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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Nox4tm1.1Hwsc
targeted mutation 1.1, Harald H H W Schmidt
MGI:4881785
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Nox4tm1.1Hwsc/Nox4tm1.1Hwsc involves: 129P2/OlaHsd * C57BL/6 MGI:4881786


Genotype
MGI:4881786
hm1
Allelic
Composition
Nox4tm1.1Hwsc/Nox4tm1.1Hwsc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nox4tm1.1Hwsc mutation (0 available); any Nox4 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• reduced disruption of the blood-brain barrier, showed by less extravasation of Evans blue (brain edema) 24 h after transient middle cerebral artery occlusion (tMCAO)
• almost no brain edema is seen in the brain regions where infarcts are regularly present
• significantly lower number of apoptotic neurons 24 h after tMCAO
• normal basal apoptotic turnover rate
• reduced infarct volume, better overall neurological function (lower Bederson scores) and grip strength in 6- to 8-week-old homozygous mice than in wild-type controls 24 h after tMCAO and permanent middle cerebral artery occlusion (pMCAO) and cortical photothrombosis
• seven of ten mice (70%) survive until day 5 after tMCAO , and five of these are still alive after 1 wk, versus 15 of 15 wild-type mice die by day5
• reduced infarct volume, better overall neurological function (lower Bederson scores) and grip strength in 18- to 20-week-old homozygous mice than in wild-type controls 24 h after tMCAO
• significantly smaller infarct volumes in 6- to 8-week-old and 18- to 20-week-old male and female homozygous mice than in wild-type sex-matched controls 24 h after subjected to tMCAO
• all infarcts are restricted to the basal ganglia
• neocortex is not affected
• infarct volume did not increase over time

cellular
• significantly lower number of apoptotic neurons 24 h after tMCAO
• normal basal apoptotic turnover rate
• reduced oxidative stress in brains from homozygous mice 24 h after tMCAO and pMACO
• very small ischemia-induced increases in reactive oxygen species (ROS) 24 h after tMCAO and pMCAO
• tissue nitration occurs to a lesser extent in ischemic brains from homozygous mice 24 h after tMCAO

cardiovascular system
N
• no abnormal vascular phenotype
• normal systemic blood pressure, renal and pulmonary functions
• normal cerebral blood flow, cerebral vasculature
• reduced disruption of the blood-brain barrier, showed by less extravasation of Evans blue (brain edema) 24 h after transient middle cerebral artery occlusion (tMCAO)
• almost no brain edema is seen in the brain regions where infarcts are regularly present

homeostasis/metabolism
• reduced infarct volume, better overall neurological function (lower Bederson scores) and grip strength in 6- to 8-week-old homozygous mice than in wild-type controls 24 h after tMCAO and permanent middle cerebral artery occlusion (pMCAO) and cortical photothrombosis
• seven of ten mice (70%) survive until day 5 after tMCAO , and five of these are still alive after 1 wk, versus 15 of 15 wild-type mice die by day5
• reduced infarct volume, better overall neurological function (lower Bederson scores) and grip strength in 18- to 20-week-old homozygous mice than in wild-type controls 24 h after tMCAO
• significantly smaller infarct volumes in 6- to 8-week-old and 18- to 20-week-old male and female homozygous mice than in wild-type sex-matched controls 24 h after subjected to tMCAO
• all infarcts are restricted to the basal ganglia
• neocortex is not affected
• infarct volume did not increase over time





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last database update
07/31/2018
MGI 6.12
The Jackson Laboratory