Phenotypes associated with this allele

• Allele Symbol: Hmox1^tm1Ysh
• Allele Name: targeted mutation 1, Ye-Shih Ho
• Allele ID: MGI:3526703
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Hmox1^tm1Ysh/Hmox1^tm1Ysh	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3526729
ht2	Hmox1^tm1Ysh/Hmox1^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3526730

Genotype
MGI:3526729

hm1

• Allelic Composition: Hmox1^tm1Ysh/Hmox1^tm1Ysh
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6

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

mortality/aging

prenatal lethality, complete penetrance ( J:95461 )

• no homozygous mice were detected, indicating embryonic lethality

Genotype
MGI:3526730

ht2

• Allelic Composition: Hmox1^tm1Ysh/Hmox1⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6

cardiovascular system

myocardium necrosis ( J:95461 )

• significantly higher myocardial necrosis after ischemia than in wild-type

abnormal cardiovascular system physiology ( J:95461 )

• increased release of creatine kinase and production of malonaldehyde (MDA) in the heart during reperfusion compared to wild-type

abnormal cardiac muscle contractility ( J:95461 )

• significantly lower contractile recovery after 30 minutes of ischemia

• the force developed by the heart (DF) during reperfusion was lower than in wild-type and did not recover beyond 87% of baseline

• preconditioning, which renders the heart tolerant to subsequent ischemia/reperfusion, did not result in an improvement in contractile recovery after injury as in wild-type

increased myocardial infarct size ( J:95461 )

• infarct size was significantly higher (48.5%) than in wild-type (28.5%) after ischemia/reperfusion

muscle

myocardium necrosis ( J:95461 )

• significantly higher myocardial necrosis after ischemia than in wild-type

abnormal cardiac muscle contractility ( J:95461 )

• significantly lower contractile recovery after 30 minutes of ischemia

• the force developed by the heart (DF) during reperfusion was lower than in wild-type and did not recover beyond 87% of baseline

• preconditioning, which renders the heart tolerant to subsequent ischemia/reperfusion, did not result in an improvement in contractile recovery after injury as in wild-type

homeostasis/metabolism

increased myocardial infarct size ( J:95461 )

• infarct size was significantly higher (48.5%) than in wild-type (28.5%) after ischemia/reperfusion