,电子逃逸到线粒体基质中或线粒体内膜中,经过一系列下游途径导致疾病的产生。

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