Phenotypes associated with this allele

• Allele Symbol: F3^tm1.1Dwr
• Allele Name: targeted mutation 1.1, Mieke Dewerchin
• Allele ID: MGI:2178048
• Summary: 5 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	F3^tm1.1Dwr/F3^tm1.1Dwr	B6.129-F3^tm1.1Dwr	MGI:4829886
hm2	F3^tm1.1Dwr/F3^tm1.1Dwr	involves: 129S1/Sv * 129X1/SvJ * BALB/c * C57BL/6	MGI:3846601
hm3	F3^tm1.1Dwr/F3^tm1.1Dwr	involves: 129S1/Sv * 129X1/SvJ * MF1 * Swiss	MGI:3846611
cx4	F2r^tm1Pago/F2r^tm1Pago F3^tm1.1Dwr/F3^tm1.1Dwr	B6.129-F3^tm1.1Dwr F2r^tm1Pago	MGI:4829887
cx5	F2rl1^tm1Bpd/F2rl1^tm1Bpd F3^tm1.1Dwr/F3^tm1.1Dwr	B6.129-F3^tm1.1Dwr F2rl1^tm1Bpd	MGI:4829888

Genotype
MGI:4829886

hm1

• Allelic Composition: F3^tm1.1Dwr/F3^tm1.1Dwr
• Genetic Background: B6.129-F3^tm1.1Dwr

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cardiovascular system

abnormal induced retina neovascularization ( J:135087 )

• mice exhibit enhanced retinal revascularization following oxygen induced retinopathy; the superficial vascular plexus reforms more quickly than in wild-type mice

vision/eye

abnormal induced retina neovascularization ( J:135087 )

• mice exhibit enhanced retinal revascularization following oxygen induced retinopathy; the superficial vascular plexus reforms more quickly than in wild-type mice

Genotype
MGI:3846601

hm2

• Allelic Composition: F3^tm1.1Dwr/F3^tm1.1Dwr
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * BALB/c * C57BL/6

hematopoietic system

hematopoietic system phenotype ( J:71271 )

N • mice exhibit normal homeostasis and pathological thrombosis

Genotype
MGI:3846611

hm3

• Allelic Composition: F3^tm1.1Dwr/F3^tm1.1Dwr
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * MF1 * Swiss

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:91165 )

• mice challenged with endotoxin exhibit increased survival compared with similarly treated wild-type mice

immune system

abnormal cellular extravasation ( J:91165 )

• reduced after endotoxin challenge

abnormal leukocyte adhesion ( J:91165 )

• reduced after endotoxin challenge

impaired leukocyte tethering or rolling ( J:91165 )

• leukocyte rolling is reduced after endotoxin challenge while rolling velocity is increased compared to in similarly treated wild-type mice

decreased leukocyte cell number ( J:91165 )

• 6 hours after endotoxin challenge, leukocytosis is attenuated compared to in similarly treated wild-type mice

• 1 hour after endotoxin challenge, accumulation of pulmonary leukocytes as measured by MPO activity is decreased compared to in similarly treated wild-type mice

decreased neutrophil cell number ( J:91165 )

• 6 and 24 hours after endotoxin challenge

decreased B cell number ( J:91165 )

• 6 hours after endotoxin challenge

decreased circulating interleukin-1 beta level ( J:91165 )

• following endotoxin challenge, mice exhibit a slower increase in IL1b levels compared with similarly treated wild-type mice

decreased circulating interleukin-6 level ( J:91165 )

• following endotoxin challenge, mice exhibit a sharper decline in IL6 levels 24 hours after challenge compared with similarly treated wild-type mice

decreased circulating tumor necrosis factor level ( J:91165 )

• following endotoxin challenge, mice exhibit decreased peak serum TNF-alpha levels compared with similarly treated wild-type mice

decreased susceptibility to endotoxin shock ( J:91165 )

• mice challenged with endotoxin exhibit increased survival, and decreased peak serum TNF-alpha levels, a slower rise in IL1b levels, a sharper decline in IL6 levels 24 hours after challenge, attenuated leukocytosis 6 hours after challenge, decreased neutrophil counts 6 and 24 hours after challenge, decreased B cell numbers 6 hours after challenge, decreased MPO activity 1 hour after challenge, decreased polymononuclear infiltration, and reduced leukocyte recruitment parameterd compared with similarly treated wild-type mice

homeostasis/metabolism

abnormal vascular wound healing ( J:111390 )

• following transluminal wire injury or ligation of the carotid artery, the intima to media ratio is decreased compared to in similarly treated wild-type mice due to a 54% and 32% increase, respectively, in medial area

• after artery injury, the number of proliferating VSMCs in media is increased compared to wild-type cells

• however, neointimal area is not statistically different

decreased circulating interleukin-1 beta level ( J:91165 )

• following endotoxin challenge, mice exhibit a slower increase in IL1b levels compared with similarly treated wild-type mice

decreased circulating interleukin-6 level ( J:91165 )

• following endotoxin challenge, mice exhibit a sharper decline in IL6 levels 24 hours after challenge compared with similarly treated wild-type mice

decreased circulating tumor necrosis factor level ( J:91165 )

• following endotoxin challenge, mice exhibit decreased peak serum TNF-alpha levels compared with similarly treated wild-type mice

abnormal blood coagulation ( J:91165 )

• 6 hours after endotoxin challenge, mice exhibit increased TAT (thrombin-antithrombin) complexes compared to in similarly treated wild-type mice

• however, TAT levels are normal 24 hours after endotoxin challenge

hematopoietic system

abnormal cellular extravasation ( J:91165 )

• reduced after endotoxin challenge

abnormal leukocyte adhesion ( J:91165 )

• reduced after endotoxin challenge

impaired leukocyte tethering or rolling ( J:91165 )

• leukocyte rolling is reduced after endotoxin challenge while rolling velocity is increased compared to in similarly treated wild-type mice

decreased leukocyte cell number ( J:91165 )

• 6 hours after endotoxin challenge, leukocytosis is attenuated compared to in similarly treated wild-type mice

• 1 hour after endotoxin challenge, accumulation of pulmonary leukocytes as measured by MPO activity is decreased compared to in similarly treated wild-type mice

decreased neutrophil cell number ( J:91165 )

• 6 and 24 hours after endotoxin challenge

decreased B cell number ( J:91165 )

• 6 hours after endotoxin challenge

cardiovascular system

abnormal vascular smooth muscle physiology ( J:111390 )

• vascular smooth muscle cells (VSMCs) fail to exhibit an increase in FFR-FVIIa-induced migration compared with wild-type cells

• however, migration of VSMCs towards fibronectin and neointimal proliferation of VSMCs after wire injury are normal

increased vascular smooth muscle cell proliferation ( J:111390 )

• after artery injury, the number of proliferating VSMCs in media is increased compared to wild-type cells

• VSMCs isolated from the aorta exhibit increased proliferation compared to wild-type cells independent of FFR-FVIIa

abnormal vascular wound healing ( J:111390 )

• following transluminal wire injury or ligation of the carotid artery, the intima to media ratio is decreased compared to in similarly treated wild-type mice due to a 54% and 32% increase, respectively, in medial area

• after artery injury, the number of proliferating VSMCs in media is increased compared to wild-type cells

• however, neointimal area is not statistically different

muscle

abnormal vascular smooth muscle physiology ( J:111390 )

• vascular smooth muscle cells (VSMCs) fail to exhibit an increase in FFR-FVIIa-induced migration compared with wild-type cells

• however, migration of VSMCs towards fibronectin and neointimal proliferation of VSMCs after wire injury are normal

increased vascular smooth muscle cell proliferation ( J:111390 )

• after artery injury, the number of proliferating VSMCs in media is increased compared to wild-type cells

• VSMCs isolated from the aorta exhibit increased proliferation compared to wild-type cells independent of FFR-FVIIa

cellular

increased vascular smooth muscle cell proliferation ( J:111390 )

• after artery injury, the number of proliferating VSMCs in media is increased compared to wild-type cells

• VSMCs isolated from the aorta exhibit increased proliferation compared to wild-type cells independent of FFR-FVIIa

abnormal cellular extravasation ( J:91165 )

• reduced after endotoxin challenge

abnormal leukocyte adhesion ( J:91165 )

• reduced after endotoxin challenge

impaired leukocyte tethering or rolling ( J:91165 )

• leukocyte rolling is reduced after endotoxin challenge while rolling velocity is increased compared to in similarly treated wild-type mice

Genotype
MGI:4829887

cx4

• Allelic Composition: F2r^tm1Pago/F2r^tm1Pago; F3^tm1.1Dwr/F3^tm1.1Dwr
• Genetic Background: B6.129-F3^tm1.1Dwr F2r^tm1Pago

cardiovascular system

abnormal induced retina neovascularization ( J:135087 )

• mice exhibit enhanced retinal revascularization following oxygen induced retinopathy; the superficial vascular plexus reforms more quickly than in wild-type mice

vision/eye

abnormal induced retina neovascularization ( J:135087 )

• mice exhibit enhanced retinal revascularization following oxygen induced retinopathy; the superficial vascular plexus reforms more quickly than in wild-type mice

Genotype
MGI:4829888

cx5

• Allelic Composition: F2rl1^tm1Bpd/F2rl1^tm1Bpd; F3^tm1.1Dwr/F3^tm1.1Dwr
• Genetic Background: B6.129-F3^tm1.1Dwr F2rl1^tm1Bpd

cardiovascular system

cardiovascular system phenotype ( J:135087 )

N • retinal neoangiogenesis after oxygen induced retinopathy is similar to wild-type mice with mice showing normal regrowth of the retinal vascular network under hypoxia