About   Help   FAQ
Phenotypes Associated with This Genotype
Genotype
MGI:5693947
Allelic
Composition
Abcb1atm1Bor/Abcb1atm1Bor
Genetic
Background
FVB.129P2-Abcb1atm1Bor/TacImx
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcb1atm1Bor mutation (3 available); any Abcb1a mutation (59 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• dysregulated epithelial cell growth in areas of inflammation
• intestinal inflammation is characterized by massive thickening of the mucosa and inflammatory cell infiltrates into the lamina propria
• crypt length is increased in mice with colitis, with about 3-5 fold more epithelial cells per crypt
• occasional crypt abscesses extending through the mucosa to the muscular layer are seen in mice with colitis
• occasional ulcerations extending through the mucosa to the muscular layer are seen in mice with colitis
• about 20-25% of mice develop loose stools and anal mucous discharge by 1 year of age
• active intestinal inflammation that is primarily restricted to the large intestine
• inflammation spreads along the entire length of the colon
• increase in number of infiltrating CD3+ T cells scattered diffusely throughout the lamina propria; majority of infiltrating T cells are CD4+TCRalphabeta+
• presence of numerous B220+ B cell clusters/follicles within the lamina propria
• Gr1+ cellular infiltrates are prominent throughout the lamina propria of the large intestine
• mice develop spontaneous colitis with an average age of onset at 20 weeks, although the first signs of colitis can be seen between 8 and 36 weeks of age
• severe inflammation of the large intestine resembles human inflammatory bowel disease, ulcerative colitis
• prophylactic treatment with oral antibiotics prevents spontaneous colitis
• mice with active colitis treated with antibiotics show reversal of active inflammation within 3 weeks of continuous treatment

endocrine/exocrine glands
• crypt length is increased in mice with colitis, with about 3-5 fold more epithelial cells per crypt
• occasional crypt abscesses extending through the mucosa to the muscular layer are seen in mice with colitis

growth/size/body
• some mice with colitis develop a wasting-type disease
• however, majority of mice with colitis are maintained for up to 3 months without signs of cachexia

hematopoietic system
• lymphocytes from colitic mice have enhanced proliferative reactivity to bacterial Ags
• mice with active colitis show increased serum antibody titers
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis

immune system
• active intestinal inflammation that is primarily restricted to the large intestine
• inflammation spreads along the entire length of the colon
• increase in number of infiltrating CD3+ T cells scattered diffusely throughout the lamina propria; majority of infiltrating T cells are CD4+TCRalphabeta+
• presence of numerous B220+ B cell clusters/follicles within the lamina propria
• Gr1+ cellular infiltrates are prominent throughout the lamina propria of the large intestine
• mice develop spontaneous colitis with an average age of onset at 20 weeks, although the first signs of colitis can be seen between 8 and 36 weeks of age
• severe inflammation of the large intestine resembles human inflammatory bowel disease, ulcerative colitis
• prophylactic treatment with oral antibiotics prevents spontaneous colitis
• mice with active colitis treated with antibiotics show reversal of active inflammation within 3 weeks of continuous treatment
• lymphocytes from colitic mice have enhanced proliferative reactivity to bacterial Ags
• mice with active colitis show increased serum antibody titers
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis
• increased in mutants with colitis but not in mutants without active colitis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
inflammatory bowel disease 13 DOID:0110893 OMIM:612244
J:51190


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)
Citing These Resources
Funding Information
Warranty Disclaimer & Copyright Notice
Send questions and comments to User Support.
last database update
02/16/2021
MGI 6.16
The Jackson Laboratory