Phenotypes Associated with This Genotype

Genotype
MGI:3762560

• Allelic Composition: Tg(Nphs1-IL2RA)18Mska/0
• Genetic Background: B6N.Cg-Tg(Nphs1-IL2RA)18Mska

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

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:127013 )

• 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

increased systemic arterial blood pressure ( J:240316 )

• 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

increased urine protein level ( J:127013 , J:240316 )

• 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)

glomerulosclerosis ( J:240316 )

• LMB2 injected mice develop glomerulosclerosis

• LMB2 injected mice to induce glomerular injury that are treated with ARB show attenuation of glomerulosclerosis progression

kidney failure ( J:127013 )

• after LMB2 injection, transgenic mice display renal failure; wild-type or untreated transgenic mice show no abnormal morphological or physiological phenotype

homeostasis/metabolism

decreased circulating total protein level ( J:127013 )

• after LMB2 injection, transgenic mice show hypoproteinemia; wild-type or untreated transgenic mice show no abnormal morphological or physiological phenotype

edema ( J:127013 )

• after LMB2 injection, transgenic mice show edema; wild-type or untreated transgenic mice show no abnormal morphological or physiological phenotype

ascites ( J:127013 )

• after LMB2 injection, transgenic mice display ascites; wild-type or untreated transgenic mice show no abnormal morphological or physiological phenotype

increased urine protein level ( J:127013 , J:240316 )

• 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)