The role of WRN in DNA repair is affected by post-translational modifications |
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Authors: | Kusumoto Rika Muftuoglu Meltem Bohr Vilhelm A |
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Affiliation: | Laboratory of Molecular Gerontology, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA. |
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Abstract: | Werner syndrome (WS) is an autosomal recessive progeroid disease characterized by genomic instability. WRN gene encodes one of the RecQ helicase family proteins, WRN, which has ATPase, helicase, exonuclease and single stranded DNA annealing activities. There is accumulating evidence suggesting that WRN contributes to the maintenance of genomic integrity through its involvement in DNA repair, replication and recombination. The role of WRN in these pathways can be modulated by its post-translational modifications in response to DNA damage. Here, we review the functional consequences of post-translational modifications on WRN as well as specific DNA repair pathways where WRN is involved and discuss how these modifications affect DNA repair pathways. |
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Keywords: | WS, Werner syndrome HGPS, Hutchinson-Gilford syndrome BS, Bloom syndrome RTS, Rothmund-Thomson syndrome ssDNA, single stranded DNA 4-NQO, 4-nitroquinoline-1-oxide RPA, replication protein A PCNA, proliferating cell nuclear antigen CPT, camptothecin pol δ, DNA polymerase δ BER, base excision repair APE1, apurinic/apyrimidinic endonuclease 1 PARP-1, poly(ADP-ribose) polymerase 1 pol β, DNA polymerase β NHEJ, non-homologous end-joining MRN, Mre11/Rad50/Nbs1 HR, homologous recombination TRF2, telomere repeat binding factor 2 ALT, alternative lengthening of telomeres SSBs, single strand breaks ROS, reactive oxygen species MMS, methyl methanesulfonate FEN1, flap endonuclease 1 DSB, DNA double strand break DNA-PKcs, DNA-dependent protein kinase catalytic subunit X4L4, XRCC4/DNA ligase IV SUMO-1, small ubiquitin-related modifier1 |
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