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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Prkcitm1Rfar
targeted mutation 1, Robert V Farese Sr
MGI:3720810
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Prkcitm1Rfar/Prkcitm1Rfar
Tg(Ckmm-cre)5Khn/0
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:3721144
cn2
Prkcitm1Rfar/Prkci+
Tg(Ckmm-cre)5Khn/?
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:3721145
cn3
Prkcitm1Rfar/Prkcitm1Rfar
Tg(NPHS2-cre)295Lbh/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5446036


Genotype
MGI:3721144
cn1
Allelic
Composition
Prkcitm1Rfar/Prkcitm1Rfar
Tg(Ckmm-cre)5Khn/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prkcitm1Rfar mutation (0 available); any Prkci mutation (54 available)
Tg(Ckmm-cre)5Khn mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• males and females have more serum lipid than wild-type mice
• serum free fatty acid levels are increased by 40% relative to wild-type mice
• fasting triglyceride levels are increased relative to in wild-type mice
• in a euglycemic clamp assay, mice require a reduced rate of glucose infusion compared to wild-type mice to maintain euglycemia
• in mice fed ad libitum, serum glucose levels are increased
• circulating glucose levels are higher in males than in females
• circulating insulin levels are higher in males than in females
• in mice fed ad libitum, glucose tolerance impairment is comparable to or less severe than in heterozygotes
• in mice fed ad libitum, insulin tolerance is impairment
• in a euglycemic clamp assay, whole-body insulin resistance is accounted for by decreases in insulin-stimulated whole-body glucose uptake and muscle glucose uptake of 25% and 30%, respectively

cardiovascular system
• glucose uptake in heart muscle, basally and during insulin treatment, is reduced

muscle
• glucose uptake in muscle (vastus laterallis and heart), basally and during insulin treatment, is reduced
• insulin-stimulated [3H]2-deoxyglucose uptake is reduced in slow-twitch (soleus) and fast-twitch (extensor digitorum longus) muscles
• glucose uptake in heart muscle, basally and during insulin treatment, is reduced

liver/biliary system
• even on a low-fat diet, hepatostetosis occurs and is more pronounced in heterogyzotes than in homozygotes

adipose tissue
• insulin-stimulated glucose transport is impaired

growth/size/body
• body weight is increased relative to wild-type mice but is less than for heterozygous mice

endocrine/exocrine glands

cellular
• insulin-stimulated glucose transport is impaired
• glucose uptake in muscle (vastus laterallis and heart), basally and during insulin treatment, is reduced
• insulin-stimulated [3H]2-deoxyglucose uptake is reduced in slow-twitch (soleus) and fast-twitch (extensor digitorum longus) muscles
• glucose uptake in heart muscle, basally and during insulin treatment, is reduced




Genotype
MGI:3721145
cn2
Allelic
Composition
Prkcitm1Rfar/Prkci+
Tg(Ckmm-cre)5Khn/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prkcitm1Rfar mutation (0 available); any Prkci mutation (54 available)
Tg(Ckmm-cre)5Khn mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• males and females have more serum lipid than wild-type mice
• serum free fatty acid levels are increased by 90% relative to wild-type mice
• fasting triglyceride levels are increased relative to in wild-type mice
• in a euglycemic clamp assay, mice require a reduced rate of glucose infusion compared to wild-type mice to maintain euglycemia
• in mice fed ad libitum, serum glucose levels are increased
• fasting glucose levels during insulin and glucose tolerance tests is increased by 20% to 25%
• when dietary fat content is increased from 5% to 10% for 2 months, mice exhibit higher glucose levels than in wild-type mice at all time points and during fasting glucose tolerance testing
• in mice fed ad libitum, serum insulin levels are increased
• in mice fed ad libitum, glucose tolerance impairment is comparable to or more severe than in homozygotes
• in mice fed ad libitum, insulin tolerance is impairment is comparable to or more severe than in homozygotes
• in a euglycemic clamp assay, whole-body insulin resistance is accounted for by decreases in insulin-stimulated whole-body glucose uptake and muscle glucose uptake of 25% and 30%, respectively

cardiovascular system

muscle
• insulin-stimulated uptake of glucose and [3H]2-deoxyglucose in vastus laterallis, soleus and extensor digitorum longus, and heart muscles is reduced by 50% to 60% compared to in wild-type mice

liver/biliary system
• even on a low-fat diet, hepatostetosis occurs and is more pronounced in heterogyzotes than in homozygotes

adipose tissue
• insulin-stimulated glucose transport is impaired

growth/size/body
• body weight is increased relative to wild-type mice and homozygous mice
• mice develop an obesity/diabetes syndrome associated with increased food intake

behavior/neurological
• mice consume 20% more regular chow than wild-type mice

immune system
• mice develop an obesity/diabetes syndrome associated with increased food intake

endocrine/exocrine glands

cellular
• insulin-stimulated glucose transport is impaired
• insulin-stimulated uptake of glucose and [3H]2-deoxyglucose in vastus laterallis, soleus and extensor digitorum longus, and heart muscles is reduced by 50% to 60% compared to in wild-type mice




Genotype
MGI:5446036
cn3
Allelic
Composition
Prkcitm1Rfar/Prkcitm1Rfar
Tg(NPHS2-cre)295Lbh/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prkcitm1Rfar mutation (0 available); any Prkci mutation (54 available)
Tg(NPHS2-cre)295Lbh mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice are born healthy but die of renal failure within 4 to 5 weeks of birth
• however, mice appear normal up to 2 weeks after birth

growth/size/body
• at ~4 weeks of age, mice exhibit significant growth retardation relative to controls

renal/urinary system
• at ~4 weeks of age, mice exhibit significant proteinuria relative to controls
• at 4 weeks, nephrin expression appears reduced while the polarity protein Par3, the tight junction marker ZO-1, and the slit diaphragm molecules nephrin and podocin exhibit a significantly impaired, granular distribution along the glomerular basement membrane, unlike the linear pattern seen in wild-type controls
• at ~4 weeks of age, foot processes appear globally effaced
• at ~4 weeks of age, severe junctional abnormalities are observed
• at ~4 weeks of age, foot processes often display significant slit diaphragm displacement
• at ~4 weeks of age, mice develop segmental glomerulosclerosis
• at ~4 weeks of age, mice exhibit renal tubule dilation
• at ~4 weeks of age, mice exhibit proteinuric casts in the tubule system
• mice develop nephrotic syndrome and die of renal failure

homeostasis/metabolism
• at ~4 weeks of age, mice exhibit significant proteinuria relative to controls





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last database update
10/08/2019
MGI 6.14
The Jackson Laboratory