P53 phosphorylation

Liu, C., R. M. Russell, and X. D. Wang. 2006. Lycopene supplementation prevents smoke-induced changes in p53, p53 phosphorylation, cell proliferation, and apoptosis in the gastric mucosa of ferrets. J Nutr 136(1) 106—111. 

Blattner C, Tobiasch E, Litfen M, Rahmsdorf HJ, Herrlich P (1999) DNA damage induced p53 stabilization no inchcation for an involvement of p53 phosphorylation. Oncogene 18 1723-1732... 

Figure 15.4 Mechanisms of apoptosis induction by resveratrol. Resveratrol selectively induces apoptosis in various cancer cells in culture by several mechanisms including activation of death receptor-mediated signaling, mitochondria-dependent cytochrome c release and caspase activation, induction of p53 and p53-regulated proapototic genes, activation of MAP kinase-mediated p53 phosphorylation, blockade of Akt-mediated cell survival pathways, and accumulation of intracellular ceramide level.

Figure 2 Resveratrol may induce apoptosis and cell cycle arrest through p53 phosphorylation mediated hy MAPKs.

Other researchers have followed related strategies as described above for detection of IL-6. For example, Wang et. al. [75] reported an amperometric immunosensor to detect interleukin-6 (lL-6) using a AuNP-Poly-dopamine sensor platform and multienzyme-antibody functionalized AuNPs on carbon nanotubes. They obtained a DL of 1 pg mL for lL-6 in buffer. Du et. al. [76] used AuNP-modified screen printed carbon electrode to detect p53 phosphorylated at Ser392 (phospho-p53 ) along with multi-enzyme labeled graphene oxide (GO). 

Inhibitor of cydin dependent kinases inhibition of Bd-2 expression upregulation of death receptor Fas, some DNA intercalation activation of caspase-3 DNA fragmentation depolarization of mitochondrial membranes, apoptotic Apoptotic inhibition of p53 phosphorylation inhibition of cdk2 kinase... 

The double edged sword effect of Cd ", namely apoptosis and cancer progression, is reflected in its opposing effects on p53. Cd " inhibits DNA base excision repair in p53-dependent and -independent manners [593], increases p53 phosphorylation as a prelude to apoptosis [594,595], and arrests cells in G1 and G2/M checkpoints via p53-dependent [510] and -independent [596] mechanisms. Cd " can affect p53 in two ways p53 is activated by phosphorylation via phosphatidylinositol-3-kinase related kinases [479] or Cd replaces zinc to maintain its mutated non-DNA binding form preventing apoptosis induction [597]. 

Another important signaling aspect involves the temporal properties of NO. Though NO is short lived, the sustained NO flux generated by NOS can vary in duration from seconds to days. NO-mediated HIF-la stabilization correlates directly with concentration and time, (Thomas et al. 2008). While pERK increases immediately in response to NO, it also transiently decreases despite the maintenance of steady-state NO levels. Moreover, NO-induced p53 phosphorylation remains stably elevated even after the dissipation of steady-state NO. Thus, signaling responses to NO are temporally and spatially deflned (Thomas et al. 2008). 

Lin T, Mak NK, Yang MS MAPK regulate p53-dependent cell death induced by benzo[a]pyrene involvement of p53 phosphorylation and acetylation. Toxicology 2008, 247 145-153. 

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