Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk14tm1.2Otsu mutation
(1 available);
any
Mapk14 mutation
(41 available)
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normal phenotype
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• appeared normal and indistinguishable from wild-type
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk14tm1.1Otsu mutation
(0 available);
any
Mapk14 mutation
(41 available)
Mapk14tm1.2Otsu mutation
(1 available);
any
Mapk14 mutation
(41 available)
Slc6a3tm1(cre)Xz mutation
(2 available);
any
Slc6a3 mutation
(66 available)
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behavior/neurological
N |
• performance on the rotarod is similar to controls, although there is a slight trend toward improved performance
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• resistant to agonist U50,488-induced conditioned place aversion (CPA)
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk14tm1.2Otsu mutation
(1 available);
any
Mapk14 mutation
(41 available)
Tg(Myh6-cre)2182Mds mutation
(3 available)
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mortality/aging
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• 30% of mutants died one week after TAC induced pressure overload compared to 8% in controls
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cardiovascular system
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• heart was larger than in controls after TAC induced pressure overload or adrenergic stimulation
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• heart weight, left ventricle weight, and average ratio of left ventricle weight to tibial length or body weight were significantly greater than in controls after TAC induced pressure overload, however no difference in cardiomyocyte cell area was observed
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• observed intermuscular and perivascular fibrosis in mutants compared to only slight perivascular fibrosis in controls after TAC induced pressure overload
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• mice exhibit normal cardiac function and structure under baseline conditions, however cardiac contractility was significantly reduced after thoracic transverse aortic constriction (TAC) induced pressure overload and chronic adrenergic stimulation
• increased left ventricle end-diastolic and end-systolic diameters compared to controls after TAC induced pressure overload
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• the number of apoptotic cardiac myocytes was 3.7 times that in controls after TAC induced pressure overload and was also increased in response to chronic adrenergic stimulation
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• after TAC induced pressure overload, exhibit greater increases in mortality, heart size and weight, cardiac fibrosis, and cardiomyocyte apoptosis and decreased cardiac contractility compared to controls
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muscle
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• mice exhibit normal cardiac function and structure under baseline conditions, however cardiac contractility was significantly reduced after thoracic transverse aortic constriction (TAC) induced pressure overload and chronic adrenergic stimulation
• increased left ventricle end-diastolic and end-systolic diameters compared to controls after TAC induced pressure overload
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• the number of apoptotic cardiac myocytes was 3.7 times that in controls after TAC induced pressure overload and was also increased in response to chronic adrenergic stimulation
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homeostasis/metabolism
cellular
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• the number of apoptotic cardiac myocytes was 3.7 times that in controls after TAC induced pressure overload and was also increased in response to chronic adrenergic stimulation
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growth/size/body
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• heart was larger than in controls after TAC induced pressure overload or adrenergic stimulation
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• heart weight, left ventricle weight, and average ratio of left ventricle weight to tibial length or body weight were significantly greater than in controls after TAC induced pressure overload, however no difference in cardiomyocyte cell area was observed
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk14tm1.2Otsu mutation
(1 available);
any
Mapk14 mutation
(41 available)
Tg(Col2a1-cre)1Bhr mutation
(3 available)
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skeleton
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• at 6 months in male mice
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• at 6 months in male mice
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• exaggerated in male mice at 6 months
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• short at 6 months in male mice
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growth/size/body
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• by 3 to 4 weeks in female and male mice
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• in male and female mice
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homeostasis/metabolism
limbs/digits/tail
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• at 6 months in male mice
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• at 6 months in male mice
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