APLF facilitates interstrand DNA crosslink repair and replication fork protection to confer cisplatin resistance

Replication stress converts the stalled forks into reversed forks, which is an important protection mechanism to prevent fork degradation and collapse into poisonous DNA double-strand breaks (DSBs). Paradoxically, the mechanism also acts in cancer cells to contribute to chemoresistance against vario...

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Veröffentlicht in:	Nucleic acids research 2024-06, Vol.52 (10), p.5676-5697
Hauptverfasser:	Wu, Cheng-Kuei, Shiu, Jia-Lin, Wu, Chao-Liang, Hung, Chi-Feng, Ho, Yen-Chih, Chen, Yen-Tzu, Tung, Sheng-Yung, Yeh, Cheng-Fa, Shen, Che-Hung, Liaw, Hungjiun, Su, Wen-Pin
Format:	Artikel
Sprache:	eng
Schlagworte:	Antineoplastic Agents - pharmacology Cell Line, Tumor Cisplatin - pharmacology DNA - genetics DNA - metabolism DNA Breaks, Double-Stranded DNA Damage DNA Repair DNA Replication - drug effects DNA-(Apurinic or Apyrimidinic Site) Lyase DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Drug Resistance, Neoplasm - genetics Fanconi Anemia Complementation Group D2 Protein - genetics Fanconi Anemia Complementation Group D2 Protein - metabolism Genome Integrity, Repair and Humans Poly (ADP-Ribose) Polymerase-1 - genetics Poly (ADP-Ribose) Polymerase-1 - metabolism Poly-ADP-Ribose Binding Proteins
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