Name | SOD1 |
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Synonyms | ALS; ALS 1; ALS1; IPOA; Indophenoloxidase A; SOD; SOD 1; SOD1… |
Name | acrolein |
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CAS | 2-propenal |
PubMed | Abstract | RScore(About this table) | |
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19515016 | Iuchi Y, Okada F, Takamiya R, Kibe N, Tsunoda S, Nakajima O, Toyoda K, Nagae R, Suematsu M, Soga T, Uchida K, Fujii J: Rescue of anaemia and autoimmune responses in SOD1-deficient mice by transgenic expression of human SOD1 in erythrocytes. Biochem J. 2009 Aug 13;422(2):313-20. The production of antibodies against lipid peroxidation products, and acrolein, as well as autoantibodies against RBCs and carbonic anhydrase II were elevated in the SOD1 (-/-) mice, but were suppressed in the SOD1 (-/-);hSOD1 (tg/+) mice. |
88(1,1,1,8) | Details |
10965797 | Shibata N, Nagai R, Miyata S, Jono T, Horiuchi S, Hirano A, Kato S, Sasaki S, Asayama K, Kobayashi M: Nonoxidative protein glycation is implicated in familial amyotrophic lateral sclerosis with superoxide dismutase-1 mutation. Acta Neuropathol. 2000 Sep;100(3):275-84. To assess a role for oxidative stress in the pathogenesis of amyotrophic lateral sclerosis (ALS), we analyzed the immunohistochemical localization of 8-hydroxy2'- (OHdG) as a nucleic acid oxidation product, acrolein-protein adduct and (HNE)-protein adduct as lipid peroxidation products, Nepsiloncarboxymethyl- (CML) as a lipid peroxidation or protein glycoxidation product, as a protein glycoxidation product, and and pyrraline as nonoxidative protein glycation products in the spinal cord of three familial ALS patients with superoxide dismutase (SOD 1) A4V mutation, six sporadic ALS patients, and six age-matched control individuals. |
33(0,1,1,3) | Details |
11045671 | Kato S, Horiuchi S, Liu J, Cleveland DW, Shibata N, Nakashima K, Nagai R, Hirano A, Takikawa M, Kato M, Nakano I, Ohama E: Advanced glycation endproduct-modified superoxide dismutase-1 (SOD1)-positive inclusions are common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutations and transgenic mice expressing human SOD1 with a G85R mutation. Acta Neuropathol. 2000 Nov;100(5):490-505. Both types of inclusions were negative for stress-response proteins (SRPs), (HNE), acrolein, synthases (NOSs) and nitrotyrosine as representative markers of oxidative stress. |
4(0,0,0,4) | Details |
20079426 | Iuchi Y, Kibe N, Tsunoda S, Suzuki S, Mikami T, Okada F, Uchida K, Fujii J: Implication of oxidative stress as a cause of autoimmune hemolytic anemia in NZB mice. Free Radic Biol Med. 2010 Apr 1;48(7):935-44. Epub 2010 Jan 14. We have recently shown that deficiency of the superoxide dismutase 1 gene (SOD1) causes anemia and autoimmune responses against red blood cells (RBCs) and that transgenic expression of human SOD1 in erythroid cells rescues them. Levels of antibodies against and acrolein were also elevated in NZB mice. |
3(0,0,0,3) | Details |
12111360 | Shibata N, Hirano A, Hedley-Whyte ET, Dal Canto MC, Nagai R, Uchida K, Horiuchi S, Kawaguchi M, Yamamoto T, Kobayashi M: Selective formation of certain advanced glycation end products in spinal cord astrocytes of humans and mice with superoxide dismutase-1 mutation. Acta Neuropathol. 2002 Aug;104(2):171-8. Epub 2002 Apr 18. In the spinal cords from six familial ALS patients with SOD1 A4V mutation and six transgenic mice expressing G93A mutant human SOD1, immunoreactivities for N (epsilon)-(carboxyethyl) argpyrimidine, pyrraline and N (epsilon)-(carboxymethyl) as AGEs were distinct in almost all of the reactive astrocytes and obscure in the residual neurons, whereas no immunoreactivity for as an AGE, or - malondialdehyde- or acrolein- as ALEs was detectable. |
2(0,0,0,2) | Details |
19749434 | Cimini A, Moreno S, D'Amelio M, Cristiano L, D'Angelo B, Falone S, Benedetti E, Carrara P, Fanelli F, Cecconi F, Amicarelli F, Ceru MP: Early biochemical and morphological modifications in the brain of a transgenic mouse model of Alzheimer's disease: a role for peroxisomes. J Alzheimers Dis. 2009 Jan 1;18(4):935-52. The expression and localization of peroxisomal (PMP70, CAT, AOX, and THL) and peroxisome-related proteins (PEX5p, GPX1, SOD1, and SOD2) were studied in the neocortex and hippocampus of transgenic and wild-type animals. Oxidative stress markers (TBARS, acrolein, and 8-OHG) were also evaluated. |
1(0,0,0,1) | Details |