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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
P2rx4tm1Ando
targeted mutation 1, Joji Ando
MGI:3612982
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
P2rx4tm1Ando/P2rx4tm1Ando Not Specified MGI:3613446


Genotype
MGI:3613446
hm1
Allelic
Composition
P2rx4tm1Ando/P2rx4tm1Ando
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
P2rx4tm1Ando mutation (0 available); any P2rx4 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• the diameter of the right common carotid artery is reduced and its walls are thicker
• homozygotes display a higher mean arterial pressure than wild-type controls
• however, no significant difference in heart rate is observed
• unlike in wild-type controls, chronic ligation of the left external carotid artery fails to result in a reduction in the lumen diameter of the left common carotid artery and medial wall thickness is increased, indicating a defect in flow-dependent vascular remodeling
• in response to blood flow stimulation, isolated mutant endothelial cells fail to exhibit a shear stress-dependent increase in Ca2+ influx and subsequent production of the potent vasodilator nitric oxide (NO)
• adenovirus vector-mediated gene transfer rescues the impaired flow-induced influx of Ca2+ and production of NO in cultured endothelial cells
• ATP-, but not acetylcholine-induced, vasodilation is significantly suppressed in preconstricted mutant cremaster muscle arterioles relative to wild-type arterioles
• following occlusion of one arteriole branch with a glass micropipette to increase blood flow through the other branch, flow-induced vasodilation is significantly reduced in mutant cremaster muscle arterioles relative to wild-type arterioles
• both ATP- and flow-induced (shear stress, 20 dynes/cm2), but not acetylcholine-induced, vasodilation is significantly reduced in mutant mesenteric arteries relative to wild-type arteries
• addition of EGTA or L-NAME significantly reduces flow-induced vasodilation in both genotypes, indicating that Ca2+ influx and NO mediate the vasodilatory response

muscle
• ATP-, but not acetylcholine-induced, vasodilation is significantly suppressed in preconstricted mutant cremaster muscle arterioles relative to wild-type arterioles
• following occlusion of one arteriole branch with a glass micropipette to increase blood flow through the other branch, flow-induced vasodilation is significantly reduced in mutant cremaster muscle arterioles relative to wild-type arterioles
• both ATP- and flow-induced (shear stress, 20 dynes/cm2), but not acetylcholine-induced, vasodilation is significantly reduced in mutant mesenteric arteries relative to wild-type arteries
• addition of EGTA or L-NAME significantly reduces flow-induced vasodilation in both genotypes, indicating that Ca2+ influx and NO mediate the vasodilatory response

homeostasis/metabolism
• mutant endothelial cells fail to exhibit flow-induced production of NO
• homozygotes excrete reduced amounts of NO products in urine
• homozygotes show a significant reduction in the daily amount of nitrite (and nitrate) excreted in urine relative to wild-type controls

renal/urinary system
• homozygotes show a significant reduction in the daily amount of nitrite (and nitrate) excreted in urine relative to wild-type controls





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory