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Drug-Target Interaction

Drug

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PubChem ID:23663939
Structure:
Synonyms:
1476-53-5
46531_FLUKA
46531_RIEDEL
7-(4-(Carbamoyloxy)tetrahydro-3-hydroxy-5-methoxy-6,6-dimethylpyran-2-ylox
7-(4-(Carbamoyloxy)tetrahydro-3-hydroxy-5-methoxy-6,6-dimethylpyran-2-yloxy)-4-hydroxy-3-(4-hydroxy-3-(4-hydroxy-3-(3-methyl-2-butenyl)benzamido)-8-methylcoumarin monosodium salt
Albamycin
Albamycin (TN)
C12609
CCG-40336
D01209
HMS1920D04
HMS2091L04
HMS500M22
MolPort-002-526-534
N1628_SIAL
N1628_SIGMA
N6160_SIAL
Novobiocin
Novobiocin sodium
Novobiocin sodium (JAN/USP)
Novobiocin sodium salt
SPECTRUM1500444
STOCK1N-53214

Target

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Uniprot ID:Q7VFP2_HELHP
Synonyms:
DNA gyrase
EC-Numbers:5.99.1.3
Organism:Helicobacter hepaticus
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

7616959
RNA polymerase (rpoB) mutants selected for increased resistance to gyrase inhibitors in Salmonella typhimurium.. A B Blanc-Potard; E Gari; F Spirito; N Figueroa-Bossi; L Bossi (1995) Molecular & general genetics : MGG display abstract
Some rifampicin-resistance (RifR) mutations make bacteria slightly resistant to the gyrase inhibitors novobiocin (Nov) and nalidixic acid (Nal). This suggested that it might be possible to isolate rpoB mutants using either drug for positive selection. In an initial test, we confirmed the presence of Rif-resistant isolates among clones selected for Nov resistance. These mutants are also more resistant to Nal. In a subsequent experiment, we found that mutants selected for low-level resistance to Nal include isolates harboring mutations genetically linked to the rpoB locus; of two such mutants studied, one is temperature-sensitive for growth. These two mutants, which are only marginally affected in their response to Nov, are normally sensitive to Rif and thus might be representative of a new class of rpoB alleles. The Rif-resistant and Rif-sensitive rpoB alleles that increase resistance to gyrase inhibitors have one property in common: they all suppress, to varying degrees, the defect in his operon regulation (transcriptional deattenuation) caused by a gyrase defect or inhibition by novobiocin. To further analyse the transcription-supercoiling relationships in these mutants, we examined the ability of RNA polymerase to recruit gyrase activity during transcription. This was done by two independent approaches: (i) observing transcription-induced accumulation of hyper-negatively supercoiled plasmid DNA in a topA mutant background and (ii) measuring transcription-induced plasmid DNA cleavage in the presence of oxolinic acid. Results indicate that the rpoB alleles described in this study diminish the recruitment of gyrase activity by the transcription process. This property correlates with a decrease in the rate of transcription initiation.