Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
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muscle
N |
• no change in the abundance of slow fibers
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
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cardiovascular system
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• by 8 months of age mutant hearts are 20% larger than wild-type due to hypertrophy
• the hypertrophic response induced by increased afterload is increased in mutants compared to wild-type mice
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growth/size/body
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• by 8 months of age mutant hearts are 20% larger than wild-type due to hypertrophy
• the hypertrophic response induced by increased afterload is increased in mutants compared to wild-type mice
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac4tm1Eno mutation
(0 available);
any
Hdac4 mutation
(110 available)
Hdac4tm2.1Eno mutation
(0 available);
any
Hdac4 mutation
(110 available)
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
Tg(Myog-cre)1Eno mutation
(0 available)
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muscle
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• soleus muscles show an increase in the percentage of slow myofibers
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac4tm1Eno mutation
(0 available);
any
Hdac4 mutation
(110 available)
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
Hdac9tm1Eno mutation
(0 available);
any
Hdac9 mutation
(49 available)
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muscle
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• increase in slow fibers
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
Pkd2tm2Som mutation
(0 available);
any
Pkd2 mutation
(84 available)
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mortality/aging
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• only 1 mouse is present at E18.5
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
Pkd2tm2Som mutation
(0 available);
any
Pkd2 mutation
(84 available)
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renal/urinary system
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• mice exhibit reduced kidney cyst formation compared with Pkd2tm2Som homozygotes
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growth/size/body
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• mice exhibit reduced kidney cyst formation compared with Pkd2tm2Som homozygotes
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
Hdac9tm1Eno mutation
(0 available);
any
Hdac9 mutation
(49 available)
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mortality/aging
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• double homozygous embryos begin to die around E15.5 with only about 12% of double homozygotes surviving to adulthood
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cardiovascular system
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• at E15.5 ventricular septal defects were seen in 77% of double homozygous embryos often associated with hemorrhages
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• 1 month old mutant heart to body weight ratios are increased and markers of cardiac hypertrophy are upregulated
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• at E15.5 thin ventricular walls were seen in 20% of double homozygous embryos often associated with hemorrhages
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• hemorrhages are seen throughout the body of some mutant embryos at E15.5
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growth/size/body
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• 1 month old mutant heart to body weight ratios are increased and markers of cardiac hypertrophy are upregulated
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• severe growth retardation is seen with surviving adults weighing 1/3 as much as wild-type mice
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muscle
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• soleus muscles show an increase in the percentage of slow myofibers
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
Tg(Myh6-Camta2)1Eno mutation
(0 available)
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cardiovascular system
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• exhibit even more enhanced cardiac hypertrophy (twice the amount) than single transgenic Tg(Myh6-Camta2)1Eno mice
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growth/size/body
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• exhibit even more enhanced cardiac hypertrophy (twice the amount) than single transgenic Tg(Myh6-Camta2)1Eno mice
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac5tm1Eno mutation
(0 available);
any
Hdac5 mutation
(56 available)
Tg(Myh6-Ppp3ca)37Eno mutation
(1 available)
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mortality/aging
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• transgenic mice are highly susceptible to sudden death from heart failure with none surviving beyond 8 weeks of age
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cardiovascular system
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• by 4 weeks of age mutant hearts are 3-fold larger than wild-type due to hypertrophy
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growth/size/body
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• by 4 weeks of age mutant hearts are 3-fold larger than wild-type due to hypertrophy
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