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Literature summary extracted from

  • Chaudhuri, A.; Ahuja, A.; Herrador, R.; Lopes, M.
    Poly(ADP-ribosyl) glycohydrolase prevents the accumulation of unusual replication structures during unperturbed S phase (2015), Mol. Cell. Biol., 35, 856-865 .
No PubMed abstract available

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
3.2.1.143 poly(ADP-ribose) + H2O Homo sapiens
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Organism

EC Number Organism UniProt Comment Textmining
3.2.1.143 Homo sapiens Q86W56
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Source Tissue

EC Number Source Tissue Comment Organism Textmining
3.2.1.143 HeLa cell
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Homo sapiens
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Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
3.2.1.143 poly(ADP-ribose) + H2O
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Homo sapiens ?
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Synonyms

EC Number Synonyms Comment Organism
3.2.1.143 PARG
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Homo sapiens
3.2.1.143 poly(ADP-ribosyl) glycohydrolase
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Homo sapiens

General Information

EC Number General Information Comment Organism
3.2.1.143 malfunction poly(ADP-ribosyl) glycohydrolase (PARG) depletion affects cell proliferation and DNA synthesis, leading to replication-coupled H2AX phosphorylation. PARG depletion or inhibition per se slows down individual replication forks similarly to mild chemotherapeutic treatment. Electron microscopic analysis of replication intermediates reveals marked accumulation of reversed forks and single-stranded DNA (ssDNA) gaps in unperturbed PARG-defective cells. PARG-defective cells display both ataxia-telangiectasia-mutated (ATM) and ataxia-Rad3-related (ATR) activation, as well as chromatin recruitment of standard double-strand-break-repair factors, such as 53BP1 and RAD51, but no physical evidence for chromosomal breakage. PARG-deficient cell phenotype, detailed overview. PARG depletion results in slow replication fork progression even in the absence of genotoxic treatments. PARG downregulation and inhibition lead to similar phenotypic consequences Homo sapiens
3.2.1.143 physiological function a single poly(ADP-ribosyl) glycohydrolase (PARG) mediates PAR degradation. PARG prevents the accumulation of unusual replication structures during unperturbed S phase. Role of PARG in the replication of human chromosomes. PAR degradation is essential to promote resumption of replication at endogenous and e-exogenous lesions, preventing idle recruitment of repair factors to remodeled replication forks Homo sapiens