EC Number | Inhibitors | Comment | Organism | Structure |
---|---|---|---|---|
2.7.99.B1 | 2-[(3,5-dibromo-4-methylphenyl)amino]-N'-[(E)-(2-hydroxy-5-nitrophenyl)methylidene]acetohydrazide | the Lig III inhibitor L67 leads to a 5fold increase in Ap4A, suggesting that Lig III may synthesize Ap4A in vivo when prevented from associating with DNA even in the absence of DNA damage | Cricetulus griseus | |
2.7.99.B1 | DNA | the enzyme activity is inhibited by DNA-binding | Cricetulus griseus | |
2.7.99.B1 | additional information | the Lig I-specific inhibitor L82, which prevents DNA-binding but not adenylation activity, causes only a slight, 1.3fold increase in the level of Ap4A in AA8 cells treated for 18 h | Cricetulus griseus |
EC Number | Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|---|
2.7.99.B1 | 2 ATP | Cricetulus griseus | the enzyme synthesizes Ap4A by transfer of AMP from the enzyme-adenylate intermediate to an ATP acceptor | diadenosine 5',5'''-P1,P4-tetraphosphate + diphosphate | - |
? |
EC Number | Organism | UniProt | Comment | Textmining |
---|---|---|---|---|
2.7.99.B1 | Cricetulus griseus | - |
- |
- |
EC Number | Source Tissue | Comment | Organism | Textmining |
---|---|---|---|---|
2.7.99.B1 | CHO-AA8 cell | - |
Cricetulus griseus | - |
2.7.99.B1 | EM-9 cell | - |
Cricetulus griseus | - |
EC Number | Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|---|
2.7.99.B1 | 2 ATP | the enzyme synthesizes Ap4A by transfer of AMP from the enzyme-adenylate intermediate to an ATP acceptor | Cricetulus griseus | diadenosine 5',5'''-P1,P4-tetraphosphate + diphosphate | - |
? |
EC Number | Synonyms | Comment | Organism |
---|---|---|---|
2.7.99.B1 | LigIII | - |
Cricetulus griseus |
EC Number | Organism | Comment | Expression |
---|---|---|---|
2.7.99.B1 | Cricetulus griseus | stress-induced increases inAp4A by DNA addition. Lig III-mediated Ap4A synthesis in response to an increased level of unrepaired strand breaks in APTX-deficient cells | up |
EC Number | General Information | Comment | Organism |
---|---|---|---|
2.7.99.B1 | malfunction | deletion of Lig I (PFL13) causes only a slight, 1.6fold increase in background Ap4A but has no effect on the level reached after treatment with MMC, indicating that Lig I cannot be responsible for the MMC-induced increase in Ap4A. Lig III, cf. EC 6.5.1.1, is the most likely, if not sole ligase, contributing to MMC-enhanced Ap4A synthesis. Normal NUDT2 expression does appear to limit the extent of Ap4A accumulation after DNA damage, but suppression of the activity of a hydrolytic activity such as the NUDT2 Ap4A hydrolase does not seem to be reponsible for Ap4A increase after DNA damage | Cricetulus griseus |
2.7.99.B1 | metabolism | no significant difference in the activity of NUDT2 between AA8 cells when cell extracts are assayed for NUDT2 activity in the 16-20 kDa region or when AA8 cells are treated with MMC | Cricetulus griseus |
2.7.99.B1 | physiological function | non-cytotoxic doses of certain DNA damaging agents increase diadenosine 5',5'''-P1,P4-tetraphosphate, Ap4A, to concentrations that can inhibit the initiation of DNA replication in a mammalian cell-free system and provide some pointers to the mechanism underlying this increase and its function. Accumulation occurs in vivo of ADP-ribosylated derivatives of Ap4A in response to DNA damage. Lig III is the most likely, if not sole ligase, contributing to MMC-enhanced Ap4A synthesis. Lig III-mediated Ap4A synthesis in response to an increased level of unrepaired strand breaks in APTX-deficient cells | Cricetulus griseus |