Neuhoff V, Schill W B, Sternbach H
Biochem J. 1970 Apr;117(3):623-31. doi: 10.1042/bj1170623.
By using micro disc electrophoresis and micro-diffusion techniques, the interaction of pure DNA-dependent RNA polymerase (EC 2.7.7.6) from Escherichia coli with the template, the substrates and the inhibitors heparin and rifampicin was investigated. The following findings were obtained: (1) heparin converts the 24S and 18S particles of the polymerase into the 13S form; (2) heparin inhibits RNA synthesis by dissociating the enzyme-template complex; (3) rifampicin does not affect the attachment of heparin to the enzyme; (4) the substrates ATP and UTP are bound by enzyme loaded with rifampicin; (5) rifampicin is bound by an enzyme-template complex to the same extent as by an RNA-synthesizing enzyme-template complex. From this it is concluded that the mechanism of the inhibition of RNA synthesis by rifampicin is radically different from that by heparin. As a working hypothesis to explain the inhibitory mechanism of rifampicin, it is assumed that it becomes very firmly attached to a position close to the synthesizing site and only blocks this when no synthesis is in progress.
通过使用微量圆盘电泳和微量扩散技术,对来自大肠杆菌的纯依赖DNA的RNA聚合酶(EC 2.7.7.6)与模板、底物以及抑制剂肝素和利福平之间的相互作用进行了研究。获得了以下发现:(1)肝素将聚合酶的24S和18S颗粒转化为13S形式;(2)肝素通过解离酶-模板复合物来抑制RNA合成;(3)利福平不影响肝素与酶的结合;(4)底物ATP和UTP被加载有利福平的酶结合;(5)利福平与酶-模板复合物的结合程度与与RNA合成酶-模板复合物的结合程度相同。由此得出结论,利福平抑制RNA合成的机制与肝素的机制截然不同。作为解释利福平抑制机制的一个工作假设,假定它非常牢固地附着在靠近合成位点的位置,并且仅在没有合成进行时才阻断该位点。