All Phenotypes Trp53inp1<tm1Acar> MGI Mouse

increased susceptibility to xenobiotic induced morbidity/mortality ( J:118867 )

• less than 50% of mutants with DSS-induced colitis survive to day 15, while less than 10% mortality is observed in controls

increased body fat mass ( J:233434 )

• increase in fat mass

• supplementation with the anti-oxidant N-acetylcysteine abolishes the increased fat mass

abnormal epididymal fat pad morphology ( J:233434 )

• mice fed a high-fat diet show a higher epididymal fat mass than controls

abnormal renal fat pad morphology ( J:233434 )

• mice fed a high-fat diet show higher renal fat mass than controls

increased body fat mass ( J:233434 )

• increase in fat mass

• supplementation with the anti-oxidant N-acetylcysteine abolishes the increased fat mass

increased body weight ( J:233434 )

• increase in body weight of 5 month old mice

increased susceptibility to weight gain ( J:118867 )

• weight gain in AZO-DSS treated mutants is twice that in controls

increased susceptibility to diet-induced obesity ( J:233434 )

• 8 week old mice fed a high-fat diet show a higher body weight gain than wild-type mice, even though food consumption does not differ

• treatment with N-acetylcysteine at the starting of a high-fat diet abolishes body weight difference between mutant and wild-type mice

increased liver weight ( J:233434 )

• high-fat diet induced liver weight is increased compared to controls

increased liver weight ( J:233434 )

• high-fat diet induced liver weight is increased compared to controls

hepatic steatosis ( J:233434 )

• high-fat diet induced steatosis is greater in mutants than in wild-type mice

• treatment with N-acetylcysteine at the starting of a high-fat diet abolishes the hepatic steatosis difference between mutant and wild-type mice

neoplasm ( J:118867 )

N	• mice observed for up to 2 years do not develop tumors

increased colon adenoma incidence ( J:118867 )

increased incidence of tumors by chemical induction ( J:118867 )

• in mutant and control mice treated with azoxymethane (AZO) and cycles of dextran sodium sulfate (DSS) ingestion, macroscopic tumors in the colon are observed in ~92% of mutants at 9 weeks, compared to ~61% of controls

• multiplicity is 2-fold higher in mutants

• treatment of mice with either AZO or DSS alone is sufficient to induce tumors in mutants after 7 months, whereas no treated wild-type mice develop tumors

abnormal intestinal mucosa morphology ( J:118867 )

• after 9 days of DSS treatment, mucosal ulcerations are more severe in mutants

abnormal crypts of Lieberkuhn morphology ( J:118867 )

• crypt damage is greater in mutants than in wild-type with induced colitis

increased colon adenoma incidence ( J:118867 )

large intestinal inflammation ( J:118867 )

• inflammation is exacerbated in mutants with colitis than in diseased wild-type mice

• 3-fold higher higher numbers of cells showing NF kappaB activation are observed in mutants with colitis

increased susceptibility to induced colitis ( J:118867 )

• mutant mice are more sensitive to DSS-induced colitis than wild-type

abnormal crypts of Lieberkuhn morphology ( J:118867 )

• crypt damage is greater in mutants than in wild-type with induced colitis

large intestinal inflammation ( J:118867 )

• inflammation is exacerbated in mutants with colitis than in diseased wild-type mice

• 3-fold higher higher numbers of cells showing NF kappaB activation are observed in mutants with colitis

increased susceptibility to induced colitis ( J:118867 )

• mutant mice are more sensitive to DSS-induced colitis than wild-type

abnormal cell morphology ( J:233434 )

• large number of lipid droplets in immortalized MEFs

• upon oxidative stress with hydrogen peroxide treatment, immortalized MEFs show an increase in lipid droplets compared to wild-type MEFs

• treatment of MEFs with the antioxidant NAC results in a reduction in lipid droplets

• treatment of MEFs with a PPAR-gamma inhibitor (GW-9662) prevents lipid droplet accumulation

abnormal mitochondrial morphology ( J:233434 )

• mitochondrial mass is higher in immortalized MEFs

increased mitochondrial number ( J:233434 )

• increase in the number of mitochondria in immortalized MEFs

abnormal mitophagy ( J:233434 )

• immortalized MEFs exhibit impaired mitophagy of dysfunctional mitochondrial pool

• immortalized MEFs show accumulation of autophagic vacuoles containing mitochondria, indicating a block in late stage of mitophagy

• treatment with hydrogen peroxide has no effect on autophagic vacuole accumulation

abnormal mitochondrial physiology ( J:233434 )

• increase in mitochondrial reactive oxygen species-producing activity in immortalized MEFs

• mitochondria occupy a smaller surface in hydrogen peroxide-treated immortalized MEFs than in wild-type MEFs, suggesting impaired ability of mitochondria to cope with stress

abnormal respiratory electron transport chain ( J:233434 )

• analysis of respiratory chain complexes shows decreased activity of complex IV in immortalized MEFs

abnormal oxidative phosphorylation ( J:233434 )

• mitochondrial oxygen consumption analysis shows decreased oxygen flow in immortalized MEFs, indicating impaired oxidative phosphorylation

oxidative stress ( J:118867 , J:233434 )

• mutants show increased plasma and colon radical-induced oxidative stress vs wild-type (J:118867)

• after colitis-induction, mutant colons produce more free radicals than wild-type and have lower antioxidant ascorbate levels (J:118867)

• increase in mitochondrial reactive oxygen species-producing activity in immortalized MEFs (J:233434)

abnormal mitophagy ( J:233434 )

• immortalized MEFs exhibit impaired mitophagy of dysfunctional mitochondrial pool

• immortalized MEFs show accumulation of autophagic vacuoles containing mitochondria, indicating a block in late stage of mitophagy

• treatment with hydrogen peroxide has no effect on autophagic vacuole accumulation

increased susceptibility to diet-induced obesity ( J:233434 )

• 8 week old mice fed a high-fat diet show a higher body weight gain than wild-type mice, even though food consumption does not differ

• treatment with N-acetylcysteine at the starting of a high-fat diet abolishes body weight difference between mutant and wild-type mice

hyperglycemia ( J:233434 )

• mice fed a high-fat diet develop hyperglycemia

• however, mice fed a standard diet are not hyperglycemic

increased circulating insulin level ( J:233434 )

• mice fed a high-fat diet exhibit greater hyperinsulinemia than wild-type mice

• however, mice fed a standard diet are not hyperinsulinemic

impaired glucose tolerance ( J:233434 )

• mice fed a standard diet are glucose intolerant

• mice fed a high-fat diet show further development of glucose intolerance

insulin resistance ( J:233434 )

• mice fed a standard diet are insulin resistant

• mice fed a high-fat diet show further development of insulin resistance

increased susceptibility to diet-induced non-insulin dependent diabetes ( J:233434 )