About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Klf5tm1Rng
targeted mutation 1, Ryozo Nagai
MGI:3038696
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Klf5tm1Rng/Klf5tm1Rng involves: 129/Sv * C57BL/6 MGI:3038737
ht2
Klf5tm1Rng/Klf5+ involves: 129 MGI:4421820
ht3
Klf5tm1Rng/Klf5+ involves: 129/Sv * C57BL/6 MGI:3038738


Genotype
MGI:3038737
hm1
Allelic
Composition
Klf5tm1Rng/Klf5tm1Rng
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Klf5tm1Rng mutation (0 available); any Klf5 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygous mutant embryos die prior to E8.5




Genotype
MGI:4421820
ht2
Allelic
Composition
Klf5tm1Rng/Klf5+
Genetic
Background
involves: 129
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Klf5tm1Rng mutation (0 available); any Klf5 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Pressure overload-induced cardiac hypertophy and fibrosis are reduced in Klf5tm1Rng/Klf5+ mice

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

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

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




Genotype
MGI:3038738
ht3
Allelic
Composition
Klf5tm1Rng/Klf5+
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Klf5tm1Rng mutation (0 available); any Klf5 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• heterozygotes exhibit abnormal thinning of the medial and adventitial layers of the aortic wall
• 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
• 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)
• 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
• 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
• 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)
• 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
• 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
• 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
• heterozygotes display abnormally shaped villi in the jejunum





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
04/30/2024
MGI 6.23
The Jackson Laboratory