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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Juptm1.1Glr
targeted mutation 1.1, Glenn L Radice
MGI:4947239
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Juptm1.1Glr/Juptm1.1Glr
Tg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/N * SJL MGI:4947241


Genotype
MGI:4947241
cn1
Allelic
Composition
Juptm1.1Glr/Juptm1.1Glr
Tg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Juptm1.1Glr mutation (1 available); any Jup mutation (138 available)
Tg(Myh6-cre/Esr1*)1Jmk mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increase in cardiac death compared to controls beginning about 3 months after tamoxifen treatment

cardiovascular system
N
• unlike in human patients with Arrhythmogenic Right Ventricular Dysplasia replacement of myocytes with adipocytes is not seen in tamoxifen treated mice and tamoxifen treated mice are not more susceptible to induced arrhythmias
• decrease in the number and length of desmosomes in tamoxifen treated mice
• adherens-type junctions with less submembranous electron-dense material are prominently seen in tamoxifen treated mice
• mislocalization of desmosomal proteins to the intercalated disc in tamoxifen treated mice
• increase in cardiomyocyte cross sectional area with age in tamoxifen treated mice
• increase in the heart to body weight ratio with age in tamoxifen treated mice
• by about 5 months after tamoxifen treatment
• mild left ventricle hypertrophy in tamoxifen treated mice
• modest left ventricle dilation in tamoxifen treated mice
• progressive thinning of the right ventricular free wall is seen after tamoxifen treatment
• by about 5 months after tamoxifen treatment
• focal areas of myocyte loss and replacement with fibrous tissue are seen after tamoxifen treatment
• increased apoptosis is seen at 5 months after tamoxifen treatment
• apoptotic cells are associated with fibrotic areas
• heart failure is seen in some tamoxifen treated mice
• reduction of left ventricular fractional shortening and ejection fraction in tamoxifen treated mice
• infiltration of activated macrophages/monocytes in areas adjacent to apoptotic myocytes in tamoxifen treated mice
• neutrophil infiltrations are also seen in tamoxifen treated mice

muscle
• decrease in the number and length of desmosomes in tamoxifen treated mice
• adherens-type junctions with less submembranous electron-dense material are prominently seen in tamoxifen treated mice
• mislocalization of desmosomal proteins to the intercalated disc in tamoxifen treated mice
• increase in cardiomyocyte cross sectional area with age in tamoxifen treated mice
• reduction of left ventricular fractional shortening and ejection fraction in tamoxifen treated mice
• cardiomyocyte sarcomeres have wider, less dense Z lines in tamoxifen treated mice
• cardiomyocyte sarcomeres appear distorted and compressed in tamoxifen treated mice
• decreased cardiomyocyte sarcomere length in tamoxifen treated mice

homeostasis/metabolism
• seen at 9 - 12 months after tamoxifen treatment, associated with heart failure
• increase in the IL6 and IL1B levels in heart lysates from tamoxifen treated mice
• increase in cytokine expression is associated with the severity of myocyte loss

immune system
• infiltration of activated macrophages/monocytes in areas adjacent to apoptotic myocytes in tamoxifen treated mice
• neutrophil infiltrations are also seen in tamoxifen treated mice
• increase in the IL6 and IL1B levels in heart lysates from tamoxifen treated mice
• increase in cytokine expression is associated with the severity of myocyte loss

respiratory system
• seen at 9 - 12 months after tamoxifen treatment, associated with heart failure





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last database update
05/17/2016
MGI 6.03
The Jackson Laboratory