Analysis Tools|
Allele Symbol Allele Name Allele ID |
Fkbp1atm1.1Shou targeted mutation 1.1, Weinian Shou MGI:5319193 |
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| Summary |
9 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• animals show normal ventricular chamber formation; no hypertrabeculation or noncompaction is detected with cardiomyocyte-specific Fkbp1a ablation
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| N |
• mice survive to adulthood
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• death occurs between E14.5 and birth
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• mutants phenocopy Fkbp1atm1Zuk mice, showing hypertrabeculation, noncompaction, and ventral septal defects (VSDs) with complete penetrance
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• animals show normal ventricular chamber formation; normal trabeculation and compaction in ventricles are observed
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• animals show normal ventricular chamber formation; normal trabeculation and compaction in ventricles are observed
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• all mutants survive through birth, but all die within 1 month of birth (proposed to be due to defective thymus development)
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| N |
• animals show normal ventricular chamber formation; normal trabeculation and compaction in ventricles are observed
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• most animals survive through gestation, but most survivors die within 8 weeks of birth likely as result of compromised cardiac function
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• edematous embryos at E13.5-14.5 have enlarged hearts
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• affected mutants phenocopy Fkbp1atm1Zuk mice, showing ventricular hypertrabeculation and noncompaction
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• observed in affected mutants at E13.5-14.5
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• prominent defects (both membranous and muscular) in origin are observed in ~40% of affected embryos at E13.5-14.5
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• affected embryos at E13.5-14.5 have hearts that are that are 'pumpkin-shaped', lacking the ventricular groove
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• edematous (affected) embryos at E13.5-14.5 show signs of failing hearts
• surviving mice at 8 weeks display compromised cardiac function
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• edematous embryos at E13.5-14.5 have enlarged hearts
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• observed in affected mutants at E13.5-14.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• cardiac development appears normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• cardiac development appears normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• shorter PP interval
• significant acceleration of the maximal phase 0 upstroke velocity in the left ventricle
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• mean peak macroscopic voltage-gated Na+ current densities are increased more than 2 fold in ventricular cardiomyocytes
• acceleration of both the early and late component of voltage-gated Na+ current inactivation in ventricular cardiomyocytes
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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 11/19/2024 MGI 6.24 |
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