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 (93 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• about 20-25% of mice develop loose stools and anal mucous discharge by 1 year of age
• 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
• 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, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
11/12/2024
MGI 6.24
The Jackson Laboratory