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Phenotypes Associated with This Genotype
Genotype
MGI:3038598
Allelic
Composition
F2rtm1Pago/F2rtm1Pago
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rtm1Pago mutation (0 available); any F2r mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• a large portion of embryos are resorbed after E10, though some mice develop normally and survive to adulthood

cardiovascular system
N
• mice that survive to adulthood exhibit normal platelet number and function, coagulation parameters, basal heart rate, and arterial blood pressure (J:38032)
• mutants exhibit normal pulmonary vasoreactivity to vasoactive mediators (J:124465)
• cell density is greater in normal carotids from mutants than in wild-type mice
• mutants exhibit a reduction of the hypertensive response to the selective thrombin receptor activating peptide, SFLLRN-NH2, before and after L-NAME (an inhibitor of nitric oxide synthesis) and absence of hypertension in the presence of L-NAME
• mutants show absence of an arterial pressure response to the selective thrombin receptor activating peptide, TFLLRNPNDK-NH2
• the hypertensive response and heart rate decrease in response to TFLLRNPNDK, a F2r (PAR-1) selective activating peptide, is absent
• SFLLRN, a nonselective receptor activating peptide, was able to induce hypotension in mutants as in wild-type mice but the heart rate decrease and secondary hypotension following L-NAME are absent
• the thrombin-induced increase in pulmonary microvessel permeability seen in controls is absent in mutants
• vessel diameter is unchanged and lumen diameter decreases following vascular injury unlike in wild-type mice in which vessel and lumen diameters increase following injury
• area of neointima formation following vascular injury is slightly less than in wild-type mice
• however, medial cell loss, incidence of thrombosis, endothelial regrowth, and medial thickening after injury are similar to wild-type

reproductive system
• matings between homozygous mice occur infrequently and produce less than 3 offspring

homeostasis/metabolism
• vessel diameter is unchanged and lumen diameter decreases following vascular injury unlike in wild-type mice in which vessel and lumen diameters increase following injury
• area of neointima formation following vascular injury is slightly less than in wild-type mice
• however, medial cell loss, incidence of thrombosis, endothelial regrowth, and medial thickening after injury are similar to wild-type

digestive/alimentary system
• mutants have a lower baseline short-circuit current in the colon than wild-type mice but no difference in the short-circuit current response to electrical field stimulation, indicating abnormal basal ion secretion in the colon
• trinitrobenzene sulfonic acid (TNBS) induced colitis is less severe in mutants than in wild-type mice

immune system
• absence of human trypsin IV and rat p23 induced edema and granulocyte infiltration after intraplantar injection
• trinitrobenzene sulfonic acid (TNBS) induced colitis is less severe in mutants than in wild-type mice


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
06/12/2024
MGI 6.13
The Jackson Laboratory