Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
poly(ADP-ribose) + H2O | Homo sapiens | - |
? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q86W56 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
HeLa cell | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
poly(ADP-ribose) + H2O | - |
Homo sapiens | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
PARG | - |
Homo sapiens |
poly(ADP-ribosyl) glycohydrolase | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
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 |
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 |