» Articles » PMID: 33398053

DNA-protein Crosslink Proteases in Genome Stability

Overview
Journal Commun Biol
Specialty Biology
Date 2021 Jan 5
PMID 33398053
Citations 37
Authors
Affiliations
Soon will be listed here.
Abstract

Proteins covalently attached to DNA, also known as DNA-protein crosslinks (DPCs), are common and bulky DNA lesions that interfere with DNA replication, repair, transcription and recombination. Research in the past several years indicates that cells possess dedicated enzymes, known as DPC proteases, which digest the protein component of a DPC. Interestingly, DPC proteases also play a role in proteolysis beside DPC repair, such as in degrading excess histones during DNA replication or controlling DNA replication checkpoints. Here, we discuss the importance of DPC proteases in DNA replication, genome stability and their direct link to human diseases and cancer therapy.

Citing Articles

Elevated reactive oxygen species can drive the alternative lengthening of telomeres pathway in ATRX-null cancers.

Goncalves T, Cunniffe S, Ma T, Mattis N, Rose A, Kent T Nucleic Acids Res. 2025; 53(4).

PMID: 39921567 PMC: 11806356. DOI: 10.1093/nar/gkaf061.


Flap endonuclease 1 repairs DNA-protein cross-links via ADP-ribosylation-dependent mechanisms.

Sun Y, Jenkins L, El Touny L, Zhu L, Yang X, Jo U Sci Adv. 2025; 11(2):eads2919.

PMID: 39792662 PMC: 11721697. DOI: 10.1126/sciadv.ads2919.


Understanding DNA replication and replication stress as avenues to combat cancer.

Naim V Commun Biol. 2024; 7(1):1578.

PMID: 39592851 PMC: 11599382. DOI: 10.1038/s42003-024-07250-x.


Homozygous synonymous FAM111A variant underlies an autosomal recessive form of Kenny-Caffey syndrome.

Bonde L, Abdelrazek I, Seif L, Alawi M, Matrawy K, Nabil K J Hum Genet. 2024; 70(2):87-97.

PMID: 39501122 PMC: 11762410. DOI: 10.1038/s10038-024-01301-1.


Causes and consequences of DNA double-stranded breaks in cardiovascular disease.

Marian A Mol Cell Biochem. 2024; .

PMID: 39404936 DOI: 10.1007/s11010-024-05131-9.


References
1.
Verma R, Oania R, Fang R, Smith G, Deshaies R . Cdc48/p97 mediates UV-dependent turnover of RNA Pol II. Mol Cell. 2011; 41(1):82-92. PMC: 3063307. DOI: 10.1016/j.molcel.2010.12.017. View

2.
Nakano T, Katafuchi A, Matsubara M, Terato H, Tsuboi T, Masuda T . Homologous recombination but not nucleotide excision repair plays a pivotal role in tolerance of DNA-protein cross-links in mammalian cells. J Biol Chem. 2009; 284(40):27065-76. PMC: 2785636. DOI: 10.1074/jbc.M109.019174. View

3.
Reinking H, Hofmann K, Stingele J . Function and evolution of the DNA-protein crosslink proteases Wss1 and SPRTN. DNA Repair (Amst). 2020; 88:102822. DOI: 10.1016/j.dnarep.2020.102822. View

4.
Maskey R, Flatten K, Sieben C, Peterson K, Baker D, Nam H . Spartan deficiency causes accumulation of Topoisomerase 1 cleavage complexes and tumorigenesis. Nucleic Acids Res. 2017; 45(8):4564-4576. PMC: 5416836. DOI: 10.1093/nar/gkx107. View

5.
Hoffmann S, Pentakota S, Mund A, Haahr P, Coscia F, Gallo M . FAM111 protease activity undermines cellular fitness and is amplified by gain-of-function mutations in human disease. EMBO Rep. 2020; 21(10):e50662. PMC: 7534640. DOI: 10.15252/embr.202050662. View