Title : Gap Junction Intercellular Communication Positively Regulates Cisplatin Toxicity by Inducing DNA Damage through Bystander Signaling.

Pub. Date : 2018 Oct 2

PMID : 30279363






4 Functional Relationships(s)
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1 Finally, we also showed that cells deficient in the structure-specific DNA endonuclease ERCC1-ERCC4 (ERCC1-XPF), an important mediator of cisplatin resistance, further sensitized when treated with cisplatin in the presence of gap junction forming density. Cisplatin ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens
2 Finally, we also showed that cells deficient in the structure-specific DNA endonuclease ERCC1-ERCC4 (ERCC1-XPF), an important mediator of cisplatin resistance, further sensitized when treated with cisplatin in the presence of gap junction forming density. Cisplatin ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens
3 Finally, we also showed that cells deficient in the structure-specific DNA endonuclease ERCC1-ERCC4 (ERCC1-XPF), an important mediator of cisplatin resistance, further sensitized when treated with cisplatin in the presence of gap junction forming density. Cisplatin ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens
4 Finally, we also showed that cells deficient in the structure-specific DNA endonuclease ERCC1-ERCC4 (ERCC1-XPF), an important mediator of cisplatin resistance, further sensitized when treated with cisplatin in the presence of gap junction forming density. Cisplatin ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens