All Phenotypes Nr3c1<tm2.1Ljm> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Nr3c1^tm2.1Ljm/Nr3c1^tm2.1Ljm Lyz2^tm1(cre)Ifo/Lyz2⁺	involves: 129P2/OlaHsd * 129S6/SvEvTac	MGI:5803964
cn2	Nr3c1^tm2.1Ljm/Nr3c1^tm2.1Ljm Tg(Camk2a-cre)T29-1Stl/0	involves: 129S6/SvEvTac * BALB/c * C57BL	MGI:5803966

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

cellular

decreased susceptibility to neuronal excitotoxicity ( J:197150 )

• with prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion

hematopoietic system

abnormal monocyte cell number ( J:197150 )

• prior to glucocorticoid stress hormone treatments fail to exhibit a reduction in numbers of infiltrating monocytes in infarcted hemisphere unlike in wild-type mice

homeostasis/metabolism

decreased susceptibility to neuronal excitotoxicity ( J:197150 )

• with prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion

abnormal response to CNS ischemic injury ( J:197150 )

• prior treatment with glucocorticoid stress hormone fail to exhibit a reduction in numbers of infiltrating monocytes and IL6 protein levels in infarcted hemisphere after middle cerebral artery occlusion unlike in wild-type mice

immune system

abnormal monocyte cell number ( J:197150 )

• prior to glucocorticoid stress hormone treatments fail to exhibit a reduction in numbers of infiltrating monocytes in infarcted hemisphere unlike in wild-type mice

increased interleukin-1 beta secretion ( J:197150 )

• in the ischemic cortex after middle cerebral artery occlusion

• in the hippocampus 12, but not 72, hours after kainic acid treatment

abnormal interleukin-6 secretion ( J:197150 )

• prior treatment with glucocorticoid stress hormone fails to induce a decrease in IL6 levels in the ischemic cortex 24 h after middle cerebral artery occlusion

nervous system

decreased susceptibility to neuronal excitotoxicity ( J:197150 )

• with prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion

abnormal response to CNS ischemic injury ( J:197150 )

Allelic Composition	Nr3c1^tm2.1Ljm/Nr3c1^tm2.1Ljm Tg(Camk2a-cre)T29-1Stl/0
Genetic Background	involves: 129S6/SvEvTac * BALB/c * C57BL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nr3c1^tm2.1Ljm mutation (1 available); any Nr3c1 mutation (34 available)
Tg(Camk2a-cre)T29-1Stl mutation (2 available)

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

nervous system

nervous system phenotype ( J:197150 )

N	• as in wild-type mice, prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion sensitizes neurons to excityotoxicity

abnormal response to CNS ischemic injury ( J:197150 )

• prior treatment with glucocorticoid stress hormone fail to exhibit a reduction in numbers of infiltrating monocytes after middle cerebral artery occlusion unlike in wild-type mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:197150 )

N	• as in wild-type mice, prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion sensitizes neurons to excityotoxicity

abnormal response to CNS ischemic injury ( J:197150 )

• prior treatment with glucocorticoid stress hormone fail to exhibit a reduction in numbers of infiltrating monocytes after middle cerebral artery occlusion unlike in wild-type mice

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)
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