The use of transgenic and mutant mice to study oxygen free radical metabolism.
about
Pol II-expressed shRNA knocks down Sod2 gene expression and causes phenotypes of the gene knockout in mice.Induced overexpression of mitochondrial Mn-superoxide dismutase extends the life span of adult Drosophila melanogasterSuperoxide dismutase 2 knockdown leads to defects in locomotor activity, sensitivity to paraquat, and increased cuticle pigmentation in Tribolium castaneum.Mitochondrial alterations caused by defective peroxisomal biogenesis in a mouse model for Zellweger syndrome (PEX5 knockout mouse)Adaptation of the myoglobin knockout mouse to hypoxic stressReactive oxygen species on bone mineral density and mechanics in Cu,Zn superoxide dismutase (Sod1) knockout mice.Sustained oxidative stress causes late acute renal failure via duplex regulation on p38 MAPK and Akt phosphorylation in severely burned rats.NF-kappaB protects cells from gamma interferon-induced RIP1-dependent necroptosis.Superoxide dismutases, SOD1 and SOD2, play a distinct role in the fat body during pupation in silkworm Bombyx moriLack of extracellular superoxide dismutase (EC-SOD) in the microenvironment impacts radiation-induced changes in neurogenesisAbsence of mitochondrial superoxide dismutase results in a murine hemolytic anemia responsive to therapy with a catalytic antioxidant.Pharmacological lifespan extension of invertebratesOxidant conditioning protects cartilage from mechanically induced damage.Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival.Neural precursor cells and central nervous system radiation sensitivity.Superoxide dismutase 1 knockdown induces oxidative stress and DNA methylation loss in the prostate.2001 William Allan Award Address. From Down syndrome to the "human" in "human genetics"Radiation-induced reductions in neurogenesis are ameliorated in mice deficient in CuZnSOD or MnSOD.Mice deficient in both Mn superoxide dismutase and glutathione peroxidase-1 have increased oxidative damage and a greater incidence of pathology but no reduction in longevity.Transplantation of neural stem cells that overexpress SOD1 enhances amelioration of intracerebral hemorrhage in mice.Mammalian NADH:ubiquinone oxidoreductase (Complex I) and nicotinamide nucleotide transhydrogenase (Nnt) together regulate the mitochondrial production of H₂O₂--implications for their role in disease, especially cancer.The role of mitochondria in mTOR-regulated longevity.Vitamin B12 protects against superoxide-induced cell injury in human aortic endothelial cells.Radioprotective effects of manganese-containing superoxide dismutase mimics on ataxia-telangiectasia cells.Neural stem cells genetically modified to overexpress cu/zn-superoxide dismutase enhance amelioration of ischemic stroke in mice.Loss of manganese superoxide dismutase leads to abnormal growth and signal transduction in mouse embryonic fibroblastsEndogenous mitochondrial oxidative stress in MnSOD-deficient mouse embryonic fibroblasts promotes mitochondrial DNA glycation.Superoxide levels and function of cerebral blood vessels after inhibition of CuZn-SOD.Changes in NO bioavailability regulate cardiac O2 consumption: control by intramitochondrial SOD2 and intracellular myoglobin.Vasomotor responses in MnSOD-deficient mice.Protection against bleomycin-induced lung injury by IL-18 in mice.CuZn-SOD deficiency, rather than overexpression, is associated with enhanced recovery and attenuated activation of NF-kappaB after brain trauma in mice.Essential fatty acids enhance free radical generation and lipid peroxidation to induce apoptosis of tumor cells
P2860
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P2860
The use of transgenic and mutant mice to study oxygen free radical metabolism.
description
1999 nî lūn-bûn
@nan
1999 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հունվարին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
The use of transgenic and mutant mice to study oxygen free radical metabolism.
@ast
The use of transgenic and mutant mice to study oxygen free radical metabolism.
@en
type
label
The use of transgenic and mutant mice to study oxygen free radical metabolism.
@ast
The use of transgenic and mutant mice to study oxygen free radical metabolism.
@en
prefLabel
The use of transgenic and mutant mice to study oxygen free radical metabolism.
@ast
The use of transgenic and mutant mice to study oxygen free radical metabolism.
@en
P2093
P1476
The use of transgenic and mutant mice to study oxygen free radical metabolism.
@en
P2093
P304
P356
10.1111/J.1749-6632.1999.TB07820.X
P407
P577
1999-01-01T00:00:00Z