Fig. 7. p53 deletion rescues the pancreatic defects caused by MDM2 or MDMX deletion.

A) Random blood Glucose level of neonatal mice (left, n=10), and 2-month-old adult male mice with indicated genotypes was measured at least 3 times on different day (right, n=9). B) Fasting Insulin level of 2-month-old male MDM2/p53-double knockout and control mice was measured (n=9). C) GTT was performed with 2-month-old male MDM2/p53-double knockout and control mice (n=9). D) Representative images of immunostaining with anti-Insulin and anti-Glucagon antibodies on pancreas cryo-sections of 2-month-old male MDM2/p53-double knockout and control mice. E) Representative images of TUNEL staining (upper), and co-immunostaining with anti-Ki67 and anti-PDX1 antibodies (lower) on pancreas cryo-sections of MDM2/p53 double knockout and control mice at the indicated embryonic stages. The percentage of PDX1 positive cells in pancreas and percentage of Ki67 positive cells in PDX1 positive cell population were calculated, respectively (right panels). F) Loss of p53 completely rescued the decreased survival rate of MDMX-conditional male mice. G) Random blood Glucose level (left panel) of 2-and 7-month-old adult male mice with indicated genotypes was measured at least 3 times on different days (n=8~10 / group). Fasting Insulin level (middle panel) of 7-month-old male mice with indicated genotypes was measured (n=6 / group). GTT (right panel) was performed with 2-month-old male MDMX/p53-double knockout and control mice (n=8~9 / group). H) Representative images of co-immunostaining with anti-Ki67 and anti-PDX1 antibodies on pancreas cryo-sections of MDMX/p53 double knockout and control mice at postnatal day 10. The percentage of PDX1 positive cells in pancreas and percentage of Ki67 positive cells in PDX1 positive cell population were calculated, respectively (right panels).