The p38 - mediated
p53 phosphorylation at Ser15 and subsequent p53 induction has been reported to be responsible for apoptosis induced by nitric oxide, hypoxic conditions, DNA - damaging agents, 1 - nitropyrene, and benzo [a] pyrene [30 - 32].
Low levels of glutathione peroxidase 1 activity in selenium - deficient mouse liver affect c - Jun N - terminal kinase activation and
p53 phosphorylation on Ser - 15 in pro-oxidant-induced aponecrosis.
Aldo - keto reductase 1C2 is essential for 1 - nitropyrene's but not for benzo [a] pyrene's induction of
p53 phosphorylation and apoptosis.
Uteroplacental insufficiency increases
p53 phosphorylation without triggering the p53 - MDM2 functional circuit response in the IUGR rat kidney.
Not exact matches
Gene - specific requirement for P - TEFb activity and RNA polymerase II
phosphorylation within the
p53 transcriptional program.
Phosphorylation of Ser15 in
p53 is a sign that
p53 is activated [25].
Ji H, Ding Z, Hawke D, Xing D, Jiang BH, Mills GB and Lu Z. AKT - dependent
phosphorylation of Niban regulates nucleophosmin - and MDM2 - mediated
p53 stability and cell apoptosis.
Although
p53 protein levels decreased after reaching the maximal level with treatment of 30 nM ActD,
phosphorylation of
p53 still increased with treatment of high doses (100 and 300 nM) of ActD.
However, it is unclear whether this enhanced interaction selectively facilitates transcription of specific
p53 target genes, including sestrins, or whether
p53 serine18
phosphorylation also regulates specific target genes by altering interactions of
p53 with other coactivators such as chromatin modifying enzymes.
Although
p53 protein levels decreased after reaching the maximal level with treatment of 100 nM ActD,
phosphorylation of
p53 still increased with treatment of a high dose (300 nM) of ActD.
First, we will use our unique DNA - and chromatin - templated in vitro transcription systems to investigate the direct role of
p53 serine18
phosphorylation in sestrin gene activation through modulation of
p53 - coactivator interactions.
p38 inhibitor (SB203580) caused a minor reduction in the ActD - induced increase in the expression and
phosphorylation of
p53 in the 293T and Hepa - 1c1c7 cells, but not in the 293 and HepG2 cells.
In the dosage studies, the expression and
phosphorylation of
p53 reached a maximal level with treatment of 10 nM ActD for 24 h in the 293 and 293T cells (Fig. 1B).
However, the ActD - induced
phosphorylation (Ser15) of
p53 was not inhibited by the inhibitors of p38, JNKs and ERKs in the current study, indicating that the
phosphorylation (Ser15) of
p53 was independent of these three MAP kinases.
HDM2 was transcribed by the
p53 transcription factor, and the patterns of expression and
phosphorylation of HDM2 were parallel to those of
p53 at low doses (5 or 10 nM) of ActD treatment.
The expression and
phosphorylation (Ser15) of
p53 is independent of JNKs, ERKs, and p38.
In contrast, treatment with ActD (10 nM) distinctly induced the expression and
phosphorylation of
p53 at 3 h, reaching a maximal response at 6 h, and maintaining a high level of
p53 for up to 12 h in the HepG2 cells.
p38 kinase regulates nitric oxide - induced apoptosis of articular chondrocytes by accumulating
p53 via NFkappa B - dependent transcription and stabilization by serine 15
phosphorylation.
In the Hepa - 1c1c7 cells, treatment with ActD (10 nM) distinctly induced the expression and
phosphorylation of
p53 at 6 h, and a high level of
p53 was maintained for up to 12 h (Fig. 1A).