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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Biochem J. 1967 Jun;103(3):714-9. doi: 10.1042/bj1030714.

Escherichia coli 156:53D2 synthesized ubiquinone only when the growth medium was supplemented with 4-hydroxybenzoate acid. 2. Little or no vitamin K(2) was formed by the mutant under the growth conditions employed, in contrast with wild-type strains. 3. In the mutant ubiquinone deficiency was correlated with low respiration and with low particulate NADH-oxidase and NADH-cytochrome b(1)-reductase activity. 4. Preincubation of ubiquinone-deficient particles with ubiquinone-30 largely restored the NADH-oxidase and NADH-cytochrome b(1)-reductase activities. 5. Various NADH-dye-linked reductases which may be associated with NADH dehydrogenase were not affected by the absence of ubiquinone. 6. The succinate-oxidase complex was less affected than the particulate NADH oxidase by ubiquinone deficiency. 7. A pathway for electrons in the NADH-oxidase complex of the auxotroph of E. coli is proposed and its relationship to the pathway in the wild-type strain is discussed.

大肠杆菌156:53D2只有在生长培养基中添加4-羟基苯甲酸时才合成泛醌。2. 与野生型菌株相比，该突变体在所用生长条件下几乎不形成维生素K(2)。3. 在该突变体中，泛醌缺乏与低呼吸作用以及低颗粒状NADH氧化酶和NADH-细胞色素b(1)-还原酶活性相关。4. 用泛醌-30对缺乏泛醌的颗粒进行预孵育，很大程度上恢复了NADH氧化酶和NADH-细胞色素b(1)-还原酶的活性。5. 各种可能与NADH脱氢酶相关的NADH-染料偶联还原酶不受泛醌缺乏的影响。6. 泛醌缺乏对琥珀酸氧化酶复合物的影响小于对颗粒状NADH氧化酶的影响。7. 提出了大肠杆菌营养缺陷型NADH氧化酶复合物中的电子传递途径，并讨论了其与野生型菌株中途径的关系。

Biochem J. 1967 Jun;103(3):714-9. doi: 10.1042/bj1030714.

Escherichia coli 156:53D2 synthesized ubiquinone only when the growth medium was supplemented with 4-hydroxybenzoate acid. 2. Little or no vitamin K(2) was formed by the mutant under the growth conditions employed, in contrast with wild-type strains. 3. In the mutant ubiquinone deficiency was correlated with low respiration and with low particulate NADH-oxidase and NADH-cytochrome b(1)-reductase activity. 4. Preincubation of ubiquinone-deficient particles with ubiquinone-30 largely restored the NADH-oxidase and NADH-cytochrome b(1)-reductase activities. 5. Various NADH-dye-linked reductases which may be associated with NADH dehydrogenase were not affected by the absence of ubiquinone. 6. The succinate-oxidase complex was less affected than the particulate NADH oxidase by ubiquinone deficiency. 7. A pathway for electrons in the NADH-oxidase complex of the auxotroph of E. coli is proposed and its relationship to the pathway in the wild-type strain is discussed.

大肠杆菌156:53D2只有在生长培养基中添加4-羟基苯甲酸时才合成泛醌。2. 与野生型菌株相比，该突变体在所用生长条件下几乎不形成维生素K(2)。3. 在该突变体中，泛醌缺乏与低呼吸作用以及低颗粒状NADH氧化酶和NADH-细胞色素b(1)-还原酶活性相关。4. 用泛醌-30对缺乏泛醌的颗粒进行预孵育，很大程度上恢复了NADH氧化酶和NADH-细胞色素b(1)-还原酶的活性。5. 各种可能与NADH脱氢酶相关的NADH-染料偶联还原酶不受泛醌缺乏的影响。6. 泛醌缺乏对琥珀酸氧化酶复合物的影响小于对颗粒状NADH氧化酶的影响。7. 提出了大肠杆菌营养缺陷型NADH氧化酶复合物中的电子传递途径，并讨论了其与野生型菌株中途径的关系。