EC Number   |
Inhibitors |
Structure  |
|---|
   2.7.7.6 | more |
no inhibition by NEM and iodoacetamide |
 |
| 2.7.7.6 | more |
no inhibition by epigallocatechin gallate |
|
| 2.7.7.6 | more |
no inhibition by ent-16-ketobeyeran-19-oic acid, i.e. isosteviol, and related compounds |
|
| 2.7.7.6 | more |
despite relatively high overall sequence and structural homology between bacterial and mammalian core RNAP enzymes, there are sufficient differences between the enzyme classes for exploitation in the discovery of selective bacterial inhibitors |
|
| 2.7.7.6 | more |
gamma irradiation leads to a transient inhibition of rRNA synthesis, but Pol I transcription is not blocked by DNA damage itself, but by the action of DNA repair enzymes |
|
| 2.7.7.6 | more |
inactivation of RNase P, by knockdown of RNase P subunits Rpp21, Rpp29 or Rpp38 by RNA interference, reduces the level of nascent transcription by Pol I, and more considerably that of Pol III, e.g. causing marked reduction in transcription of rDNA by Pol I |
|
| 2.7.7.6 | more |
oncogenes and tumor suppressors control Pol I transcription, overview. Development of drugs that target the Pol I transcription machinery at different points, overveiw |
|
| 2.7.7.6 | more |
synthesis of simplified etnangien analogues and analysis of their antimicrobial activities, overview |
|
| 2.7.7.6 | more |
no inhibition of RNA transcription by RECQL5 helicase-deficient point mutant RECQL5D157A, and another human RECQ family helicase, RECQL1 |
|
| 2.7.7.6 | more |
Top1 inhibition favors Pol II escape from a promoter-proximal pausing site of the human HIF-1alpha gene in living cells. Top1 inhibition can trigger a transcriptional stress, involving antisense transcription and increased chromatin accessibility, which is dependent on cdk activity and deregulated Pol II pausing |
|
