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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Mapk14tm1.2Otsu
targeted mutation 1.2, Kinya Otsu
MGI:3525576
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Mapk14tm1.2Otsu/Mapk14tm1.2Otsu involves: C57BL/6J MGI:3525857
cn2
Mapk14tm1.1Otsu/Mapk14tm1.2Otsu
Slc6a3tm1(cre)Xz/0
involves: 129S1/Sv * C57BL/6 MGI:5824896
cn3
Mapk14tm1.2Otsu/Mapk14tm1.2Otsu
Tg(Myh6-cre)2182Mds/0
involves: C57BL/6J MGI:3525858
cn4
Mapk14tm1.2Otsu/Mapk14tm1.2Otsu
Tg(Col2a1-cre)1Bhr/0
involves: C57BL/6 * SJL MGI:5532835


Genotype
MGI:3525857
hm1
Allelic
Composition
Mapk14tm1.2Otsu/Mapk14tm1.2Otsu
Genetic
Background
involves: C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk14tm1.2Otsu mutation (1 available); any Mapk14 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• appeared normal and indistinguishable from wild-type




Genotype
MGI:5824896
cn2
Allelic
Composition
Mapk14tm1.1Otsu/Mapk14tm1.2Otsu
Slc6a3tm1(cre)Xz/0
Genetic
Background
involves: 129S1/Sv * C57BL/6
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)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• performance on the rotarod is similar to controls, although there is a slight trend toward improved performance
• resistant to agonist U50,488-induced conditioned place aversion (CPA)




Genotype
MGI:3525858
cn3
Allelic
Composition
Mapk14tm1.2Otsu/Mapk14tm1.2Otsu
Tg(Myh6-cre)2182Mds/0
Genetic
Background
involves: C57BL/6J
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)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 30% of mutants died one week after TAC induced pressure overload compared to 8% in controls

cardiovascular system
• heart was larger than in controls after TAC induced pressure overload or adrenergic stimulation
• 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
• observed intermuscular and perivascular fibrosis in mutants compared to only slight perivascular fibrosis in controls after TAC induced pressure overload
• 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
• 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
• 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

muscle
• 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
• 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

homeostasis/metabolism
• 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

cellular
• 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

growth/size/body
• heart was larger than in controls after TAC induced pressure overload or adrenergic stimulation
• 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




Genotype
MGI:5532835
cn4
Allelic
Composition
Mapk14tm1.2Otsu/Mapk14tm1.2Otsu
Tg(Col2a1-cre)1Bhr/0
Genetic
Background
involves: C57BL/6 * SJL
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)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• at 6 months in male mice
• at 6 months in male mice
• exaggerated in male mice at 6 months
• short at 6 months in male mice

growth/size/body
• by 3 to 4 weeks in female and male mice
• in male and female mice

homeostasis/metabolism
N
• mice exhibit normal IGF1 serum levels

limbs/digits/tail
• at 6 months in male mice
• at 6 months in male mice





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last database update
05/07/2024
MGI 6.23
The Jackson Laboratory