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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Itga1tm1Gdnr
targeted mutation 1, Humphrey Gardner
MGI:2451067
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Itga1tm1Gdnr/Itga1tm1Gdnr involves: 129S4/SvJae * BALB/c MGI:2451068
cx2
Ins2Akita/Ins2Akita
Itga1tm1Gdnr/Itga1tm1Gdnr
C.Cg-Ins2Akita Itga1tm1Gdnr MGI:5508896
cx3
Col4a3tm1Dec/Col4a3tm1Dec
Itga1tm1Gdnr/Itga1tm1Gdnr
involves: 129S4/SvJae * 129X1/SvJ * BALB/c MGI:3583734


Genotype
MGI:2451068
hm1
Allelic
Composition
Itga1tm1Gdnr/Itga1tm1Gdnr
Genetic
Background
involves: 129S4/SvJae * BALB/c
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itga1tm1Gdnr mutation (0 available); any Itga1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• increased apoptosis 1 week after treatment with adriamycin
• increased foot process effacement 1 day after treatment with adriamycin
• smaller glomeruli and glomerular tuft area
• increased mesangial matrix accumulation
• mesangial expansion 1 day after treatment with adriamycin
• focal mesangiolysis and lesions 1 day after treatment with adriamycin
• increased succeptibility to adriamycin induced kidney damage
• increased glomerular matrix deposition and hyalinosis by 1 week after treatment with adriamycin
• serious interstitial damage and increased apoptosis 1 week after treatment with adriamycin

homeostasis/metabolism
• abnormally increased creatinine levels as a result of adriamycin treatment
• abnormally increased albuminuria as a result of treatment with adriamycin
• increased susceptibility to glomerulopathy in response to adriamycin-induced kidney injury

cellular
• increased apoptosis 1 week after treatment with adriamycin




Genotype
MGI:5508896
cx2
Allelic
Composition
Ins2Akita/Ins2Akita
Itga1tm1Gdnr/Itga1tm1Gdnr
Genetic
Background
C.Cg-Ins2Akita Itga1tm1Gdnr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ins2Akita mutation (13 available); any Ins2 mutation (23 available)
Itga1tm1Gdnr mutation (0 available); any Itga1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 40% of mutants fail to thrive and have to be euthanized before 6 months of age

cardiovascular system
• mice show a a greater decrease in CD31 positive structures in the glomeruli than in single Ins2Akita homozygotes, indicating collapse of the glomerular tufts

growth/size/body
• decreased body weight at 4 and 6 months of age compared to wild-type mice or single Itgal1tm1Gdnr homozygotes

homeostasis/metabolism
• develop a similar level of hyperglycemia as in single Ins2Akita homozygotes
• 16-fold increase in albumin-to-creatine ratio at 4 months of age

renal/urinary system
• 16-fold increase in albumin-to-creatine ratio at 4 months of age
• glomerular basement membrane thickening is more severe than in single Ins2Akita homozygotes
• increase in glomerular collagen IV deposition at 6 months of age is more abundant than in single Ins2Akita homozygotes
• mice show a a greater decrease in CD31 positive structures in the glomeruli than in single Ins2Akita homozygotes, indicating collapse of the glomerular tufts
• excessive fibrillar collagen deposition in diffuse and nodular mesangial lesions
• increase in mesangial matrix expansion at 4 and 6 months of age is greater than in single Ins2Akita homozygotes
• diffuse and nodular mesangial sclerosis
• small increase in collagen I in the tubulointerstitial compartment of the kidney
• however tubulointerstitial fibrosis is not observed
• glomerular filtration rate is increased at 4 months of age to a similar level as in single Ins2Akita homozygotes
• by 6 months of age, glomerular filtration rate is decreased compared to controls, with an overall 50% decline compared to at 4 months

Mouse Models of Human Disease
OMIM ID Ref(s)
Diabetes Mellitus, Insulin-Dependent; IDDM 222100 J:198186




Genotype
MGI:3583734
cx3
Allelic
Composition
Col4a3tm1Dec/Col4a3tm1Dec
Itga1tm1Gdnr/Itga1tm1Gdnr
Genetic
Background
involves: 129S4/SvJae * 129X1/SvJ * BALB/c
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col4a3tm1Dec mutation (1 available); any Col4a3 mutation (35 available)
Itga1tm1Gdnr mutation (0 available); any Itga1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• decreased accumulation of myofibroblasts in kidneys of 7 week old mice compared to mice only homozygous for the collagen deficiency
• infiltration of the kidney tubular interstitium by macrophage is less in 4 week old mice than in mice only homozygous for the collagen deficiency
• attenuated damage to the glomerular basement membrane although damage still present
• slower rate of renal disease progression
• end stage renal failure delayed to 14.5 weeks rather than 8.5 weeks as in mice only homozygous for the collagen deficiency

homeostasis/metabolism
• onset of proteinuria is delayed relative to mice only homozygous for the collagen deficiency

immune system
• infiltration of the kidney tubular interstitium by macrophage is less in 4 week old mice than in mice only homozygous for the collagen deficiency





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
11/29/2016
MGI 6.06
The Jackson Laboratory