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Phenotypes Associated with This Genotype
Genotype
MGI:3760247
Allelic
Composition
Smad3tm1Par/Smad3tm1Par
Genetic
Background
129-Smad3tm1Par/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smad3tm1Par mutation (2 available); any Smad3 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants maintained free of the gram-negative enterohepatic bacteria Helicobacter for up to 9 months do not develop colon cancer as do mutants housed under normal conditions
• infection of mutants with Helicobacter triggers colon cancer in 50-66% of mutants; mucinous adenocarcinomas develop 5 to 30 weeks after infection

immune system
• at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (25 min in duration), homozygotes fail to exhibit a significant increase in plasma IL-6 levels, unlike similarly-treated wild-type controls
• at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury, homozygotes exhibit a significant reduction in the renal expression of IL-6 and endothelin-1 mRNA, unlike similarly-treated wild-type controls
• however, expression of other cytokines known to contribute to ischemic acute kidney injury is not significantly altered
• at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury, homozygotes exhibit a drastic reduction in renal expression of IL-6, unlike similarly-treated wild-type controls
• colonic tissue of uninfected mutants is in a proinflammatory state as indicated by increased mRNA levels of IL-6, TNF-alpha, IFN-gamma, and IL-4, which is exacerbated by Helicobacter infection

renal/urinary system
• at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (either 22.5 or 25 min in duration), homozygotes exhibit better preservation of renal function as measured by serum BUN and creatinine levels
• renal histological injury is significantly reduced as shown by decreased acute tubular necrosis, intratubular sloughing and cast formation

homeostasis/metabolism
• at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (either 22.5 or 25 min in duration), homozygotes exhibit significantly reduced serum creatinine levels relative to wild-type controls
• at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (either 22.5 or 25 min in duration), homozygotes exhibit significantly reduced serum BUN levels relative to wild-type controls
• at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (25 min in duration), homozygotes fail to exhibit a significant increase in plasma IL-6 levels, unlike similarly-treated wild-type controls
• at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (either 22.5 or 25 min in duration), homozygotes exhibit better preservation of renal function as measured by serum BUN and creatinine levels
• renal histological injury is significantly reduced as shown by decreased acute tubular necrosis, intratubular sloughing and cast formation

digestive/alimentary system
• mutants maintained free of the gram-negative enterohepatic bacteria Helicobacter for up to 9 months do not develop colon cancer as do mutants housed under normal conditions
• infection of mutants with Helicobacter triggers colon cancer in 50-66% of mutants; mucinous adenocarcinomas develop 5 to 30 weeks after infection


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
12/17/2024
MGI 6.24
The Jackson Laboratory