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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Prdx3tm1Hjha
targeted mutation 1, Hunjoo Ha
MGI:5749424
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Prdx3tm1Hjha/Prdx3tm1Hjha involves: 129S4/SvJae * C57BL/6 MGI:5781002


Genotype
MGI:5781002
hm1
Allelic
Composition
Prdx3tm1Hjha/Prdx3tm1Hjha
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prdx3tm1Hjha mutation (0 available); any Prdx3 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• increased fat mass by 20 months of age
• body weight is normal at 4 months but significantly increased by 20 months of age

adipose tissue
• increased white adipose tissue amount (WAT) at 4 and 20 months of age
• increased fat mass by 20 months of age
• increased adipogenic gene expression in differentiated adipocyte-derived stem cells (ASCs) isolated from subcutaneous fat pads of mutant mice relative to wild-type controls
• white fat cell hypertrophy at 4 and 20 months of age
• significant increase in epididymal WAT by 20 months of age
• significant increase in perirenal fat by 20 months of age
• downregulation of adiponectin mRNA and protein expression in mutant adipocytes isolated from epididymal WAT
• upregulation of plasminogen activator inhibitor-1 (PAI-1) mRNA and protein expression in mutant adipocytes isolated from epididymal WAT

cellular
• increased adipogenic gene expression in differentiated adipocyte-derived stem cells (ASCs) isolated from subcutaneous fat pads of mutant mice relative to wild-type controls
• severe downregulation of mitochondrial proteins involved in oxidative phosphorylation and fatty acid metabolism in mutant adipocytes isolated from epididymal WAT relative to wild-type controls
• impaired mitochondrial biogenesis in mutant adipocytes as shown by a significant reduction in mtDNA and a trend towards downregulation of genes related to mitochondrial biosynthesis
• increased mitochondrial protein carbonylation in mutant subcutaneous, epididymal, and omental WAT relative to wild-type controls
• downregulation of mitochondrial enzymes involved in fatty acid oxidation in mutant adipocytes, suggesting impaired ability to burn excessive fat
• aberrant mitochondrial redox state resulting in abnormal adipocyte differentiation
• increased mitochondrial oxidative stress as shown by downregulation of antioxidant genes, including manganese superoxide dismutase, heme oxygenase-1 and quinone oxidoreductase 1, in mutant adipocytes relative to wild-type controls
• increased oxidative stress as shown by increased plasma lipid peroxidation levels (measured as thiobarbituric acid reactive substance levels) and HSP60/nitrotyrosine staining in WAT relative to wild-type controls
• increased mitochondrial protein carbonylation in mutant subcutaneous, epididymal, and omental WAT relative to wild-type controls

homeostasis/metabolism
• downregulation of mitochondrial enzymes involved in fatty acid oxidation in mutant adipocytes, suggesting impaired ability to burn excessive fat
• increased plasma glucose levels in the fasted state, with no change in fed glucose levels, relative to wild-type controls
• increased plasma insulin levels in the fasted state relative to wild-type controls
• significantly increased total plasma cholesterol levels relative to wild-type controls
• trend towards lower plasma triglyceride levels, likely due to increased level of Lpl mRNA levels in mutant adipocytes
• significantly increased plasma plasminogen activator inhibitor-1 (PAI-1) levels at 20 months of age
• mice are glucose intolerant in an oral glucose tolerance test
• mice show significantly decreased sensitivity to insulin in an insulin tolerance test
• downregulation of adiponectin mRNA and protein expression in mutant adipocytes isolated from epididymal WAT
• in contrast, adipocyte leptin levels remain normal
• significantly decreased plasma adiponectin levels at 20 months of age
• in contrast, plasma leptin levels remain normal
• increased lipid metabolism in mutant adipocytes as shown by upregulation of genes related to lipid homeostasis





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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
04/23/2024
MGI 6.23
The Jackson Laboratory