About   Help   FAQ
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 (26 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





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)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
11/19/2024
MGI 6.24
The Jackson Laboratory