Phenotypes associated with this allele

• Allele Symbol: Nlrp6^tm1Macha
• Allele Name: targeted mutation 1, Mathias Chamaillard
• Allele ID: MGI:5140329
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Nlrp6^tm1Macha/Nlrp6^tm1Macha	involves: 129S5/SvEvBrd * C57BL/6J	MGI:5140342

Genotype
MGI:5140342

hm1

• Allelic Composition: Nlrp6^tm1Macha/Nlrp6^tm1Macha
• Genetic Background: involves: 129S5/SvEvBrd * C57BL/6J

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

Increased susceptibility to induced colitis in Nlrp6^tm1Macha/Nlrp6^tm1Macha mice

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:173352 )

• in 20% of mice treated with azoxymethane and DSS

digestive/alimentary system

rectal hemorrhage ( J:173352 )

• in DSS-treated mice

• in mice treated with azoxymethane and DSS

abnormal intestinal mucosa morphology ( J:173352 )

• colonic mucosa shrinkage in DSS-treated mice

intestinal ulcer ( J:173352 )

• in DSS-treated mice

decreased colon length ( J:173352 )

• greater shortening in DSS-treated mice than in similarly treated wild-type mice

intestinal edema ( J:173352 )

• in DSS-treated mice

increased gastrointestinal tumor incidence ( J:173352 )

• mice treated with azoxymethane and DSS exhibit increased colorectal tumorigenesis compared with wild-type mice

abnormal intestine physiology ( J:173352 )

• DSS-treated mice exhibit increased colonic permeability, edema, and cell cycle arrest compared with wild-type mice

abnormal enterocyte proliferation ( J:173352 )

• DSS-treated mice exhibit enhanced cell cycle arrest in the colon compared with similarly treated wild-type mice

increased susceptibility to induced colitis ( J:173352 )

• mice treated with dextran sodium sulfate (DSS) exhibit persistent signs of colitis (weight loss, hunched posture, rectal bleeding, diarrhea, ulcerations, reduced colon length, increased leukocyte infiltration, colonic permeability, colonic mucosa shrinkage, edema formation, and mucosal damage) even 10 days after a return to regular water compared with similarly treated wild-type mice

• anakinra therapy fails to rescue DSS-induced injury

• mice treated with azoxymethane and DSS exhibit increased colorectal tumorigenesis compared with wild-type mice

neoplasm

increased gastrointestinal tumor incidence ( J:173352 )

• mice treated with azoxymethane and DSS exhibit increased colorectal tumorigenesis compared with wild-type mice

increased incidence of tumors by chemical induction ( J:173352 )

• mice treated with azoxymethane and DSS exhibit increased colorectal tumorigenesis compared with wild-type mice

behavior/neurological

hunched posture ( J:173352 )

• in DSS-treated mice

cardiovascular system

rectal hemorrhage ( J:173352 )

• in DSS-treated mice

• in mice treated with azoxymethane and DSS

growth/size/body

increased susceptibility to weight loss ( J:173352 )

• in DSS-treated mice

• in mice treated with azoxymethane and DSS

homeostasis/metabolism

intestinal edema ( J:173352 )

• in DSS-treated mice

increased susceptibility to xenobiotic induced morbidity/mortality ( J:173352 )

• in 20% of mice treated with azoxymethane and DSS

increased incidence of tumors by chemical induction ( J:173352 )

• mice treated with azoxymethane and DSS exhibit increased colorectal tumorigenesis compared with wild-type mice

impaired wound healing ( J:173352 )

• of a mucosal wound

immune system

increased susceptibility to induced colitis ( J:173352 )

• mice treated with dextran sodium sulfate (DSS) exhibit persistent signs of colitis (weight loss, hunched posture, rectal bleeding, diarrhea, ulcerations, reduced colon length, increased leukocyte infiltration, colonic permeability, colonic mucosa shrinkage, edema formation, and mucosal damage) even 10 days after a return to regular water compared with similarly treated wild-type mice

• anakinra therapy fails to rescue DSS-induced injury

• mice treated with azoxymethane and DSS exhibit increased colorectal tumorigenesis compared with wild-type mice

cellular

abnormal enterocyte proliferation ( J:173352 )

• DSS-treated mice exhibit enhanced cell cycle arrest in the colon compared with similarly treated wild-type mice