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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tnfrsf1btm1Imx
targeted mutation 1, Immunex Research and Development Corporation
MGI:1860087
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx B6.129S7-Tnfrsf1btm1Imx MGI:4830692
hm2
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx involves: 129S7/SvEvBrd * C57BL/6 MGI:2175020
cx3
Birc2tm1.1Rbr/Birc2tm1.1Rbr
Birc3tm1.1Rbr/Birc3tm1.1Rbr
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx
involves: 129S7/SvEvBrd * BALB/cJ * C57BL/6 * SJL MGI:5319379
cx4
Lepob/Lepob
Tnfrsf1atm1Imx/Tnfrsf1atm1Imx
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx
involves: 129S7/SvEvBrd * C57BL/6 MGI:2176437
cx5
Tnfrsf1atm1Imx/Tnfrsf1atm1Imx
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx
involves: 129S7/SvEvBrd * C57BL/6 MGI:3689914


Genotype
MGI:4830692
hm1
Allelic
Composition
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx
Genetic
Background
B6.129S7-Tnfrsf1btm1Imx
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1btm1Imx mutation (3 available); any Tnfrsf1b mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
N
• no increase in bone mineral density (J:135519)
• no increase in bone mineral density (J:135519)

respiratory system
N
• display a rapid increase in peak inspiratory pressure when exposed to high stretch ventilation, as is seen in controls (J:143836)
• display a rapid increase in peak inspiratory pressure when exposed to high stretch ventilation, as is seen in controls (J:143836)

homeostasis/metabolism
• decreased arterial pO2 after 2 hours of high stretch ventilation (J:143836)
• increased arterial pCO2 after 2 hours of high stretch ventilation (J:143836)
• decreased arterial pO2 after 2 hours of high stretch ventilation (J:143836)
• increased arterial pCO2 after 2 hours of high stretch ventilation (J:143836)

cardiovascular system
• drops below 45mm Hg by 70 minutes of high stretch ventilation whereas controls require 90 minutes (J:143836)
• drops below 45mm Hg by 70 minutes of high stretch ventilation whereas controls require 90 minutes (J:143836)




Genotype
MGI:2175020
hm2
Allelic
Composition
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1btm1Imx mutation (3 available); any Tnfrsf1b mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• numbers of microglial cells significantly increased relative to controls after epileptic stimulation (J:112713)
• numbers of microglial cells significantly increased relative to controls after epileptic stimulation (J:112713)
• two hours post i.v. lipopolysaccharide (LPS) challenge serum levels are 5 fold higher than controls, however, TNF kinetics and activity are not altered (J:45147)
• two hours post i.v. lipopolysaccharide (LPS) challenge serum levels are 5 fold higher than controls, however, TNF kinetics and activity are not altered (J:45147)
• increased pulmonary neutrophil accumulation in response to intranasal instillation of M. faeni as compared to control, however monocyte and lymphocyte levels are comparable to control (J:45147)
• increased pulmonary neutrophil accumulation in response to intranasal instillation of M. faeni as compared to control, however monocyte and lymphocyte levels are comparable to control (J:45147)
• increased numbers of T-gamma,delta cells in broncho-alveolar lavage fluid (J:120174)
• increased numbers of T-gamma,delta cells in broncho-alveolar lavage fluid (J:120174)

homeostasis/metabolism
N
• normal recovery after superficial injury causes an increased trans-epidermal water loss (J:59056)
• normal recovery after superficial injury causes an increased trans-epidermal water loss (J:59056)
• 41% loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• 41% loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• two hours post i.v. lipopolysaccharide (LPS) challenge serum levels are 5 fold higher than controls, however, TNF kinetics and activity are not altered (J:45147)
• two hours post i.v. lipopolysaccharide (LPS) challenge serum levels are 5 fold higher than controls, however, TNF kinetics and activity are not altered (J:45147)

nervous system
• 41% loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• 41% loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• numbers of microglial cells significantly increased relative to controls after epileptic stimulation (J:112713)
• numbers of microglial cells significantly increased relative to controls after epileptic stimulation (J:112713)
• increased glutamate currents (J:152590)
• increased glutamate currents (J:152590)

tumorigenesis
• development after DMPA/TPA treatment is reduced (J:89088)
• development after DMPA/TPA treatment is reduced (J:89088)

respiratory system
• increased numbers of T-gamma,delta cells in broncho-alveolar lavage fluid (J:120174)
• increased numbers of T-gamma,delta cells in broncho-alveolar lavage fluid (J:120174)

hematopoietic system
• numbers of microglial cells significantly increased relative to controls after epileptic stimulation (J:112713)
• numbers of microglial cells significantly increased relative to controls after epileptic stimulation (J:112713)

integument
• development after DMPA/TPA treatment is reduced (J:89088)
• development after DMPA/TPA treatment is reduced (J:89088)

cellular
• 41% loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• 41% loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)

Mouse Models of Human Disease
OMIM ID Ref(s)
NOT Hyperlipidemia, Familial Combined; FCHL 144250 J:45147
NOT Hypertension, Essential 145500 J:45147




Genotype
MGI:5319379
cx3
Allelic
Composition
Birc2tm1.1Rbr/Birc2tm1.1Rbr
Birc3tm1.1Rbr/Birc3tm1.1Rbr
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx
Genetic
Background
involves: 129S7/SvEvBrd * BALB/cJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Birc2tm1.1Rbr mutation (0 available); any Birc2 mutation (5 available)
Birc3tm1.1Rbr mutation (0 available); any Birc3 mutation (7 available)
Tnfrsf1btm1Imx mutation (3 available); any Tnfrsf1b mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• around E10.5 (J:182515)
• around E10.5 (J:182515)




Genotype
MGI:2176437
cx4
Allelic
Composition
Lepob/Lepob
Tnfrsf1atm1Imx/Tnfrsf1atm1Imx
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepob mutation (6 available); any Lep mutation (10 available)
Tnfrsf1atm1Imx mutation (4 available); any Tnfrsf1a mutation (22 available)
Tnfrsf1btm1Imx mutation (3 available); any Tnfrsf1b mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• plasma insulin levels are reduced significantly compared to homozygous Lep mutants (J:55722)
• plasma insulin levels are reduced significantly compared to homozygous Lep mutants (J:55722)
• 52% reduction in plasminogen activator inhibitor (PAI-1) antigen in the plasma (J:55722)
• 78% reduction in PAI-1 mRNA expression and 80% reduction in TGF-beta gene expression in adipose tissue (J:55722)
• 52% reduction in plasminogen activator inhibitor (PAI-1) antigen in the plasma (J:55722)
• 78% reduction in PAI-1 mRNA expression and 80% reduction in TGF-beta gene expression in adipose tissue (J:55722)

adipose tissue
• 78% reduction in PAI-1 mRNA expression and 80% reduction in TGF-beta gene expression in adipose tissue (J:55722)
• 78% reduction in PAI-1 mRNA expression and 80% reduction in TGF-beta gene expression in adipose tissue (J:55722)




Genotype
MGI:3689914
cx5
Allelic
Composition
Tnfrsf1atm1Imx/Tnfrsf1atm1Imx
Tnfrsf1btm1Imx/Tnfrsf1btm1Imx
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Imx mutation (4 available); any Tnfrsf1a mutation (22 available)
Tnfrsf1btm1Imx mutation (3 available); any Tnfrsf1b mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• enhanced survival after caecal ligation and puncture (J:48865)
• enhanced survival after caecal ligation and puncture (J:48865)

immune system
• reduced microglial response to excitotoxic injury (J:33864)
• reduced microglial response to excitotoxic injury (J:33864)
• two hours post lipopolysaccharide (LPS) challenge serum levels are 15-20 fold higher than controls, however, TNF kinetics and activity are not altered (J:45147)
• two hours post lipopolysaccharide (LPS) challenge serum levels are 15-20 fold higher than controls, however, TNF kinetics and activity are not altered (J:45147)
• following reverse passive Arthus reaction to induce uveitis, mice exhibit reduced cellular infiltration into the anterior and posterior segments compared with wild-type mice (J:115094)
• following reverse passive Arthus reaction to induce uveitis, mice exhibit reduced cellular infiltration into the anterior and posterior segments compared with wild-type mice (J:115094)
• do not respond to collagen type II injections as do controls by developing arthritis for at least 14 days (J:120707)
• do not respond to collagen type II injections as do controls by developing arthritis for at least 14 days (J:120707)
• M. faeni- induced neutrophil accumulation in the lung is decreased as compared to control, however monocyte and lymphocyte levels are comparable to control (J:45147)
• M. faeni- induced neutrophil accumulation in the lung is decreased as compared to control, however monocyte and lymphocyte levels are comparable to control (J:45147)
• exhibits resistance to a lethal LPS dose plus hepatoxin D-gal (increases sensitivity to LPS) (J:45147)
• exhibits resistance to a lethal LPS dose plus hepatoxin D-gal (increases sensitivity to LPS) (J:45147)
• osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp (J:58851)
• the osteolytic lesions continue to be larger for at least 38 days after innoculation (J:58851)
• osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp (J:58851)
• the osteolytic lesions continue to be larger for at least 38 days after innoculation (J:58851)
• mice have 3 log greater bacterial penetration of the dental pulp eight days after experimental bacterial infection (J:58851)
• mice have 3 log greater bacterial penetration of the dental pulp eight days after experimental bacterial infection (J:58851)

homeostasis/metabolism
• 40% larger infarction than controls after coronary artery occlusion (J:62223)
• extent of necrosis in ventricles is similar to controls (J:62223)
• apoptosis peaks earlier and higher than for controls (J:62223)
• 40% larger infarction than controls after coronary artery occlusion (J:62223)
• extent of necrosis in ventricles is similar to controls (J:62223)
• apoptosis peaks earlier and higher than for controls (J:62223)
• increased susceptibility to kainic acid damage (J:33864)
• 30-50% neuron loss at kainic acid doses causing only minimal hippocampal damage in controls (J:33864)
• susceptibility to kainic acid damage is not reduced by TNF treatment (J:33864)
• increased susceptibility to kainic acid damage (J:33864)
• 30-50% neuron loss at kainic acid doses causing only minimal hippocampal damage in controls (J:33864)
• susceptibility to kainic acid damage is not reduced by TNF treatment (J:33864)
• two hours post lipopolysaccharide (LPS) challenge serum levels are 15-20 fold higher than controls, however, TNF kinetics and activity are not altered (J:45147)
• two hours post lipopolysaccharide (LPS) challenge serum levels are 15-20 fold higher than controls, however, TNF kinetics and activity are not altered (J:45147)
• TNF alpha induced thrombus formation is delayed (J:117987)
• TNF alpha induced thrombus formation is delayed (J:117987)
• hypothermic response to caecal ligation and puncture much shorter in duration than for controls (J:48865)
• febrile response to caecal ligation and puncture earlier in onset in males (J:48865)
• hypothermic response to caecal ligation and puncture much shorter in duration than for controls (J:48865)
• febrile response to caecal ligation and puncture earlier in onset in males (J:48865)
• fail to develop fibroproliferative lesions at bronchiolar-alveolar duct junctions when exposed to chrysotile asbestos fibers (J:51349)
• fail to develop fibroproliferative lesions at bronchiolar-alveolar duct junctions when exposed to chrysotile asbestos fibers (J:51349)
• protected against loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• also protected against tyrosin hydroxylase loss (J:78637)
• no loss of tyrosine hydroxylase immunoreactive nerve terminals (J:78637)
• protected against loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• also protected against tyrosin hydroxylase loss (J:78637)
• no loss of tyrosine hydroxylase immunoreactive nerve terminals (J:78637)
• enlarged calluses formed on long bone fractures during healing at days 14, 21, and 28 (J:70467)
• bones are fragile and prone to re-breaking (J:70467)
• delayed removal of calcified cartillage (J:70467)
• delayed mesenchymal cell differentiation (J:70467)
• enlarged calluses formed on long bone fractures during healing at days 14, 21, and 28 (J:70467)
• bones are fragile and prone to re-breaking (J:70467)
• delayed removal of calcified cartillage (J:70467)
• delayed mesenchymal cell differentiation (J:70467)
• significantly increased area of infarct after middle cerebral artery occlusion (J:33864)
• significantly increased area of infarct after middle cerebral artery occlusion (J:33864)

cellular
• protected against loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• also protected against tyrosin hydroxylase loss (J:78637)
• no loss of tyrosine hydroxylase immunoreactive nerve terminals (J:78637)
• protected against loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• also protected against tyrosin hydroxylase loss (J:78637)
• no loss of tyrosine hydroxylase immunoreactive nerve terminals (J:78637)
• increased susceptibility to kainic acid damage (J:33864)
• 30-50% neuron loss at kainic acid doses causing only minimal hippocampal damage in controls (J:33864)
• susceptibility to kainic acid damage is not reduced by TNF treatment (J:33864)
• increased susceptibility to kainic acid damage (J:33864)
• 30-50% neuron loss at kainic acid doses causing only minimal hippocampal damage in controls (J:33864)
• susceptibility to kainic acid damage is not reduced by TNF treatment (J:33864)

skeleton
• enlarged calluses formed on long bone fractures during healing at days 14, 21, and 28 (J:70467)
• bones are fragile and prone to re-breaking (J:70467)
• delayed removal of calcified cartillage (J:70467)
• delayed mesenchymal cell differentiation (J:70467)
• enlarged calluses formed on long bone fractures during healing at days 14, 21, and 28 (J:70467)
• bones are fragile and prone to re-breaking (J:70467)
• delayed removal of calcified cartillage (J:70467)
• delayed mesenchymal cell differentiation (J:70467)
• do not respond to collagen type II injections as do controls by developing arthritis for at least 14 days (J:120707)
• do not respond to collagen type II injections as do controls by developing arthritis for at least 14 days (J:120707)
• osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp (J:58851)
• the osteolytic lesions continue to be larger for at least 38 days after innoculation (J:58851)
• osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp (J:58851)
• the osteolytic lesions continue to be larger for at least 38 days after innoculation (J:58851)
• no induction of intramembranous bone on periosteal surfaces after 21 days of healing (J:70467)
• lack of trabecular bridging (J:70467)
• delayed formation of new trabecular bone after bone marrow cannulation (J:70467)
• extensive necrotic tissue and hematomas remain 3 days after bone marrow cannulation (J:70467)
• no induction of intramembranous bone on periosteal surfaces after 21 days of healing (J:70467)
• lack of trabecular bridging (J:70467)
• delayed formation of new trabecular bone after bone marrow cannulation (J:70467)
• extensive necrotic tissue and hematomas remain 3 days after bone marrow cannulation (J:70467)
• there is significantly more osteoclastogenesis that occurs in molars between 7 and 21 days after bacterial infection of the dental pulp (J:58851)
• osteoclast activity of the molars is almost 2-fold higher than in wild-types 7 days after bacterial inoculation (J:58851)
• there is significantly more osteoclastogenesis that occurs in molars between 7 and 21 days after bacterial infection of the dental pulp (J:58851)
• osteoclast activity of the molars is almost 2-fold higher than in wild-types 7 days after bacterial inoculation (J:58851)

nervous system
N
• no overt phenotype when unstressed (J:33864)
• no overt phenotype when unstressed (J:33864)
• 44% higher level of generalized convulsions in the 2 hours following 1 hour of electrical stimulation in the hippocampus (J:112713)
• 44% higher level of generalized convulsions in the 2 hours following 1 hour of electrical stimulation in the hippocampus (J:112713)
• significantly increased area of infarct after middle cerebral artery occlusion (J:33864)
• significantly increased area of infarct after middle cerebral artery occlusion (J:33864)
• glial response to neuronal injury is blunted (J:78637)
• glial response to neuronal injury is blunted (J:78637)
• reduced microglial response to excitotoxic injury (J:33864)
• reduced microglial response to excitotoxic injury (J:33864)
• long term neuron survival in culture is reduced (J:33864)
• long term neuron survival in culture is reduced (J:33864)
• protected against loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• also protected against tyrosin hydroxylase loss (J:78637)
• no loss of tyrosine hydroxylase immunoreactive nerve terminals (J:78637)
• protected against loss of striatal dopaminergic neurons in MPTP model of Parkinson's disease (controls lose 70%) (J:78637)
• also protected against tyrosin hydroxylase loss (J:78637)
• no loss of tyrosine hydroxylase immunoreactive nerve terminals (J:78637)
• increased susceptibility to kainic acid damage (J:33864)
• 30-50% neuron loss at kainic acid doses causing only minimal hippocampal damage in controls (J:33864)
• susceptibility to kainic acid damage is not reduced by TNF treatment (J:33864)
• increased susceptibility to kainic acid damage (J:33864)
• 30-50% neuron loss at kainic acid doses causing only minimal hippocampal damage in controls (J:33864)
• susceptibility to kainic acid damage is not reduced by TNF treatment (J:33864)

behavior/neurological
• reduced food intake at 24 hours but not at 48 hours after caecal ligation and puncture in males (J:48865)
• reduced food intake at 24 hours but not at 48 hours after caecal ligation and puncture in males (J:48865)
• 44% higher level of generalized convulsions in the 2 hours following 1 hour of electrical stimulation in the hippocampus (J:112713)
• 44% higher level of generalized convulsions in the 2 hours following 1 hour of electrical stimulation in the hippocampus (J:112713)

respiratory system
• fail to develop fibroproliferative lesions at bronchiolar-alveolar duct junctions when exposed to chrysotile asbestos fibers (J:51349)
• fail to develop fibroproliferative lesions at bronchiolar-alveolar duct junctions when exposed to chrysotile asbestos fibers (J:51349)

cardiovascular system
• more extensive avascular region develops on the retina 17 days after treatment of mice with 75% oxygen for 5 days (J:104652)
• recovery of deep retinal vessels delayed relative to controls (J:104652)
• rate of neovascularization higher at 21 days after treatment than in controls (J:104652)
• more extensive avascular region develops on the retina 17 days after treatment of mice with 75% oxygen for 5 days (J:104652)
• recovery of deep retinal vessels delayed relative to controls (J:104652)
• rate of neovascularization higher at 21 days after treatment than in controls (J:104652)
• 40% larger infarction than controls after coronary artery occlusion (J:62223)
• extent of necrosis in ventricles is similar to controls (J:62223)
• apoptosis peaks earlier and higher than for controls (J:62223)
• 40% larger infarction than controls after coronary artery occlusion (J:62223)
• extent of necrosis in ventricles is similar to controls (J:62223)
• apoptosis peaks earlier and higher than for controls (J:62223)

renal/urinary system
• reduced interstitial volume (J:69294)
• reduced interstitial volume (J:69294)
• more modest development of progressive interstitial fibrosis after uretera; ligation than in controls (J:69294)
• collagen IV deposition (J:69294)
• improved by enalapril treatment (J:69294)
• more modest development of progressive interstitial fibrosis after uretera; ligation than in controls (J:69294)
• collagen IV deposition (J:69294)
• improved by enalapril treatment (J:69294)

muscle
• recovery after cardiotoxin damage to the soleus muscle is slowed (J:104990)
• few well defined myofibers 5 days after treatment when the control animal is almost normal (J:104990)
• severe inflammatory infiltration persists through 5 days (J:104990)
• extensive calcium deposits at 5 days (J:104990)
• cross-sectional area of myofibers at 68.7% of pretreatment condition at 12 days after treatment (J:104990)
• contractile force recovery is 53.9% of preatreatment level compared to 75.8% for controls (J:104990)
• recovery after cardiotoxin damage to the soleus muscle is slowed (J:104990)
• few well defined myofibers 5 days after treatment when the control animal is almost normal (J:104990)
• severe inflammatory infiltration persists through 5 days (J:104990)
• extensive calcium deposits at 5 days (J:104990)
• cross-sectional area of myofibers at 68.7% of pretreatment condition at 12 days after treatment (J:104990)
• contractile force recovery is 53.9% of preatreatment level compared to 75.8% for controls (J:104990)

vision/eye
• more extensive avascular region develops on the retina 17 days after treatment of mice with 75% oxygen for 5 days (J:104652)
• recovery of deep retinal vessels delayed relative to controls (J:104652)
• rate of neovascularization higher at 21 days after treatment than in controls (J:104652)
• more extensive avascular region develops on the retina 17 days after treatment of mice with 75% oxygen for 5 days (J:104652)
• recovery of deep retinal vessels delayed relative to controls (J:104652)
• rate of neovascularization higher at 21 days after treatment than in controls (J:104652)

hematopoietic system
• reduced microglial response to excitotoxic injury (J:33864)
• reduced microglial response to excitotoxic injury (J:33864)

craniofacial
• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation (J:58851)
• complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation (J:58851)
• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation (J:58851)
• complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation (J:58851)

growth/size/body
• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation (J:58851)
• complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation (J:58851)
• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation (J:58851)
• complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation (J:58851)





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last database update
02/02/2016
MGI 6.02
The Jackson Laboratory