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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Vav3tm1Xrb
targeted mutation 1, Xose R Bustelo
MGI:3514154
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Vav3tm1Xrb/Vav3tm1Xrb Not Specified MGI:3663760
cx2
Vav2tm1Tnr/Vav2tm1Tnr
Vav3tm1Xrb/Vav3tm1Xrb
involves: 129P2/OlaHsd MGI:3843285


Genotype
MGI:3663760
hm1
Allelic
Composition
Vav3tm1Xrb/Vav3tm1Xrb
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Vav3tm1Xrb mutation (0 available); any Vav3 mutation (55 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• cardiovascular defects are first detected at 4 months of age and progressively increase in aging mice; however no defects are seen in the right ventricle or in pulmonary arteries
• aorta media wall becomes thicker and disorganized, showing hyperplasia and hypertrophy of smooth muscle cells as well as increased deposition of extracellular matrix
• mice exhibit extensive vascular remodeling; administration of captopril, an angiotensin-converting enzyme inhibitor, decreases the cardiovascular remodeling
• hypertrophy of cardiomyocytes in the left heart ventricle
• left ventricular fibrosis; treatment with propranolol for 5 weeks prevents the development of fibrosis
• show high levels of angiotensin-converting enzyme in the heart
• lower +dP/dt max values
• more severe than in Vav2tm1Trn homozygotes (J:124056)
• systemic arterial hypertension, showing high systolic and diastolic blood pressure
• more severe than in Vav2tm1Trn homozygotes

growth/size/body

homeostasis/metabolism
• show an age dependent increase of angiotensin II and a concomitant reduction of bradykinin in plasma
• elevated from birth to adulthood, indicating hyperactivity of the sympathetic nervous system (J:111973)
• show an age dependent increase of angiotensin II in plasma
• exhibit high levels of vasopressin in newborns which increases further as they age
• aldosterone levels become elevated from 4 months of age onward
• elevated from birth to adulthood, indicating hyperactivity of the sympathetic nervous system (J:111973)
• activation of the renin-angiotensin system
• elevated from birth to adulthood, indicating hyperactivity of the sympathetic nervous system (J:111973)
• in the plasma (J:124056)
• show an age dependent increase of angiotensin II and a concomitant reduction of bradykinin in plasma
• potassium excretion rates of kidneys are lower
• kidneys have lower rates of sodium excretion and as a compensatory mechanism to keep the electrolyte balance, chloride excretion

nervous system
• exhibit hyperactivity of sympathetic neurons from the time of birth, as indicated by an increase in catecholamines

renal/urinary system
• potassium excretion rates of kidneys are lower
• kidneys have lower rates of sodium excretion and as a compensatory mechanism to keep the electrolyte balance, chloride excretion
• develop renal fibrosis in an age-dependent manner
• kidneys have lower rates of creatinine clearance
• urinary flow is about 85% lower than in controls

muscle
• hypertrophy of cardiomyocytes in the left heart ventricle
• lower +dP/dt max values




Genotype
MGI:3843285
cx2
Allelic
Composition
Vav2tm1Tnr/Vav2tm1Tnr
Vav3tm1Xrb/Vav3tm1Xrb
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Vav2tm1Tnr mutation (0 available); any Vav2 mutation (45 available)
Vav3tm1Xrb mutation (0 available); any Vav3 mutation (55 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in the plasma

cardiovascular system
• more severe than in Vav2tm1Trn homozygotes
• more severe than in Vav2tm1Trn homozygotes





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last database update
04/09/2024
MGI 6.23
The Jackson Laboratory