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Literature summary for 3.1.11.1 extracted from

  • Sertic, S.; Pizzi, S.; Cloney, R.; Lehmann, A.R.; Marini, F.; Plevani, P.; Muzi-Falconi, M.
    Human exonuclease 1 connects nucleotide excision repair (NER) processing with checkpoint activation in response to UV irradiation (2011), Proc. Natl. Acad. Sci. USA, 108, 13647-13652.
    View publication on PubMedView publication on EuropePMC
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Localization

Localization Comment Organism GeneOntology No. Textmining
nucleus in S-phase cells both hEXO1 isoforms accumulate in proliferating cell nuclear antigen-positive foci. After UV irradiation of cells both hEXO1a and hEXO1b accumulated similarly at local UV-induced DNA damages, LUDS, colocalizing with NER preincision factors. Inhibition of repair synthesis enhances hEXO1 accumulation at LUDs Homo sapiens 5634
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Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
additional information Homo sapiens endogenous hEXO1 interacts with XPA ?
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Organism

Organism UniProt Comment Textmining
Homo sapiens
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
additional information endogenous hEXO1 interacts with XPA Homo sapiens ?
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 ?

Synonyms

Synonyms Comment Organism
Exo1
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 Homo sapiens
exonuclease 1
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 Homo sapiens

General Information

General Information Comment Organism
evolution exonuclease 1 is highly conserved from yeast to human Homo sapiens
malfunction in nonreplicating cells, depletion or downregulation of hEXO1 reduces unscheduled DNA synthesis after UV irradiation, prevents ubiquitylation of histone H2A, and impairs activation of the checkpoint signal transduction cascade in response to UV damage Homo sapiens
physiological function exonuclease 1 is implicated in numerous DNA metabolic pathways, including repair, recombination, replication, and telomere maintenance. Key role for hEXO1 in the UV-induced DNA damage response linking NER to checkpoint activation in human cells. hEXO1 accumulation requires XPF-dependent processing of UV-induced lesions and is enhanced by inhibition of DNA repair synthesis Homo sapiens