PRMT1 and PRMT5: on the road of homologous recombination and non-homologous end joining.
DNA repair pathway choice
PRMT1
PRMT5
homologous recombination
non-homologous end joining
Journal
Genome instability & disease
ISSN: 2524-7662
Titre abrégé: Genome Instab Dis
Pays: Switzerland
ID NLM: 101774793
Informations de publication
Date de publication:
Aug 2023
Aug 2023
Historique:
pmc-release:
01
08
2024
medline:
4
9
2023
pubmed:
4
9
2023
entrez:
4
9
2023
Statut:
ppublish
Résumé
DNA double-strand breaks (DSBs) are widely accepted to be the most deleterious form of DNA lesions that pose a severe threat to genome integrity. Two predominant pathways are responsible for repair of DSBs, homologous recombination (HR) and non-homologous end-joining (NHEJ). HR relies on a template to faithfully repair breaks, while NHEJ is a template-independent and error-prone repair mechanism. Multiple layers of regulation have been documented to dictate the balance between HR and NHEJ, such as cell cycle and post-translational modifications (PTMs). Arginine methylation is one of the most common PTMs, which is catalyzed by protein arginine methyltransferases (PRMTs). PRMT1 and PRMT5 are the predominate PRMTs that promote asymmetric dimethylarginine and symmetric dimethylarginine, respectively. They have emerged to be crucial regulators of DNA damage repair. In this review, we summarize current understanding and unaddressed questions of PRMT1 and PRMT5 in regulation of HR and NHEJ, providing insights into their roles in DSB repair pathway choice and the potential of targeting them for cancer therapy.
Identifiants
pubmed: 37663901
doi: 10.1007/s42764-022-00095-w
pmc: PMC10470524
mid: NIHMS1889533
doi:
Types de publication
Journal Article
Langues
eng
Pagination
197-209Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM130457
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM146749
Pays : United States
Déclaration de conflit d'intérêts
Competing interests The authors declare that they have no competing interests.
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