Phenotypes associated with this allele

• Allele Symbol: Klf5^tm1Rng
• Allele Name: targeted mutation 1, Ryozo Nagai
• Allele ID: MGI:3038696
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Klf5^tm1Rng/Klf5^tm1Rng	involves: 129/Sv * C57BL/6	MGI:3038737
ht2	Klf5^tm1Rng/Klf5^+	involves: 129	MGI:4421820
ht3	Klf5^tm1Rng/Klf5^+	involves: 129/Sv * C57BL/6	MGI:3038738

Genotype
MGI:3038737

hm1

• Allelic Composition: Klf5^tm1Rng/Klf5^tm1Rng
• Genetic Background: involves: 129/Sv * C57BL/6

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

mortality/aging

embryonic lethality, complete penetrance ( J:78275 )

• homozygous mutant embryos die prior to E8.5

Genotype
MGI:4421820

ht2

• Allelic Composition: Klf5^tm1Rng/Klf5⁺
• Genetic Background: involves: 129

Pressure overload-induced cardiac hypertophy and fibrosis are reduced in Klf5^tm1Rng/Klf5⁺ mice

cardiovascular system

decreased heart weight ( J:156696 )

• following low-intensity transverse aortic constriction compared to in similarly treated wild-type mice

cardiac hypertrophy ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy compared with similarly treated wild-type mice

cardiac fibrosis ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced fibrosis compared with similarly treated wild-type mice

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

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy and fibrosis compared with similarly treated wild-type mice

homeostasis/metabolism

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

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy and fibrosis compared with similarly treated wild-type mice

growth/size/body

cardiac hypertrophy ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy compared with similarly treated wild-type mice

Genotype
MGI:3038738

ht3

• Allelic Composition: Klf5^tm1Rng/Klf5⁺
• Genetic Background: involves: 129/Sv * C57BL/6

cardiovascular system

abnormal aorta wall morphology ( J:78275 )

• heterozygotes exhibit abnormal thinning of the medial and adventitial layers of the aortic wall

decreased angiogenesis ( J:78275 )

• in the cuff-injured femoral artery model, heterozygotes display reduced cardiovascular remodeling and angiogenesis relative to wild-type mice

• in addition, heterozygotes show impaired angiogenic activity in a hind-limb ischemia model (where femoral arteries are ablated), and significantly attenuated angiogenic responses to implanted tumors

decreased response of heart to induced stress ( J:78275 )

• in response to external stress (cuff-injured femoral artery model), heterozygotes exhibit decreased arterial-wall thickening with no evidence of intimal hyperplasia, as well as reduced levels of angiogenesis, cardiac hypertrophy, and interstitial fibrosis relative to wild-type mice

• similarly attenuated responses to vascular injury are observed in the wire-injured femoral artery model

• following a continuous, 14-day infusion of angiotensin II, heterozygotes display significantly reduced cardiac hypertrophy, with thinner ventricular walls and lower heart weight to body weight ratios, as well as significantly reduced interstitial and perivascular fibrosis relative to wild-type mice

• attenuation of cardiovascular remodeling is associated with reduced expression of both activated platelet-derived growth factor-A (PDGF-A) and transforming growth factor-beta (TGF-beta)

abnormal vascular smooth muscle physiology ( J:78275 )

• in the cuff-injured femoral artery model, heterozygotes show impaired activation and proliferation of smooth muscle cells and fibroblasts, whereas wild-type mice display thickening of the medial and intimal layers and high proliferation of smooth muscle cells

abnormal vascular wound healing ( J:78275 )

• in the cuff-injured femoral artery model, heterozygotes display smaller areas of neointima and granulation tissue around the cuff relative to wild-type mice

• administration of LE135, a synthetic retinoic-acid receptor (RAR) antagonist, to heterozygotes with cuffed femoral arteries incrementally increases formation of granulation tissue and neointima to nearly wild-type levels

homeostasis/metabolism

decreased response of heart to induced stress ( J:78275 )

• in response to external stress (cuff-injured femoral artery model), heterozygotes exhibit decreased arterial-wall thickening with no evidence of intimal hyperplasia, as well as reduced levels of angiogenesis, cardiac hypertrophy, and interstitial fibrosis relative to wild-type mice

• similarly attenuated responses to vascular injury are observed in the wire-injured femoral artery model

• following a continuous, 14-day infusion of angiotensin II, heterozygotes display significantly reduced cardiac hypertrophy, with thinner ventricular walls and lower heart weight to body weight ratios, as well as significantly reduced interstitial and perivascular fibrosis relative to wild-type mice

• attenuation of cardiovascular remodeling is associated with reduced expression of both activated platelet-derived growth factor-A (PDGF-A) and transforming growth factor-beta (TGF-beta)

abnormal vascular wound healing ( J:78275 )

• in the cuff-injured femoral artery model, heterozygotes display smaller areas of neointima and granulation tissue around the cuff relative to wild-type mice

• administration of LE135, a synthetic retinoic-acid receptor (RAR) antagonist, to heterozygotes with cuffed femoral arteries incrementally increases formation of granulation tissue and neointima to nearly wild-type levels

muscle

abnormal vascular smooth muscle physiology ( J:78275 )

• in the cuff-injured femoral artery model, heterozygotes show impaired activation and proliferation of smooth muscle cells and fibroblasts, whereas wild-type mice display thickening of the medial and intimal layers and high proliferation of smooth muscle cells

digestive/alimentary system

abnormal intestinal mucosa morphology ( J:78275 )

• heterozygotes display abnormally shaped villi, a lower number of mesenchymal cells, and a reduced amount of extracellular matrix in the GI tract relative to wild-type mice

• administration of LE135 increases the mesenchymal components and thickness of villi in the GI tracts of heterozygous mice, making the structure of the GI mucosa comparable to that in wild-type mice

abnormal small intestinal villus morphology ( J:78275 )

• heterozygotes display abnormally shaped villi in the jejunum