Phenotypes associated with this allele
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr1atm3Tma mutation
(0 available);
any
Agtr1a mutation
(40 available)
Tg(Nphs1-cre)10Mska mutation
(0 available)
Tg(Nphs1-IL2RA)18Mska mutation
(0 available)
|
|
|
renal/urinary system
N |
• mice do not show proteinuria and renal morphology is normal
• mice injected with an immunotoxin, anti-Tac(Fv)-PE38 (LMB2) develop the same level of glomerulosclerosis as controls
• mice injected with LMB2 to induce glomerular injury that are treated with angiotensin II type 1 receptor blocker (ARB) show attenuation of glomerulosclerosis progression
|
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation
(7 available);
any
Gt(ROSA)26Sor mutation
(993 available)
Tg(Nphs1-cre)33Mska mutation
(0 available)
Tg(Nphs1-IL2RA)18Mska mutation
(0 available)
|
|
|
renal/urinary system
|
• proliferation of parietal epithelial cells, not podocytes, is observed; proliferating cells are lacZ-negative, whereas podocytes express beta-galactosidase
|
|
• vacuolar degeneration of parietal epithelial cells is observed after LMB2 treatment
• proliferation of parietal epithelial cells, not podocytes, is also seen; proliferating cells are lacZ-negative, whereas podocytes express beta-galactosidase
|
|
• vacuolar degeneration of podocytes is observed after LMB2 treatment; podocytes are identified by lacZ staining
• podocytes are lost temporally after LMB2 treatment, correlating with progression of sclerosis
|
|
• hyalinosis is seen after LMB2 treatment
|
|
• mesangiolysis is seen after LMB2 treatment
|
|
• after treatment with the immunotoxin LMB2, transgenic animal rapidly develop glomerulosclerosis
• 18%, 23%, and 60% of glomeruli show segmental or global sclerosis at 10, 14 or 21 days after treatment, respectively
|
cellular
|
• proliferation of parietal epithelial cells, not podocytes, is observed; proliferating cells are lacZ-negative, whereas podocytes express beta-galactosidase
|
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
|
|
|
mortality/aging
|
• with injection of 20-50 ng/g LMB2, most transgenic mice die from severe edema and/or renal failure by 5-6 days, while doses of 5 ng/g induce mortality in 7 to 8 days, 2.5 ng/g LMB2 produces mortality in 8 to 9 days and 1.25 ng/g induces mortality within 11 to 14 days; untreated transgenic mice or treated wild-type mice show no abnormal phenotype
• at 0.625 ng/g body weight of toxin, majority of transgenic mice show mild and transient ascites and survive for >28 days
|
cardiovascular system
|
• mice injected with the immunotoxin LMB2 (a human CD25-targeted recombinant immunotoxin, anti-Tac(Fv)-PE38) exhibit increased blood pressure
• LMB2 injected mice to induce glomerular injury that are treated with angiotensin II type 1 receptor blocker (ARB) show lower systolic blood pressure than control mice without ARB treatment
|
renal/urinary system
|
• 2-3 days after injection of 1.25ng/g body weight or higher of the immunotoxin LMB2 transgenic mice develop nonselective proteinuria, with proteinuria developing more rapidly with higher doses; wild-type or untreated transgenic mice show no abnormal morphological or physiological phenotype
(J:127013)
• at a dose of 0.625 ng/g toxin, proteinuria peaks at day 7 and returns to normal range by 28 days
(J:127013)
• LMB2 injected mice show moderate proteinuria
(J:240316)
• LMB2 injected mice to induce glomerular injury that are treated with ARB or an angiotensin I-converting enzyme inhibitor show a decrease in proteinuria
(J:240316)
|
|
• LMB2 injected mice develop glomerulosclerosis
• LMB2 injected mice to induce glomerular injury that are treated with ARB show attenuation of glomerulosclerosis progression
|
|
• after LMB2 injection, transgenic mice display renal failure; wild-type or untreated transgenic mice show no abnormal morphological or physiological phenotype
|
homeostasis/metabolism