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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Ggt1-tTA)#Agoc
transgene insertion, Adolf Garcia-Ocana
MGI:5705528
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cx1
Tg(Ggt1-tTA)#Agoc/0
Tg(tetO/CMV-PTHLH)#Agoc/0
involves: CD-1 MGI:5705534
cx2
Tg(Ggt1-tTA)#Agoc/0
Tg(tetO/CMV-Hgf)#Agoc/0
involves: CD-1 MGI:5705535
cx3
Tg(Ggt1-tTA)#Agoc/0
Tg(tetO-MYC)36aBop/0
involves: FVB/N MGI:5705536


Genotype
MGI:5705534
cx1
Allelic
Composition
Tg(Ggt1-tTA)#Agoc/0
Tg(tetO/CMV-PTHLH)#Agoc/0
Genetic
Background
involves: CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• mild hypophosphatemia
• however, mice do not display hypercalcemia

renal/urinary system
N
• kidney weight and morphology appears normal at 4 months of age under normal physiologic conditions and circulating markers of kidney function, BUN, and plasma creatinine concentrations are normal
• mice exhibit a similar level of renal failure induced by ischemia/reperfusion and similar level of renal damage induced by FA injection as controls




Genotype
MGI:5705535
cx2
Allelic
Composition
Tg(Ggt1-tTA)#Agoc/0
Tg(tetO/CMV-Hgf)#Agoc/0
Genetic
Background
involves: CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• mice exhibit decreased renal damage induced by ischemia/reperfusion, showing reduced tubular damage with fewer obstructing casts, reduced levels of plasma creatinine and BUN levels compared to controls and increased survival rate after 48 hours after ischemia/reperfusion
• mice exhibit increased kidney tubular cell proliferation and decreased apoptosis 48 hours after ischemia/reperfusion
• however, mice treated with doxycycline to turn off expression exhibit similar renal damage to ischemia/reperfusion as controls
• under normal physiologic conditions, kidney weight and morphology appears normal at 4 months of age and circulating markers of kidney function, BUN, and plasma creatinine concentrations are normal

renal/urinary system
• mice exhibit decreased renal damage induced by ischemia/reperfusion, showing reduced tubular damage with fewer obstructing casts, reduced levels of plasma creatinine and BUN levels compared to controls and increased survival rate after 48 hours after ischemia/reperfusion
• mice exhibit increased kidney tubular cell proliferation and decreased apoptosis 48 hours after ischemia/reperfusion
• however, mice treated with doxycycline to turn off expression exhibit similar renal damage to ischemia/reperfusion as controls
• under normal physiologic conditions, kidney weight and morphology appears normal at 4 months of age and circulating markers of kidney function, BUN, and plasma creatinine concentrations are normal




Genotype
MGI:5705536
cx3
Allelic
Composition
Tg(Ggt1-tTA)#Agoc/0
Tg(tetO-MYC)36aBop/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Ggt1-tTA)#Agoc mutation (0 available)
Tg(tetO-MYC)36aBop mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• removal of doxycycline (dox) results in increased kidney size
• removal of dox results in the development of rapidly progressing of renal cell carcinoma
• marker analysis indicates that tumor subtype is of the collecting-duct carcinoma which exhibits a distinct lipid signature
• treatment with dox reverses tumor and results in regression of the renal cell carcinoma
• initiation of renal cell carcinoma is associated with the activation of glutaminolysis
• treatment with dox to suppress MYC protein expression results in regression of the renal cell carcinoma due to inhibition of proliferation accompanied by the persistence of apoptosis
• treatment with an inhibitor of kidney type glutaminase BPTES slows progression of renal cell carcinoma tumors, reduces neoplastic cells, and decreases kidney cell proliferation

neoplasm
• removal of dox results in the development of rapidly progressing of renal cell carcinoma
• marker analysis indicates that tumor subtype is of the collecting-duct carcinoma which exhibits a distinct lipid signature
• treatment with dox reverses tumor and results in regression of the renal cell carcinoma
• initiation of renal cell carcinoma is associated with the activation of glutaminolysis
• treatment with dox to suppress MYC protein expression results in regression of the renal cell carcinoma due to inhibition of proliferation accompanied by the persistence of apoptosis
• treatment with an inhibitor of kidney type glutaminase BPTES slows progression of renal cell carcinoma tumors, reduces neoplastic cells, and decreases kidney cell proliferation

growth/size/body
• removal of doxycycline (dox) results in increased kidney size





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last database update
12/10/2024
MGI 6.24
The Jackson Laboratory