Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rac1tm1.1Djk mutation
(0 available);
any
Rac1 mutation
(21 available)
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mortality/aging
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• no viable homozygous mutant embryos are found at E8.5 or later
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immune system
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• in vitro, mutant bone marrow neutrophils show a ~50% reduction in fMLP-induced chemotaxis relative to wild-type neutrophils both at 1 and 10 uM fMLP
• mutant neutrophils show a significant reduction in fMLP-induced F-actin formation, with a slower rate of actin polymerization relative to wild-type neutrophils
• however, both PMA- and fMLP-stimulated mutant bone marrow neutrophils exhibit normal superoxide production relative to wild-type neutrophils
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• 3 hrs after induction of peritonitis by sodium periodate injection, circulating leukocyte counts are not significantly increased, unlike in wild-type controls
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• 3 hrs after induction of peritonitis, only a small increase in peripheral neutrophil counts is observed, unlike in wild-type controls where circulating neutrophil counts are increased by >3-fold
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• 3 hrs after sodium periodate injection into the peritoneum, mutant mice exhibit a >50% reduction in neutrophil accumulation at the site of inflammation relative to wild-type controls
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• 3 hrs after i.p. injection of sodium periodate, mutant mice display impaired neutrophil chemotaxis and in vivo recruitment to sites of acute inflammation relative to wild-type controls
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hematopoietic system
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• in vitro, mutant bone marrow neutrophils show a ~50% reduction in fMLP-induced chemotaxis relative to wild-type neutrophils both at 1 and 10 uM fMLP
• mutant neutrophils show a significant reduction in fMLP-induced F-actin formation, with a slower rate of actin polymerization relative to wild-type neutrophils
• however, both PMA- and fMLP-stimulated mutant bone marrow neutrophils exhibit normal superoxide production relative to wild-type neutrophils
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• 3 hrs after induction of peritonitis by sodium periodate injection, circulating leukocyte counts are not significantly increased, unlike in wild-type controls
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• 3 hrs after induction of peritonitis, only a small increase in peripheral neutrophil counts is observed, unlike in wild-type controls where circulating neutrophil counts are increased by >3-fold
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• 3 hrs after sodium periodate injection into the peritoneum, mutant mice exhibit a >50% reduction in neutrophil accumulation at the site of inflammation relative to wild-type controls
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cellular
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• in vitro, mutant bone marrow neutrophils show a ~50% reduction in fMLP-induced chemotaxis relative to wild-type neutrophils both at 1 and 10 uM fMLP
• mutant neutrophils show a significant reduction in fMLP-induced F-actin formation, with a slower rate of actin polymerization relative to wild-type neutrophils
• however, both PMA- and fMLP-stimulated mutant bone marrow neutrophils exhibit normal superoxide production relative to wild-type neutrophils
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rac1tm1.1Djk mutation
(0 available);
any
Rac1 mutation
(21 available)
Rac1tm1Djk mutation
(1 available);
any
Rac1 mutation
(21 available)
Tg(Msx2-cre)5Rem mutation
(2 available)
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limbs/digits/tail
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• partial forelimb truncation
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rac1tm1.1Djk mutation
(0 available);
any
Rac1 mutation
(21 available)
Rac1tm1Djk mutation
(1 available);
any
Rac1 mutation
(21 available)
Tg(Myh6-cre/Esr1*)1Liao mutation
(0 available)
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cellular
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• superoxide anion production is reduced in cardiac-specific Rac1-nulls compared to wild-type in response to angiotensin II (increase of 3.3-fold in wild-type, 2.1-fold in heterozygotes and only 1.2 fold in Rac1 nulls)
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homeostasis/metabolism
cardiovascular system
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• 2 weeks after infusion of angiotensin II, hearts from cardiac-specific Rac1-deletion show reduced end-diastolic myocardial wall thickness
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• cross-sectional areas of cardiomyocytes in wild-type and Rac1 heterozygotes are increased in response to angiotensin II (300 and 270 um2 vs 200 um2 in untreated controls) but areas of cardiomyocytes from nulls show no change
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• 2 weeks after infusion of angiotensin II or saline, hearts from cardiac specific Rac1-deletion show less hypertrophy than wild-type or Rac1 heterozygotes
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• angiotensin II increases left ventricular mass of wild-type and Rac1 heterozygotes by 184 and 160% respectively, while cardiac-specific Rac1 nulls have only a 123% increase
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muscle
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• 2 weeks after infusion of angiotensin II, hearts from cardiac-specific Rac1-deletion show reduced end-diastolic myocardial wall thickness
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• cross-sectional areas of cardiomyocytes in wild-type and Rac1 heterozygotes are increased in response to angiotensin II (300 and 270 um2 vs 200 um2 in untreated controls) but areas of cardiomyocytes from nulls show no change
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growth/size/body
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• 2 weeks after infusion of angiotensin II or saline, hearts from cardiac specific Rac1-deletion show less hypertrophy than wild-type or Rac1 heterozygotes
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