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大肠杆菌中脱氧胞苷、尿苷、尿嘧啶、腺嘌呤和次黄嘌呤转运的能量偶联机制。

Mechanism of energy coupling for transport of deoxycytidine, uridine, uracil, adenine and hypoxanthine in Escherichia coli.

作者信息

Roy-Burman S, von Dippe P J, Visser D W

出版信息

Biochim Biophys Acta. 1978 Aug 4;511(2):285-96. doi: 10.1016/0005-2736(78)90321-8.

Abstract

The transport processes for uridine, deoxycytidine, uracil, adenine and hypoxanthine require an energy source and are active under anaerobic or aerobic conditions. Inhibitory effects of cyanide, arsenate, carbonylcyanide m-chlorophenylhydrazone, 2,4-dinitrophenol and N,N'-dicyclohexylcarbodiimide on the transport of uridine and deoxycytidine differ from the corresponding effects on the transport of uracil, adenine and hypoxanthine. The nature of these inhibitory effects supports the conclusion that uridine and deoxycytidine transport is energized either by electron transport or by ATP hydrolysis via (Ca2+ + Mg2+)-ATPase. The transport or uracil, adenine and hypoxanthine is dependent upon ATP or some high energy phosphate derivative of ATP, but is independent of (Ca2+ + Mg+)-ATPase and electron transport. Uptake of the ribose moiety of uridine by a mutant of Escherichia coli B, which lacks the transport system for uracil and intact uridine, is neither stimulated by energy sources nor inhibited by various inhibitors of energy metabolism under either aerobic or anaerobic conditions.

摘要

尿苷、脱氧胞苷、尿嘧啶、腺嘌呤和次黄嘌呤的转运过程需要能量来源,并且在厌氧或需氧条件下均具有活性。氰化物、砷酸盐、羰基氰化物间氯苯腙、2,4-二硝基苯酚和N,N'-二环己基碳二亚胺对尿苷和脱氧胞苷转运的抑制作用与对尿嘧啶、腺嘌呤和次黄嘌呤转运的相应作用不同。这些抑制作用的性质支持这样的结论,即尿苷和脱氧胞苷的转运是通过电子传递或经由(Ca2+ + Mg2+)-ATP酶的ATP水解来提供能量的。尿嘧啶、腺嘌呤和次黄嘌呤的转运依赖于ATP或ATP的某些高能磷酸衍生物,但不依赖于(Ca2+ + Mg+)-ATP酶和电子传递。缺乏尿嘧啶和完整尿苷转运系统的大肠杆菌B突变体对尿苷核糖部分的摄取,在有氧或厌氧条件下既不受能量来源的刺激,也不受各种能量代谢抑制剂的抑制。

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