Prostaglandin E synthase 3 (Ptges3) encodes p23, a protein that is known as a heat shock protein 90 (HSP90) co-chaperone and involved in stabilizing HSP90 with other proteins. p23 also facilitates the recruitment of PHD2, a prolyl hydroxylase domain protein responsible for hydroxylating hypoxia-inducible factor alpha (HIF-&alpha;), which is a subunit of the hypoxia-inducible factor (HIF) complex. HIF is necessary for oxygen homeostasis by regulating metabolic adaptation, erythropoiesis (red blood cell production), respiration, and angiogenesis. These p23AA mice have two amino acid substitutions (L159A and E160A) in the Ptges3 gene in a Pro-Xaa-Leu-Glu (PXLE) motif. This mutation abolishes the interaction between p23 and PHD2. Heterozygous mice are viable and fertile. Homozygous p23AA mice display an augmented hypoxic ventilatory response. The donating laboratory notes that homozygous mice are not fertile and are generated in lower than expected Mendelian ratio from heterozygous x heterozygous matings (~17%) on a mixed B6;129S background. When on a pure C57BL/6J background, homozygous production was significantly lower (~3% from heterozygous x Heterozygous matings). These mice may be useful for studying oxygen-sensing, respiration and the HIF pathway.

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p23AA knock-in (KI) mice have two amino acid substitutions (L159A and E160A) in the Ptges3 gene, resulting in modification of a PXLE motif which abolishes p23 interaction with PHD2. These mice may be useful when studying oxygen-sensing and the hypoxia-inducible factor (HIF) pathway.

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