Inhibition of DNA Repair Enzymes as a Valuable Pharmaceutical Approach

doi:10.3390/books978-3-0365-7880-4

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https://mdpi.com/books/pdfview/book/7469

Contributor(s)

Volcho, Konstantin (editor)

Lavrik, Olga (editor)

Language

English

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Abstract

Although DNA repair enzymes play a crucial role in maintaining the integrity of the genome, the hyperactivity of certain enzymes of the DNA repair system can lead to the resistance of tumors to chemo- and radiotherapy, aimed at damaging the DNA of cancer cells. Therefore, the inhibition of DNA repair enzymes could help to overcome this resistance. The reviews and research articles included in this collection describe the molecular mechanisms of action of some important enzymes of the DNA repair system, as well as some new inhibitors of such enzymes and the pharmacological properties of these inhibitors. This reprint clearly demonstrates the importance of the inhibition of DNA repair enzymes to fight various diseases, especially cancer.

URI

https://directory.doabooks.org/handle/20.500.12854/101373

Keywords

poly (ADP-ribose) polymerase inhibitor; non-small cell lung cancer; DNA damage; radiotherapy; chemotherapy; combination therapy; coumarin; neoflavone; DNA repair enzymes; Tdp1 inhibitor; cancer; tumor; topotecan; topoisomerase 1 inhibitors; molecular modeling; chemical space; morpholino nucleosides; NAD+ analogs; DNA repair; PARP; 7-methylguanine; poly(ADP-ribose) polymerase 1; inhibitor; nucleosome; trapping; docking; molecular dynamics; fluorescence anisotropy; spFRET microscopy; DNA glycosylases; drug targets; APE1; protein–protein interactions; base excision repair; multifunctional disordered protein; fluorescence techniques; cell cycle checkpoint; cancer therapy; DNA repair inhibitors; synthetic lethality; fused in sarcoma; poly(ADP-ribose) polymerase; poly(ADP-ribose); protein phase separation; berberine; tetrahydroberberine; DNA repair enzyme; SAR; poly(ADP-ribosylation); PARP-1; Olaparib; KU55933; KU-0060648; SCR7 pyrazine; VERO cells; synergism; resistance; CDKN2A; soft tissue sarcomas (STS); gastrointestinal stromal tumors (GIST); AKT signaling; Rad51 recombinase; homology-mediated DNA repair; apoptosis; sensitization; XPA; ERCC1-XPF; CSB; UVB radiation; UVB mutagenesis; nucleotide excision repair (NER); cyclobutane–pyrimidine dimer (CPD) photolesion; veliparib; resveratrol; arsenic trioxide; spironolactone; usnic acid; thioether; tyrosyl-DNA phosphodiesterase 1; TDP1 inhibitor; inhibiting activity; TDP2; PARP1; synergy; HEK293 knockout cell line; polyphenols; PARP-1 inhibitors; n/a