Sentences with phrase «p53 phosphorylation»

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).
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