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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cyp2c23Gt(OST85045)Lex
gene trap OST85045, Lexicon Genetics
MGI:4178127
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Cyp2c23Gt(OST85045)Lex/Cyp2c23Gt(OST85045)Lex 129-Cyp2c23Gt(OST85045)Lex MGI:5559332


Genotype
MGI:5559332
hm1
Allelic
Composition
Cyp2c23Gt(OST85045)Lex/Cyp2c23Gt(OST85045)Lex
Genetic
Background
129-Cyp2c23Gt(OST85045)Lex
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cyp2c23Gt(OST85045)Lex mutation (1 available); any Cyp2c23 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• primary pulmonary endothelial cells show reduced tubulogenic capacity in the absence or presence of added arachidonic acid
• the epoxygenase 11,12-epoxyeicosatrienoic acid metabolite restores the tubulogenic capacity of primary pulmonary endothelial cells
• VEGF fails to stimulate the tubulogenesis of primary pulmonary endothelial cells in culture as it does in wild-type cells
• primary pulmonary endothelial cells show reduced growth rates in culture under non-stimulated conditions
• the epoxygenase 11,12-epoxyeicosatrienoic acid metabolite restores the proliferative capacity of primary pulmonary endothelial cells
• VEGF fails to stimulate the proliferation of primary pulmonary endothelial cells in culture as it does in wild-type cells

neoplasm
• tumor vascularization and growth are blunted in mutants injected with murine p60.5 cells compared to wild-type and treatment with Wyeth 14,643, a PPARalpha-selective ligand has no effect on tumors in mutants unlike in wild-type

cellular
• primary pulmonary endothelial cells show reduced growth rates in culture under non-stimulated conditions
• the epoxygenase 11,12-epoxyeicosatrienoic acid metabolite restores the proliferative capacity of primary pulmonary endothelial cells
• VEGF fails to stimulate the proliferation of primary pulmonary endothelial cells in culture as it does in wild-type cells

cardiovascular system
• mice fed a high potassium diet show increased systemic blood pressure
• amiloride treatment abolishes the high potassium-induced hypertension

growth/size/body
• mutants fed a high potassium diet gain weight unlike wild-type mice which lose weight

homeostasis/metabolism
• the increase in plasma aldosterone levels induced by a high potassium diet in wild-type mice is smaller in mutants
• mice fed a high potassium diet show increased plasma sodium concentration
• mice fed a high potassium diet show decreased 24-hour urinary sodium excretion
• however potassium excretion is normal in mice fed a high potassium diet

renal/urinary system
• mice fed a high potassium diet show decreased 24-hour urinary sodium excretion
• however potassium excretion is normal in mice fed a high potassium diet
• high potassium intake fails to increase 11,12-epoxyeicosatrienoic acid formation in the cortical collecting ducts as it does in wild-type mice
• mice do not show an increase in whole-cell amiloride-sensitive sodium currents in principal cells of cortical collecting ducts in response to N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide, an inhibitor of CYP epoxygenase, as is seen in wild-type cells





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