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. 2014 Nov 17;53(49):7693–7705. doi: 10.1021/bi5013222

Table 1. Summary of Prx Knockout Studies in Vertebrates.

organism/enzyme ref brief phenotypic observations
Mus musculus-PrxI (66) malignant cancers, hemolytic anemia, premature death
M. musculus-PrxI (58) increased DNA oxidation, increased c-Myc activation in embryonic fibroblasts
M. musculus-PrxI (65) increased susceptibility to Ras-induced breast cancer
M. musculus-PrxII (59) increased protein oxidation in red blood cells, hemolytic anemia
M. musculus-PrxII (67) increased plaque formation, predisposition to develop atherosclerosis
M. musculus-PrxII (69) enlarged thymus, increased T cell proliferation
M. musculus-PrxII (68) increased splenocytes, bone marrow differentiation
M. musculus-PrxII (71) increased p21 and p53 levels, increased cellular senescence
M. musculus-PrxII (60) increased protein cysteine oxidation in red blood cell fractions
M. musculus-PrxIII (61) increased lung damage from inflammation, increased DNA damage
M. musculus-PrxIII (62) increased fat mass, increased protein carbonylation in adipose tissue
M. musculus-PrxIII (72) reduced litter size, increased oxidative stress in placenta tissue
M. musculus-PrxIII (73) increased macrophage apoptosis by lipopolysaccharide treatment
M. musculus-PrxIV (74) testicular atrophy, reduced sperm viability in oxidative stress
M. musculus-PrxVI (134) increased lung damage, decreased animal survival due to hyperoxia
M. musculus-PrxVI (131) increased ischemic reperfusion injury, increased cardiomyocyte apoptosis
M. musculus-PrxVI (135) decreased lung surfactant degradation
M. musculus-PrxVI (64) increased LDL oxidation by macrophages, increased plasma lipid H2O2 levels
M. musculus-PrxVI (136) increased UPR, increased apoptosis in lens epithelial and aging cells