TIGAR, a p53-inducible regulator of glycolysis and apoptosis

Article Abstract:

A p53-inducible gene named TIGAR (TP53-induced glycolysis and apoptosis regulator) is identified that lowers fructose-2,6-bisphosphate levels in cells, resulting in an inhibition of glycolysis and an overall decrease in intracellular reactive oxygen species (ROS) levels. The expression of TIGAR modulates the apoptotic response to p53 and the decrease of intracellular ROS levels in response to TIGAR plays a role in the ability of p53 to protect from the accumulation of genomic damage.

Glycolysis

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PIDD: A switch hitter

Article Abstract:

The fundamental decision making process called PIDD (p53- induced protein with a death domain), protein promotes apoptosis downstream of the tumor-suppressor protein p53. In response to such stress PIDD forms a nuclear complex that enhance sumoylation of NEMO (IKKgamma) and is important for the activation of the antiapoptotic transcription factor NF- kappaB.

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Sequential modification of NEMO/IKK(sub)gamma by SUMO-1 and ubiquitin mediates NF-kappaB activation by genotoxic stress

Article Abstract:

Results show that the two separate signaling pathways, SUMO-1 modification and ATM activation are induced by genotoxic stress. Data suggest that the two pathways work in unison and cause nuclear targeting and ubiquitylation of free NEMO, to facilitate the transcription factor NF-kappa B survival pathway.

United States, Analysis, Genetic aspects, Cellular signal transduction, Genetic transcription, Transcription (Genetics), Cellular control mechanisms, Cell regulation, Enzyme activation, Genetic toxicology

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