Phenotypes associated with this allele

• Allele Symbol: Klf5^tm2.1Rng
• Allele Name: targeted mutation 2.1, Ryozo Nagai
• Allele ID: MGI:4421792
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Klf5^tm2.1Rng/Klf5^tm2.1Rng	involves: C57BL/6	MGI:4421817
cn2	Klf5^tm2.1Rng/Klf5^tm2.1Rng Tg(Postn-cre)1Sjc/0	involves: C57BL/6	MGI:4421819
cn3	Klf5^tm2.1Rng/Klf5^tm2.1Rng Tg(Myh6-cre)2182Mds/0	involves: C57BL/6 * FVB/N	MGI:4421818

Genotype
MGI:4421817

hm1

• Allelic Composition: Klf5^tm2.1Rng/Klf5^tm2.1Rng
• Genetic Background: involves: C57BL/6

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

normal phenotype

no abnormal phenotype detected ( J:156696 )

• mice appear normal

Genotype
MGI:4421819

cn2

• Allelic Composition: Klf5^tm2.1Rng/Klf5^tm2.1Rng; Tg(Postn-cre)1Sjc/0
• Genetic Background: involves: C57BL/6

Fibroblast-specific deletion of Klf5 attenuates cardiac hypertrophy and fibrosis after TAC in Klf5^tm2.1Rng/Klf5^tm2.1Rng Tg(Postn-cre)1Sjc mice

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

increased susceptibility to xenobiotic induced morbidity/mortality ( J:156696 )

• following high-intensity transverse aortic constriction and exposure to a minimum dose of anesthetic

cardiovascular system

pulmonary vascular congestion ( J:156696 )

• following high-intensity transverse aortic constriction

abnormal myocardial fiber morphology ( J:156696 )

• following low- or high-intensity transverse aortic constriction, mice exhibit reduced cardiomyocyte hypertrophy compared with similarly treated Klf5^tm2.1Rng homozygotes

decreased heart weight ( J:156696 )

• following low- or high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

cardiac hypertrophy ( J:156696 )

• following low- or high-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy compared with similarly treated Klf5^tm2.1Rng homozygotes

abnormal heart left ventricle morphology ( J:156696 )

• following low-intensity transverse aortic constriction, left ventricle diastolic posterior wall thickness is reduced compared to in similarly treated Klf5^tm2.1Rng homozygotes

increased heart left ventricle size ( J:156696 )

• following high-intensity transverse aortic constriction and anesthesia, one mouse exhibited increased left ventricle luminal diameter compared with similarly treated Klf5^tm2.1Rng homozygotes

cardiac interstitial fibrosis ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac interstitial fibrosis compared with similarly treated Klf5^tm2.1Rng homozygotes

abnormal cardiovascular system physiology ( J:156696 )

• following high-intensity transverse aortic constriction and anesthesia, one mouse exhibited reduced systolic function compared with similarly treated Klf5^tm2.1Rng homozygotes

abnormal myocardial fiber physiology ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiomyocyte proliferation compared with similarly treated Klf5^tm2.1Rng homozygotes

abnormal response of heart to induced stress ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy and fibrosis, left ventricle diastolic posterior wall thickness, and cardiomyocyte hypertrophy and proliferation compared with similarly treated Klf5^tm2.1Rng homozygotes

• following high-intensity transverse aortic constriction, mice exhibit increased mortality with weight loss, rapid breathing, and pulmonary edema and/or hemorrhage but reduced cardiac hypertrophy, heart weight, and fibrosis compared with similarly treated Klf5^tm2.1Rng homozygotes

• following high-intensity transverse aortic constriction and anesthesia, one mouse exhibited enlarged left ventricle luminal diameter and reduced systolic function compared with similarly treated Klf5^tm2.1Rng homozygotes

respiratory system

pulmonary vascular congestion ( J:156696 )

• following high-intensity transverse aortic constriction

pulmonary edema ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

pulmonary alveolar edema ( J:156696 )

• following high-intensity transverse aortic constriction

increased wet-to-dry lung weight ratio ( J:156696 )

• following high-intensity transverse aortic constriction due to pulmonary congestion and alveolar edema

increased pulmonary respiratory rate ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

growth/size/body

cardiac hypertrophy ( J:156696 )

• following low- or high-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy compared with similarly treated Klf5^tm2.1Rng homozygotes

weight loss ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

homeostasis/metabolism

abnormal response of heart to induced stress ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy and fibrosis, left ventricle diastolic posterior wall thickness, and cardiomyocyte hypertrophy and proliferation compared with similarly treated Klf5^tm2.1Rng homozygotes

• following high-intensity transverse aortic constriction, mice exhibit increased mortality with weight loss, rapid breathing, and pulmonary edema and/or hemorrhage but reduced cardiac hypertrophy, heart weight, and fibrosis compared with similarly treated Klf5^tm2.1Rng homozygotes

• following high-intensity transverse aortic constriction and anesthesia, one mouse exhibited enlarged left ventricle luminal diameter and reduced systolic function compared with similarly treated Klf5^tm2.1Rng homozygotes

pulmonary edema ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

pulmonary alveolar edema ( J:156696 )

• following high-intensity transverse aortic constriction

increased susceptibility to xenobiotic induced morbidity/mortality ( J:156696 )

• following high-intensity transverse aortic constriction and exposure to a minimum dose of anesthetic

muscle

abnormal myocardial fiber morphology ( J:156696 )

• following low- or high-intensity transverse aortic constriction, mice exhibit reduced cardiomyocyte hypertrophy compared with similarly treated Klf5^tm2.1Rng homozygotes

cellular

cardiac interstitial fibrosis ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac interstitial fibrosis compared with similarly treated Klf5^tm2.1Rng homozygotes

Genotype
MGI:4421818

cn3

• Allelic Composition: Klf5^tm2.1Rng/Klf5^tm2.1Rng; Tg(Myh6-cre)2182Mds/0
• Genetic Background: involves: C57BL/6 * FVB/N

Cardiomyocyte-specific deletion of Klf5 does not alter pressure overload-induced hypertrophy in Klf5^tm2.1Rng/Klf5^tm2.1Rng Tg(Myh6-cre)2182Mds/0 mice

cardiovascular system

cardiovascular system phenotype ( J:156696 )

N • mice exhibit a normal response to low-intensity transverse aortic constriction