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. Author manuscript; available in PMC: 2014 Feb 5.
Published in final edited form as: Cell Metab. 2013 Feb 5;17(2):159–161. doi: 10.1016/j.cmet.2013.01.012

Figure. Schematic of p53 controlling metabolic fate upon serine starvation.

Figure

Through glycolysis, glucose is converted into 3-PG, 3-phosphoglycerate, and shuttled into the serine synthesis pathway, as the demand for serine is great. Serine is then converted into glycine, where, p53 is elevated and activates p21 to promote cell cycle arrest and replenish GSH, glutathione. Conversion to inosine monophosphate (IMP) and resultant purine biosynthesis is suppressed. GSH pools suppress reactive oxygen species (ROS) generated from the TCA cycle. Cells lacking p53 or p21 generate IMP instead of replenishing GMP pools and succumb to excessive ROS.