Analysis Tools
growth/size/body
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• lower body weight gain between 5 and 10 weeks of age than for controls
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immune system
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• mutants develop severe inflammation in the colon leading to inflammatory bowel disease
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• upon DSS exposure
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• mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice
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• CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring nave CD4 T cells into immunodeficient hosts
• however, CD25-postive CD4 T cells inhibit the expansion of naive T cells in Rag2 deficient hosts as effectively as wild-type CD25-positive CD4 T cells
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• levels of cytokines increase in the brain are greater than for controls after lipopolysaccharide treatment
(J:139972)
• in LPS-injected mice
(J:157787)
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• in LPS-injected mice
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• in LPS-injected mice
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• plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls
(J:139972)
• in LPS-injected mice
(J:157787)
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• in LPS-injected mice
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• in LPS-injected mice
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• in LPS-injected mice
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• plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls
(J:139972)
• slightly in LPS-injected mice
(J:157787)
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• in LPS-injected mice
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• LPS-injected mice exhibit increased CXCL10 and CXCL1 levels compared with similarly treated wild-type mice
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• mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice
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homeostasis/metabolism
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• time to fatigue on a motorized treadmill is reduced 24% after lipopolysaccharide treatment
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• increased toxicity of N-methyl-D-aspartate in primary neuron culture
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• lipopolysaccharide causes a very significant drop in core body temperature
|
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• levels of cytokines increase in the brain are greater than for controls after lipopolysaccharide treatment
(J:139972)
• in LPS-injected mice
(J:157787)
|
|
• in LPS-injected mice
|
|
• in LPS-injected mice
|
|
• plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls
(J:139972)
• in LPS-injected mice
(J:157787)
|
|
• in LPS-injected mice
|
|
• in LPS-injected mice
|
|
• in LPS-injected mice
|
|
• plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls
(J:139972)
• slightly in LPS-injected mice
(J:157787)
|
|
• in LPS-injected mice
|
|
• LPS-injected mice exhibit increased CXCL10 and CXCL1 levels compared with similarly treated wild-type mice
|
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• lesion volume after middle cerebral artery occlusion increases 30%
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digestive/alimentary system
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• rectal prolapse is seen at a median time of 16 weeks of age
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• 20% of mutants with colonic inflammation exhibit colon tumors; tumors are adenocarcinomas
• tumors develop between 25 and 35 weeks of age
|
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• mutants develop severe inflammation in the colon leading to inflammatory bowel disease
|
|
• upon DSS exposure
|
|
• mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice
|
cardiovascular system
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• reduced choroidal neovascularization 7 days following krypton laser exposure of the eye
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• lower under basal conditions
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• LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine
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• endothelin 1 induced contraction of Aorta and first order mesenteric arteries is greater than controls when also treated with L-NAME and indomethecine and TNFalpha
• response to endothelin 1 is eliminated in the presence of PD-98059
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muscle
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• LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine
|
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• endothelin 1 induced contraction of Aorta and first order mesenteric arteries is greater than controls when also treated with L-NAME and indomethecine and TNFalpha
• response to endothelin 1 is eliminated in the presence of PD-98059
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behavior/neurological
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• rotarod performance worsens after IP lipopolysaccharide injection
• effect persists at least 24 hours
• performance fails to improve over consecutive trials but only after IP lipopolysaccharide injection
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• more time in "slow-wave sleep" and less time awake during dark phase
• less effect of influenza virus infection on slow wave sleep during dark phase but a greater decrease in delta wave amplitude
• lipopolysaccharide causes an overall decrease in delta wave amplitude
• lipopolysaccharide causes decreased slow wave and REM sleep during light phase
• lipopolysaccharide results in increased time spent awake, particularly in light phase
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• time to fatigue on a motorized treadmill is reduced 24% after lipopolysaccharide treatment
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nervous system
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• lesion volume after middle cerebral artery occlusion increases 30%
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• increased sensitivity to oxygen or glucose deprivation
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• increased toxicity of N-methyl-D-aspartate in primary neuron culture
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vision/eye
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• reduced choroidal neovascularization 7 days following krypton laser exposure of the eye
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neoplasm
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• 20% of mutants with colonic inflammation exhibit colon tumors; tumors are adenocarcinomas
• tumors develop between 25 and 35 weeks of age
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cellular
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• increased toxicity of N-methyl-D-aspartate in primary neuron culture
|
hematopoietic system
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• CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring nave CD4 T cells into immunodeficient hosts
• however, CD25-postive CD4 T cells inhibit the expansion of naive T cells in Rag2 deficient hosts as effectively as wild-type CD25-positive CD4 T cells
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| inflammatory bowel disease | DOID:0050589 |
OMIM:PS266600 |
J:124308 , J:149347 | |
