ライフサイエンスコーパス: KMnO4

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1 KMnO4 footprinting detects solvent-accessible thymine ba

2 KMnO4 reactivity assays reveal that, at 37 degrees C, bo

3 moter DNA inefficiently, we noted additional KMnO4 sensitivity at the -11 position of the spoIIID pro

4 itrocellulose filter DNA binding assays, and KMnO4 probing of drug-DNA and drug-DNA-enzyme complexes,

5 strongly inhibited by carboxymethylation and KMnO4, suggesting the presence of SH groups at the activ

6 Using exonuclease and KMnO4 footprinting of T7RNAP transcription complexes we

7 is involves the coprecipitation of FeSO4 and KMnO4 in a kilogram-scale continuous process, in acidic

8 in gene fliC were analyzed using DNase I and KMnO4 footprinting over a range of temperatures.

9 ently accumulated complex is I2, DNase I and KMnO4 footprinting reveal a complex with a closed-start

10 lts of equilibrium and transient DNase I and KMnO4 footprinting studies which characterize I1 and I2.

11 ter complex stability assays and DNAse I and KMnO4 footprinting.

12 ter produces extended DNase I protection and KMnO4 hypersensitivity.

13 of the T4 late promoter has been analyzed by KMnO4 footprinting and transcription.

14 The reaction is promoted by KMnO4 in the presence of a carboxylic acid and its corre

15 cidic permanganate enhanced by formaldehyde (KMnO4-COH), acidic cerium (IV) and rhodamine B (Ce-RB),

16 E-RNAP with the T at -11 may protect it from KMnO4 attack.

17 is reactive with base-specific probes (e.g. KMnO4, DMS).

18 nding mode, was found to induce the greatest KMnO4 reactivity, while Hoechst 33342, a minor groove bi

19 g intercalator that alkylates N7 of guanine; KMnO4, which reacts more strongly with bases in denature

20 dividual site reactivities from multiple-hit KMnO4 footprinting of the non-template strand of Esigma7

21 Using a 0.25 M KMnO4 and 0.5 M NaOH solution, quantitative NOx collecti

22 the liquid phase was achieved with 11.5 muM KMnO4 in 2% HNO3.

23 antitative analysis of the biphasic decay of KMnO4 reactivity of RPo at 0 degreesC, we obtain the equ

24 he MHF-determined population distribution of KMnO4-reactive (RPo) and non-reactive promoter DNA to no

25 The location/distribution of KMnO4-sensitive sites on the two DNA strands suggested t

26 yl radical (*OH) and potassium permanganate (KMnO4) footprints obtained under conditions selected for

27 We used potassium permanganate (KMnO4) to identify unpaired thymidine (T) residues in pr

28 nd bottom strands to potassium permanganate (KMnO4).

29 es to probes that include hydroxyl radicals, KMnO4, the junction resolvases endonuclease VII and RuvC

30 to the single-stranded DNA-specific reagents KMnO4 and dimethyl sulfate indicated that RecBCD opened,

31 MS) strategy employing the thymine-selective KMnO4 oxidation reaction to detect conformational change

32 However, the KMnO4-COH CL system showed a higher sensitivity toward p

33 This KMnO4 oxidation/ESI-MS/MS approach is an alternative to

34 e sensitivity of the +1 T and +1 5-F-dUrd to KMnO4 oxidation.

35 m the 5' end were only partially reactive to KMnO4, suggesting that part of the 5'-terminated strand

36 Reactivity to KMnO4 (indicative of opening) within gamma ori DNA occur

37 Using reactivity to KMnO4 in vivo as an assay, we find that, like initiation

38 IHF, examined singly, enhanced reactivity to KMnO4.

39 ucleotide excision repair reaction in vitro, KMnO4 footprinting experiments were performed on a damag

40 s detected when the bent DNA was probed with KMnO4.

41 nscription start site (+1) do not react with KMnO4, indicating that this region is closed in I1.

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