Pub. Date : 2020
PMID : 32064022
6 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Thioridazine Induces Cardiotoxicity via Reactive Oxygen Species-Mediated hERG Channel Deficiency and L-Type Calcium Channel Activation. | Thioridazine | ETS transcription factor ERG | Homo sapiens |
| 2 | The present study was aimed at exploring the long-term effects of THIO on the hERG and L-type calcium channels, both of which are relevant to the development of QT prolongation. | Thioridazine | ETS transcription factor ERG | Homo sapiens |
| 3 | The ROS scavenger N-acetyl cysteine (NAC) significantly attenuated hERG reduction induced by THIO and abolished the upregulation of ER stress marker proteins. | Thioridazine | ETS transcription factor ERG | Homo sapiens |
| 4 | Meanwhile, THIO increased the degradation of hERG channels via disrupting hERG-Hsp70 interactions. | Thioridazine | ETS transcription factor ERG | Homo sapiens |
| 5 | Meanwhile, THIO increased the degradation of hERG channels via disrupting hERG-Hsp70 interactions. | Thioridazine | ETS transcription factor ERG | Homo sapiens |
| 6 | In conclusion, dysfunction of hERG channel proteins and activation of L-type calcium channels via ROS production might be the ionic mechanisms for QT prolongation induced by THIO. | Thioridazine | ETS transcription factor ERG | Homo sapiens |