All Phenotypes Tg(CAG-cre/Esr1*)86Lbgn MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Nphs2^tm1Antc/Nphs2^tm3.1Antc Tg(CAG-cre/Esr1*)86Lbgn/0	involves: 129 * C57BL/6 * DBA	MGI:4847559
cn2	Nphs2^tm2.1Antc/Nphs2^tm3.1Antc Tg(CAG-cre/Esr1*)86Lbgn/0	involves: 129S2/SvPas * C57BL/6 * DBA	MGI:6316681

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

mortality/aging

premature death ( J:166320 )

• mice die 11 weeks after tamoxifen treatment

renal/urinary system

increased urine protein level ( J:166320 )

• after 4 weeks of tamoxifen treatment, mice develop nonselective proteinuria compared with control mice

albuminuria ( J:166320 )

• after 10 days of tamoxifen treatment

• after 2 weeks of nursing from mice fed tamoxifen

abnormal kidney morphology ( J:166320 )

• after 9 weeks, tamoxifen-treated mice exhibit progressive tubular injury with basement membrane thickening and interstitial fibrosis unlike similarly treated wild-type mice

podocyte foot process effacement ( J:166320 )

• tamoxifen-treated mice exhibit focal effacement at 1 and 2 weeks then diffuse effacement at 4 weeks unlike similarly treated wild-type mice

podocyte hypertrophy ( J:166320 )

• after 2 weeks of tamoxifen treatment, mice exhibit podocyte hypertrophy compared with similarly treated control mice

abnormal renal glomerulus morphology ( J:166320 )

• after 4 weeks, tamoxifen-treated mice exhibit glomerular pseudocrescents in some glomeruli unlike in similarly treated control mice

increased mesangial cell number ( J:166320 )

• mice nursed by dams fed tamoxifen exhibit lesions of mesangial proliferation compared with similarly treated controls

expanded mesangial matrix ( J:166320 )

• after 2 weeks of tamoxifen treatment, mice exhibit minimal mesangial matrix expansion compared with similarly treated control mice

glomerulosclerosis ( J:166320 )

• after 4 weeks of tamoxifen treatment, mice exhibit focal segmental glomerulosclerosis in many glomeruli with varying severity unlike in similarly treated control mice

• mice nursed by dams fed tamoxifen exhibit lesions of focal segmental glomerulosclerosis unlike similarly treated control mice

• glomerulosclerosis worsens by 6 weeks of tamoxifen treatment

• at or near death, tamoxifen-treated mice exhibit global scelrosis

renal interstitial fibrosis ( J:166320 )

• after 9 weeks in tamoxifen-treated mice

abnormal renal tubule morphology ( J:166320 )

• tamoxifen-treated mice exhibit tubulointerstitial injury with diffuse tubular dilation, tubular atrophy and necrosis, and proteinaceous casts unlike in similarly treated control mice

renal tubule atrophy ( J:166320 )

• in tamoxifen-treated mice

dilated renal tubule ( J:166320 )

• in tamoxifen-treated mice

renal tubular necrosis ( J:166320 )

• in tamoxifen-treated mice

renal cast ( J:166320 )

• in tamoxifen-treated mice

homeostasis/metabolism

increased circulating creatinine level ( J:166320 )

• after 6 weeks of tamoxifen treatment

increased blood urea nitrogen level ( J:166320 )

• after 6 weeks of tamoxifen treatment

increased circulating cholesterol level ( J:166320 )

• after 4 weeks of tamoxifen treatment

increased urine protein level ( J:166320 )

• after 4 weeks of tamoxifen treatment, mice develop nonselective proteinuria compared with control mice

albuminuria ( J:166320 )

• after 10 days of tamoxifen treatment

• after 2 weeks of nursing from mice fed tamoxifen

cardiovascular system

increased systemic arterial systolic blood pressure ( J:166320 )

• modestly after 4 weeks of tamoxifen treatment

cellular

increased mesangial cell number ( J:166320 )

• mice nursed by dams fed tamoxifen exhibit lesions of mesangial proliferation compared with similarly treated controls

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
nephrotic syndrome		DOID:1184		J:166320

Allelic Composition	Nphs2^tm2.1Antc/Nphs2^tm3.1Antc Tg(CAG-cre/Esr1*)86Lbgn/0
Genetic Background	involves: 129S2/SvPas * C57BL/6 * DBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nphs2^tm2.1Antc mutation (0 available); any Nphs2 mutation (30 available)
Nphs2^tm3.1Antc mutation (0 available); any Nphs2 mutation (30 available)
Tg(CAG-cre/Esr1*)86Lbgn mutation (0 available)

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

Nphs2^tm2.1Antc/Nphs2^tm3.1Antc Tg(CAG-cre/Esr1*)86Lbgn/0 mice develop focal-segmental glomerulosclerosis

mortality/aging

premature death ( J:245693 )

• the median survival of tamoxifen-treated mice is 12 weeks

growth/size/body

decreased body weight ( J:245693 )

• mice exhibit lower body weight from week 6 onward after tamoxifen treatment

cardiovascular system

increased systemic arterial blood pressure ( J:245693 )

• blood pressure moderately increases after tamoxifen treatment

homeostasis/metabolism

increased urine creatinine level ( J:245693 )

• mice exhibit increased creatinine levels within a few days of tamoxifen treatment

increased circulating cholesterol level ( J:245693 )

• mice exhibit hypercholesterolemia 4 weeks after tamoxifen induction

decreased circulating serum albumin level ( J:245693 )

• mice exhibit hypoalbuminemia 4 weeks after tamoxifen induction

increased urine protein level ( J:245693 )

• mice develop proteinuria within a few days of tamoxifen treatment which increases to a maximum 4-5 weeks after induction and thereafter decreases gradually but remains elevated compared to controls

renal/urinary system

increased urine creatinine level ( J:245693 )

• mice exhibit increased creatinine levels within a few days of tamoxifen treatment

increased urine protein level ( J:245693 )

abnormal podocyte foot process morphology ( J:245693 )

• foot processes are irregularly shaped one week after tamoxifen induction, progressing to effacement

fused podocyte foot processes ( J:245693 )

• foot processes are fused one week after tamoxifen induction progressing to global fusion and effacement

podocyte foot process effacement ( J:245693 )

• in tamoxifen treated mice

decreased podocyte number ( J:245693 )

• mice show reduced podocyte number per glomerulus starting at the end of the second week after tamoxifen induction (68% of controls) to 18% of controls at 12-16 weeks

increased renal glomerulus basement membrane thickness ( J:245693 )

• glomerular basement membrane is thickened in tamoxifen-induced mice

glomerulosclerosis ( J:245693 )

• mice exhibit early glomerular sclerosis form the first week after tamoxifen induction that progresses increases until week eight when 100% of glomeruli are partially or globally sclerosed

renal interstitial fibrosis ( J:245693 )

• mice develop severe interstitial fibrosis which is visible from the first week after tamoxifen induction and increase to 12% of the total kidney area in the course of the disease

renal tubule atrophy ( J:245693 )

• mice develop tubular atrophy that is visible from the first week after tamoxifen induction

decreased creatinine clearance ( J:245693 )

• mice exhibit diminished creatinine clearance 4 weeks after tamoxifen induction

kidney failure ( J:245693 )

• mice progress to renal failure after tamoxifen-induction

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
nephrotic syndrome		DOID:1184		J:245693

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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