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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Mliptm1.1(cre)Dzw
targeted mutation 1.1, Da-Zhi Wang
MGI:5907348
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Mliptm1.1(cre)Dzw/Mliptm1.1(cre)Dzw involves: C57BL/6 MGI:5907350
cx2
Lmnatm1Stw/Lmna+
Mliptm1.1(cre)Dzw/Mliptm1.1(cre)Dzw
involves: 129S1/Sv * C57BL/6 MGI:5907352
cx3
Lmnatm1Stw/Lmnatm1Stw
Mliptm1.1(cre)Dzw/Mliptm1.1(cre)Dzw
involves: 129S1/Sv * C57BL/6 MGI:5907353
cx4
Lmnatm1Stw/Lmnatm1Stw
Mliptm1.1(cre)Dzw/Mlip+
involves: 129S1/Sv * C57BL/6 MGI:5907354
cx5
Mliptm1.1(cre)Dzw/Mliptm1.1(cre)Dzw
Tg(Myh6-Ppp3ca)37Eno/0
involves: C57BL/6 * FVB MGI:5907351


Genotype
MGI:5907350
hm1
Allelic
Composition
Mliptm1.1(cre)Dzw/Mliptm1.1(cre)Dzw
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mliptm1.1(cre)Dzw mutation (0 available); any Mlip mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• greater increase in cross-sectional area following transverse aortic constriction compared to controls
• increase in absolute and relative left ventricular mass at 11 months of age but not in mice at 3 or 6 months of age
• increase in left ventricular dimension in aged mice
• transverse aortic constriction induced dramatic left ventricular dilation unlike in wild-type controls where this treatment induces left ventricular hypertrophy
• extensive fibrosis following transverse aortic constriction
• depressed cardiac function in older mice
• however, no detectable cardiac defects in young mice
• decrease in ejection fraction and fractional shortening at 11 and 18 months of age but not at 3 or 6 months of age
• dramatic decrease following transverse aortic constriction
• transverse aortic constriction induced dramatic left ventricular dilation unlike in wild-type controls where this treatment induces left ventricular hypertrophy
• dramatic decrease in cardiac contraction and increase in fibrosis and cardiomyocyte size following transverse aortic constriction

homeostasis/metabolism
• transverse aortic constriction induced dramatic left ventricular dilation unlike in wild-type controls where this treatment induces left ventricular hypertrophy
• dramatic decrease in cardiac contraction and increase in fibrosis and cardiomyocyte size following transverse aortic constriction

muscle
• greater increase in cross-sectional area following transverse aortic constriction compared to controls
• decrease in ejection fraction and fractional shortening at 11 and 18 months of age but not at 3 or 6 months of age
• dramatic decrease following transverse aortic constriction




Genotype
MGI:5907352
cx2
Allelic
Composition
Lmnatm1Stw/Lmna+
Mliptm1.1(cre)Dzw/Mliptm1.1(cre)Dzw
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lmnatm1Stw mutation (3 available); any Lmna mutation (82 available)
Mliptm1.1(cre)Dzw mutation (0 available); any Mlip mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• progressive increase in left ventricular internal dimension at end-diastole from 6 to 12 months of age
• at 12 months of age
• progressive decrease in fractional shortening from 6 to 12 months of age

muscle
• at 12 months of age
• progressive decrease in fractional shortening from 6 to 12 months of age




Genotype
MGI:5907353
cx3
Allelic
Composition
Lmnatm1Stw/Lmnatm1Stw
Mliptm1.1(cre)Dzw/Mliptm1.1(cre)Dzw
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lmnatm1Stw mutation (3 available); any Lmna mutation (82 available)
Mliptm1.1(cre)Dzw mutation (0 available); any Mlip mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die earlier than mice homozygous for the Lmna mutation alone

cardiovascular system
• dilation is more severe than in mice homozygous for the Lmna mutation alone
• cardiac dysfunction is more severe than in mice homozygous for the Lmna mutation alone

muscle
• cardiac dysfunction is more severe than in mice homozygous for the Lmna mutation alone




Genotype
MGI:5907354
cx4
Allelic
Composition
Lmnatm1Stw/Lmnatm1Stw
Mliptm1.1(cre)Dzw/Mlip+
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lmnatm1Stw mutation (3 available); any Lmna mutation (82 available)
Mliptm1.1(cre)Dzw mutation (0 available); any Mlip mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die earlier than mice homozygous for the Lmna mutation alone




Genotype
MGI:5907351
cx5
Allelic
Composition
Mliptm1.1(cre)Dzw/Mliptm1.1(cre)Dzw
Tg(Myh6-Ppp3ca)37Eno/0
Genetic
Background
involves: C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mliptm1.1(cre)Dzw mutation (0 available); any Mlip mutation (28 available)
Tg(Myh6-Ppp3ca)37Eno mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• half die by 10 weeks of age and all die by 18 weeks of age
• die earlier than mice carrying Tg(Myh6-Ppp3ca)37Eno alone
• appear to die from heart failure

cardiovascular system
• decrease in left ventricular wall thickness
• increase in left ventricular dimension and decrease in wall thickness
• fractional shortening is around 10%

muscle
• fractional shortening is around 10%





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
05/07/2024
MGI 6.23
The Jackson Laboratory