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 (35 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)
Citing These Resources Funding Information Warranty Disclaimer, Privacy Notice, Licensing, & Copyright Send questions and comments to User Support.	last database update 10/29/2024 MGI 6.24