EC Number   |
General Information |
Reference |
|---|
  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 |
740351 |
| 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 |
740351 |
| 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 |
740351 |
