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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ptgirtm1Sna
targeted mutation 1, Shuh Narumiya
MGI:2137832
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ptgirtm1Sna/Ptgirtm1Sna B6.129P2-Ptgirtm1Sna/Sna MGI:5517586
hm2
Ptgirtm1Sna/Ptgirtm1Sna involves: 129P2/OlaHsd * C57BL/6 MGI:2175008
hm3
Ptgirtm1Sna/Ptgirtm1Sna involves: 129P2/OlaHsd * C57BL/6Cr MGI:3603299
cx4
Ptgirtm1Sna/Ptgirtm1Sna
Tbxa2rtm1Cof/Tbxa2rtm1Cof
129-Ptgirtm1Sna Tbxa2rtm1Cof MGI:3603361


Genotype
MGI:5517586
hm1
Allelic
Composition
Ptgirtm1Sna/Ptgirtm1Sna
Genetic
Background
B6.129P2-Ptgirtm1Sna/Sna
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgirtm1Sna mutation (1 available); any Ptgir mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• in a model of IgE antigen-dependent passive cutaneous anaphylaxis, mice exhibit normal dye extravasation (a measure of edema)




Genotype
MGI:2175008
hm2
Allelic
Composition
Ptgirtm1Sna/Ptgirtm1Sna
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgirtm1Sna mutation (1 available); any Ptgir mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• homozygotes that survive to birth grow normally, are fertile and live >1 year in the absence of overt abnormalities
• breeding of heterozygotes produces homozygotes at a lower frequency than the predicted Mendelian ratio, suggesting embryonic loss esp. in males

homeostasis/metabolism
• homozygotes fail to exhibit prolonged bleeding times in response to beraprost (a prostacyclin mimetic), unlike wild-type mice
• in response to catheter-induced carotid vascular injury, homozygotes display enhanced platelet activation, as shown by an increased injury-related increment in urinary excretion of metabolite 2,3-dinor-TxB2
• homozygotes do not develop spontaneous thrombosis but exhibit increased susceptibility to arterial thrombosis induced by FeCl3 (J:42275)
• at 4 hrs after FeCl3 exposure, ~2/3 of mutant arteries exhibit obstructive thrombi with reddish tails, whereas wild-type preparations display mural thrombi of yellowish color (J:42275)
• after prolonged FeCl3 treatment, 30% of homozygotes die within 1 day due to bilateral occlusions of the carotid arteries and/or embolic stroke, whereas all wild-type mice survive treatment (J:42275)
• carotid artery occlusion time after photochemical injury is shortened (J:108957)
• homozygotes show a normal prostacyclin concentration in the peritoneal lavage fluid after dilute acetic acid treatment; in contrast, PGE2 levels are reduced to ~25% of prostacyclin levels
• after catheter-induced carotid vascular injury, homozygotes show an increased periprocedural increment in urinary metabolite 2,3-dinor-TxB2

immune system
• in the carrageenin-induced paw-edema model, homozygotes exhibit reduced edema formation similar to that observed in indomethacin-pretreated wild-type mice
• in addition, homozygotes display a marked reduction of exudate volume in the carrageenin-induced pleurisy model

behavior/neurological
• in the acetic acid-induced writhing test, homozygotes exhibit reduced nociceptive perception to levels noted in indomethacin-pretreated wild-type mice
• notably, prostacyclin induces a writhing response in 60% of wild-type mice and in 0% of mutant mice, whereas PGE2 induces a response in less than 25% of animals in both genotypes

cardiovascular system
N
• under basal conditions, homozygotes are normotensive and exhibit a normal heart rate and normal bleeding times relative to wild-type mice
• in response to catheter-induced carotid vascular injury, homozygotes exhibit an increased % of luminal stenosis relative to wild-type mice
• in response to catheter-induced carotid vascular injury, homozygotes exhibit enhanced vascular proliferative indices, as shown by a significant increase in the intima-to-media ratio, % of luminal stenosis, and the number of intimal and medial BrdU-labeled cells relative to wild-type mice

hematopoietic system
• in response to catheter-induced carotid vascular injury, homozygotes display enhanced platelet activation, as shown by an increased injury-related increment in urinary excretion of metabolite 2,3-dinor-TxB2




Genotype
MGI:3603299
hm3
Allelic
Composition
Ptgirtm1Sna/Ptgirtm1Sna
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6Cr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgirtm1Sna mutation (1 available); any Ptgir mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• 9-week-old males treated with colon carcinogen azoxymethane exhibit no significant differences in the numbers of aberrant crypt (AC) foci per colon or ACs per focus relative to wild-type counterparts
• ACF formation in the distal colon is associated with a slight increase in spleen weight




Genotype
MGI:3603361
cx4
Allelic
Composition
Ptgirtm1Sna/Ptgirtm1Sna
Tbxa2rtm1Cof/Tbxa2rtm1Cof
Genetic
Background
129-Ptgirtm1Sna Tbxa2rtm1Cof
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgirtm1Sna mutation (1 available); any Ptgir mutation (32 available)
Tbxa2rtm1Cof mutation (0 available); any Tbxa2r mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• following catheter-induced carotid vascular injury, double homozygotes fail to exhibit the enhanced vascular proliferative response observed in Ptgirtm1Sna homozygotes
• in double homozygotes, the intima-to-media ratio, % of luminal stenosis, and the number of BrdU-labeled cells is comparable to observed in wild-type mice; in addition, the periprocedural increment in platelet activation noted in Ptgirtm1Sna homozygotes is abolished





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory