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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Raf1tm1.1Bgn
targeted mutation 1.1, Benjamin G Neel
MGI:5003364
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
ht1
Raf1tm1.1Bgn/Raf1+ involves: 129S6/SvEvTac * C57BL/6NCr MGI:5003451


Genotype
MGI:5003451
ht1
Allelic
Composition
Raf1tm1.1Bgn/Raf1+
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6NCr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Raf1tm1.1Bgn mutation (1 available); any Raf1 mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following transverse aortic constriction (J:172034)
• following transverse aortic constriction (J:172034)

cardiovascular system
N
• fetal cardiomyocyte proliferation and valve development are normal (J:172034)
• fetal cardiomyocyte proliferation and valve development are normal (J:172034)
• following transverse aortic constriction (J:172034)
• following transverse aortic constriction (J:172034)
• at 8 weeks of age (J:172034)
• however, treatment with a MEK inhibitor rescues cardiomyocyte enlargement (J:172034)
• at 8 weeks of age (J:172034)
• however, treatment with a MEK inhibitor rescues cardiomyocyte enlargement (J:172034)
• as early as 2 weeks after birth (J:172034)
• following transverse aortic constriction (J:172034)
• as early as 2 weeks after birth (J:172034)
• following transverse aortic constriction (J:172034)
• however, treatment with MEK inhibitor rescues cardiac hypertrophy (J:172034)
• however, treatment with MEK inhibitor rescues cardiac hypertrophy (J:172034)
• increased left ventricular diastolic posterior wall thickness (J:189143)
• increased left ventricular internal end-diastolic dimension (J:189143)
• increased left ventricular diastolic posterior wall thickness (J:189143)
• increased left ventricular internal end-diastolic dimension (J:189143)
• mice exhibit increased ventricular wall thickness compared with wild-type mice (J:172034)
• at 2 and 4 months of age, left ventricular diastolic posterior wall thickness is increased compared to in wild-type mice (J:172034)
• mice exhibit increased ventricular wall thickness compared with wild-type mice (J:172034)
• at 2 and 4 months of age, left ventricular diastolic posterior wall thickness is increased compared to in wild-type mice (J:172034)
• following transverse aortic constriction (J:172034)
• following transverse aortic constriction (J:172034)
• at 4 months, mice exhibit increased left ventricle internal end-diastolic dimension (LVIDd) compared with wild-type mice (J:172034)
• however, LVIDd is normal at 2 months of age and left ventricle internal end-systolic dimension is normal (J:172034)
• at 4 months, mice exhibit increased left ventricle internal end-diastolic dimension (LVIDd) compared with wild-type mice (J:172034)
• however, LVIDd is normal at 2 months of age and left ventricle internal end-systolic dimension is normal (J:172034)
• following transverse aortic constriction, mice exhibit severe cardiac interstitial fibrosis and perivascular fibrosis compared with wild-type mice (J:172034)
• following transverse aortic constriction, mice exhibit severe cardiac interstitial fibrosis and perivascular fibrosis compared with wild-type mice (J:172034)
• following transverse aortic constriction (J:172034)
• following transverse aortic constriction (J:172034)
• mice exhibit abnormal cardiac function compared with wild-type mice (J:172034)
• however, treatment with a MEK inhibitor normalizes cardiac function (J:172034)
• mice exhibit abnormal cardiac function compared with wild-type mice (J:172034)
• however, treatment with a MEK inhibitor normalizes cardiac function (J:172034)
• as early as 2 weeks after birth (J:172034)
• as early as 2 weeks after birth (J:172034)
• at 2 and 4 months (J:172034)
• at 2 and 4 months (J:172034)
• increased (J:189143)
• increased (J:189143)
• at 2 and 4 months, mice exhibit increased stroke volume compared with wild-type mice (J:172034)
• following transverse aortic constriction, mice exhibit increased stroke volume compared with wild-type mice (J:172034)
• at 2 and 4 months, mice exhibit increased stroke volume compared with wild-type mice (J:172034)
• following transverse aortic constriction, mice exhibit increased stroke volume compared with wild-type mice (J:172034)
• following transverse aortic constriction (J:172034)
• following transverse aortic constriction (J:172034)
• at 2 and 4 months, mice exhibit increased ejection fraction and fractional shortening compared with wild-type mice (J:172034)
• however, cardiac relaxation is normal (J:172034)
• at 2 and 4 months, mice exhibit increased ejection fraction and fractional shortening compared with wild-type mice (J:172034)
• however, cardiac relaxation is normal (J:172034)
• increased fractional shortening and ejection fraction (J:189143)
• increased fractional shortening and ejection fraction (J:189143)
• at 4 months, mice exhibit decreased left ventricle pressure compared with wild-type mice (J:172034)
• at 4 months, mice exhibit decreased left ventricle pressure compared with wild-type mice (J:172034)
• following transverse aortic constriction (J:172034)
• following transverse aortic constriction (J:172034)
• following transverse aortic constriction, mice exhibit increased lethality, ventricular and left atrial enlargement, increased heart weight, severe interstitial fibrosis, perivascular fibrosis, deteriorating cardiac function (stroke volume and fractional shortening), decreased cardiac contractility, infarct, and fatal, functional decompensation in some mice compared with wild-type mice (J:172034)
• following transverse aortic constriction, mice exhibit increased lethality, ventricular and left atrial enlargement, increased heart weight, severe interstitial fibrosis, perivascular fibrosis, deteriorating cardiac function (stroke volume and fractional shortening), decreased cardiac contractility, infarct, and fatal, functional decompensation in some mice compared with wild-type mice (J:172034)

immune system
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• increasing in severity with age (J:172034)
• increasing in severity with age (J:172034)

craniofacial
• mice exhibit facial dysmorphia compared with wild-type mice (J:172034)
• however, treatment with a MEK inhibitory rescues facial dysmorphia (J:172034)
• mice exhibit facial dysmorphia compared with wild-type mice (J:172034)
• however, treatment with a MEK inhibitory rescues facial dysmorphia (J:172034)
• blunt snout (J:172034)
• blunt snout (J:172034)

growth/size/body
• mice exhibit facial dysmorphia compared with wild-type mice (J:172034)
• however, treatment with a MEK inhibitory rescues facial dysmorphia (J:172034)
• mice exhibit facial dysmorphia compared with wild-type mice (J:172034)
• however, treatment with a MEK inhibitory rescues facial dysmorphia (J:172034)
• blunt snout (J:172034)
• blunt snout (J:172034)
• at weaning (J:172034)
• at weaning (J:172034)
• however, mice treated with a MEK inhibitor normalizes weight (J:172034)
• however, mice treated with a MEK inhibitor normalizes weight (J:172034)
• however, mice treated with a MEK inhibitor normalizes length (J:172034)
• however, mice treated with a MEK inhibitor normalizes length (J:172034)

homeostasis/metabolism
• following transverse aortic constriction, mice exhibit increased lethality, ventricular and left atrial enlargement, increased heart weight, severe interstitial fibrosis, perivascular fibrosis, deteriorating cardiac function (stroke volume and fractional shortening), decreased cardiac contractility, infarct, and fatal, functional decompensation in some mice compared with wild-type mice (J:172034)
• following transverse aortic constriction, mice exhibit increased lethality, ventricular and left atrial enlargement, increased heart weight, severe interstitial fibrosis, perivascular fibrosis, deteriorating cardiac function (stroke volume and fractional shortening), decreased cardiac contractility, infarct, and fatal, functional decompensation in some mice compared with wild-type mice (J:172034)

muscle
• at 8 weeks of age (J:172034)
• however, treatment with a MEK inhibitor rescues cardiomyocyte enlargement (J:172034)
• at 8 weeks of age (J:172034)
• however, treatment with a MEK inhibitor rescues cardiomyocyte enlargement (J:172034)
• as early as 2 weeks after birth (J:172034)
• as early as 2 weeks after birth (J:172034)
• following transverse aortic constriction (J:172034)
• following transverse aortic constriction (J:172034)
• at 2 and 4 months, mice exhibit increased ejection fraction and fractional shortening compared with wild-type mice (J:172034)
• however, cardiac relaxation is normal (J:172034)
• at 2 and 4 months, mice exhibit increased ejection fraction and fractional shortening compared with wild-type mice (J:172034)
• however, cardiac relaxation is normal (J:172034)
• increased fractional shortening and ejection fraction (J:189143)
• increased fractional shortening and ejection fraction (J:189143)

skeleton

vision/eye

hematopoietic system
• myeloid progenitors are expanded compared to in wild-type mice (J:172034)
• myeloid progenitors are expanded compared to in wild-type mice (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• at 1 year of age (J:172034)
• increasing in severity with age (J:172034)
• increasing in severity with age (J:172034)

Mouse Models of Human Disease
OMIM ID Ref(s)
Noonan Syndrome 5; NS5 611553 J:172034





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last database update
01/26/2016
MGI 6.02
The Jackson Laboratory