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1.15.1.1: superoxide dismutase

This is an abbreviated version!
For detailed information about superoxide dismutase, go to the full flat file.

Word Map on EC 1.15.1.1

Reaction

2 superoxide + 2 H+ =

O2
+
H2O2

Synonyms

AhSOD, alr2938, AmSOD, APE0743, ApMn-SOD1, ApMn-SOD2, ASAC_0498, Ca-Cu,Zn SOD, cambialistic superoxide dismutase, Cg-EcSOD, chloroplastic Fe-SOD, Cj-Cu, Zn SOD, cMn-SOD, cMnSOD, cold-active superoxide dismutase, copper, zinc superoxide dismutase, copper-zinc superoxide dismutase, copper/zinc superoxide dismutase, copper/zinc-superoxide dismutase, CpSOD, CSD1, CSD2, CtSOD, Cu, Zn SOD, Cu, Zn superoxide dismutase, Cu, Zn-superoxide dismutase, Cu, ZnSOD, Cu,Zn superoxide dismutase, Cu,Zn-SOD, Cu,Zn-superoxide dismutase, Cu,ZnSOD, Cu-Zn SOD, Cu-Zn superoxide dismutase, Cu-Zn-SOD, Cu/Zn SOD, Cu/Zn superoxide dismutase, Cu/Zn superoxide dismutase 1, Cu/Zn-SOD, Cu/Zn-SODI, Cu/Zn-SODII, Cu/Zn-superoxide dismutase, Cu/ZnSOD, cuprein, CuZn superoxide dismutase, CuZn superoxide dismutase 1, CuZn-SOD, CuZn-superoxide dismutase, CuZnSOD, cytMnSOD, cytocuprein, cytoplasmic manganese SOD, cytosolic Cu/Zn superoxide dismutase, cytosolic Cu/Zn-SOD, cytosolic manganese superoxide dismutase, DaSOD, dhsod-1, dismutase, superoxide, EC-SOD, ecCuZnSOD, ECSOD, ElFe-SOD, ElSOD, erythrocuprein, erythrocyte superoxide dismutase, eSOD, extracellular copper-zinc superoxide dismutase, extracellular CuZnSOD, extracellular SOD, extracellular superoxide dismutase, Fe-SOD, Fe-SODe, Fe-SOD_ASAC, Fe-superoxide dismutase, Fe-type SOD, Fe/Mn-SOD, Fe/Mn-type SOD, Fe/MnSOD, ferrisuperoxide dismutase, FeSOD, GTNG_2884, hEC-SOD, hemocuprein, hepatocuprein, high isoelectric point superoxide dismutase, intracellular Cu-Zn superoxide dismutase, iron SOD, iron SOD type, iron superoxide dismutase, iron-containing superoxide dismutase, iron-dependent superoxide dismutase, iron-superoxide dismutase, KmSod1p, LSOD, manganese superoxide dismutase, manganese-containing SOD, manganese-containing superoxide dismutase, MgMnSOD1, MgMnSOD2, mitMn-SOD, mitochondrial manganese superoxide dismutase, mMnSOD, Mn-containing superoxide dismutase, Mn-SOD, Mn-type SOD, Mn/Fe superoxide dismutase, MnSOD, MnSOD-2, MnSOD-3, MnSOD1, MnSOD47, More, mtMnSOD, mtSOD, nectarin I, neelaredoxin, Nlr, Of-cCu/ZnSOD, PASOD, perMn-SOD, pfSOD, PschSOD, PsSOD, PthipI-SODC, PthipI-SODC1, PthipI-SODC2, RmFeSOD, RsrSOD, SaCSD1, SaFe-SOD, sdB, SOD, SOD 1, SOD I, SOD-1, SOD-2, SOD-3, SOD-4, SOD1, SOD2, SOD3, SODA, SodB, SODB1, SODB2, SodC, SODF, SODI, SODII, SODIII, SODIV, SODS, SSO0316, superoxide dismutase, superoxide dismutase 1, superoxide dismutase I, superoxide dismutase II, superoxide dismutase [Cu-Zn]

ECTree

     1 Oxidoreductases
         1.15 Acting on superoxide as acceptor
             1.15.1 Acting on superoxide as acceptor (only sub-subclass identified to date)
                1.15.1.1 superoxide dismutase

Expression

Expression on EC 1.15.1.1 - superoxide dismutase

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
2-[(3-iodophenyl)methylsulfanyl]-5-pyridin-4-yl-1,3,4-oxadiazole, a known protein kinase inhibitor, decreases enzyme mutant G93A-SOD1 expression in vitro and in the brain and spinal cord in vivo. Compounds 3-[1-(3-hydroxypropyl)-1H-pyrrolo[2,3-b]pyridin-3-yl]-4-(pyrazin-2-yl)-1H-pyrrole-2,5-dione, 2-chloro-1-(4,5-dibromothiophen-2-yl)ethan-1-one, 2-bromo-1-(4-bromophenyl)ethan-1-one, 4-(5-[[(3-iodophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(3-methoxyphenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(3-fluorophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-[5-([[4-(trifluoromethyl)phenyl]methyl]sulfanyl)-1,3,4-oxadiazol-2-yl]pyridine, 4-(5-[[(3-chlorophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(3-nitrophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(3-bromophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(4-methoxyphenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(4-chlorophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(4-bromophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(4-iodophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(4-fluorophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(4-methylphenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(4-nitrophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine, 4-(5-[[(4-nitrophenyl)methyl]sulfanyl]-1,3,4-oxadiazol-2-yl)pyridine suppress the enzyme expression
-
4 constitutive isozymes, 3 cold-inducible isozymes in bulbs, at 4°C, overview
-
a decrease in mRNA levels is observed for Sod1 with osmotic stress treatment
-
after challenge with lipopolysaccharide (LPS), expression of pfSOD mRNA in hemocytes is increased, reaching the highest level at 8 h, then dropping to basal levels at 36 h
-
betulinic acid, i.e. BetA, from Pulsatilla chinensis suppresses SOD2 expression by BetA-induced cAMP-response element-binding protein, i.e. CREB protein, dephosphorylation at Ser133, which subsequently prevents SOD2 transcription through the required cAMP-response element-binding protein-binding motif on the SOD2 promoter, mechanism, overview
-
both gene expression and enzyme activity of recombinant SOD expressed in Brassica oleracea var. italica increase significantly in transgenic lines when challenged with Hyaloperonospora parasitica, the causal agent of downy mildew
-
challenge with Vibrio anguillarum increases Mm-icCu/Zn-SOD expression
constitutive overexpression of group IId WRKY gene GhWRKY39-1 in Nicotiana benthamiana confers a greater resistance to infection by both the bacterial pathogen Ralstonia solanacearum and the fungal pathogen Rhizoctonia solani. The transgenic plants also exhibit elevated mRNA levels of several pathogenrelated (PR) genes, including PR1c, PR2, and PR4. Moreover, the transgenic plants display enhanced tolerance to salt and oxidative stress and show elevated expression of several oxidationrelated genes encoding SOD, APX, CAT, and glutathioneS-transferase
-
docosahexaenoic acid inhibits enzyme transcription in cancer cells, involvement of hypoxia-inducible factor-2alpha signaling, but not of peroxisome proliferator-activated receptor alpha, overview. Suppression of SOD-1 expression by clofibrate also requires hypoxia-inducible factor-2alpha and the binding element in the SOD-1 promoter
-
effects of abiotic and biotic stresses on SOD expression, overview
enzyme expression is increased when cells are cultured with Cu2+, Cr2+, Fe3+ and Ni2+
expressions of Mn-SOD and Ni-SOD genes are highly induced
expressions of Mn-SOD and Ni-SOD genes are highly induced. The expression of the SOD genes from plants is influenced by plant growth stage and growth regulating substances. The effects of the hormone abscisic acid and osmotic stress can induce expression of Cu/Zn-SOD and Mn-SOD genes in maize
-
Fe-SODs and Cu/Zn-SODs are constitutively expressed. Effects of abiotic and biotic stresses on SOD expression, overview
gene sodB gene, encoding Fe-SOD, is expressed highly in logarithmic phase cells but is downregulated in stationaryphase cells, except when the medium is amended with FeCl3 suggesting that downregulation of Pseudomonas putida sodB in stationary phase cells is due to Fe2+ depletion in this phase of growth. Removal of Fe2+ by adding a Fe-chelator decreases the sodB transcript level, even in logarithmicphase cells
GSK3B-IX and aloisine-A induce the enzyme expression
-
in Pennisetum seedlings, abiotic stress-induced PgCuZnSOD transcript upregulation directly correlates to high protein and activity induction. PgCuZnSOD mRNA levels gradually increase to several folds on exposure of Pennisetum seedlings corresponding to gradual increase in the time period of different stress treatments i.e. dehydration, methyl viologen, NaCl and high temperature (48°C) with an exception in cold stress (4°C) where the transcript initially increased (0-12 h time-point) in comparison to control and later decreased (24 h time-point) with regards to initial rise
in Portunus trituberculatus challenged with the Hematodinium parasite, transcripts in hemocytes are decreased significantly at 3 h, and then increased significantly at 12 and 24 h, followed by significant reduction from 48 to 192 h
induced overproduction of the CyAbrB transcription factor CalA (cyanobacterial AbrBlike, Alr0946) in the cyanobacterium Nostoc sp. PCC 7120 downregulates the abundance of Fe-SOD, one of two types of SODs in strain PCC 7120. Purified recombinant CalA interacts with the promoter region of alr2938, encoding Fe-SOD, indicating a transcriptional regulation of Fe-SOD by CalA
infection of the organism by white spot syndrome virus increases the expression of cMn-SOD. Transcript levels increase transiently 1 h post-infection and then decrease as the viral infection progresses to levels significantly lower than uninfected controls by 12 h post-infection
-
KCN inhibits Cu,Zn-SOD expression
microRNA miR398, conserved in several plant species, targets two of the three Cu/Zn-SODs of Arabidopsis thaliana (CSD1 and CSD2) by triggering cleavage or inhibiting translation of their mRNAs
mRNA transcription of enzyme ecCuZnSOD in hemocytes and gill is upregulated after inoculation with Spiroplasma eriocheiris and Aeromonas hydrophila. mtMnSOD in hepatopancreas is upregulated after Aeromonas hydrophila inoculation, whereas it is downregulated after Spiroplasma eriocheiris challenge, enzyme expression pattern, overview
mRNA transcription of enzyme ecCuZnSOD in the hepatopancreas, hemocytes, and gill is upregulated after inoculation with Spiroplasma eriocheiris and Aeromonas hydrophila, enzyme expression pattern, overview
mtMnSOD in hepatopancreas is upregulated after Aeromonas hydrophila inoculation, whereas it is downregulated after Spiroplasma eriocheiris challenge, enzyme expression pattern, overview
NaCl treatment increases the transcript level of cytosolic Cu/Zn-SOD in young and mature leaves rather than in old leaves. Expression of the cytosolic Cu/Zn-SOD gene is induced by exogenous abscisic acid
-
no suppression of MnSOD by KCN
other transcription factors such as NAC, GRAS, MYB, and C3H are also involved in the regulation of SOD genes. Effects of abiotic and biotic stresses on SOD expression, overview
-
overexpression of yeast transcription factor ACE1 in Arabidopsis thaliana increases the activities of Cu/Zn-SOD, indicating that ACE1 plays an important role in the regulation of SOD gene expression. The Cu/ZnSOD gene is remarkably activated by ginsenoside Rb2 through transcription factor AP2 binding sites and its induction
regulation of the expression of miR398, overview. Effects of abiotic and biotic stresses on SOD expression, overview
salinity (50 mM NaCl) causes a decrease in activities of SOD during germination. After stress the activity increases in recovered plants. During vegetative growth, the activity of SOD is strongly enhanced and responsible for salt tolerance
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screening of Of-cCu/ZnSOD 5'-flanking region reveal the presence of several important transcription factor binding sites that potentially govern the Cu/ZnSOD expression
Sod1 mRNA levels are induced by iron, light stress and by direct H2O2stress treatment, thus confirming their role in oxidative stress response
-
temporal expression of SOD in hemocytes of bay scallops is challenged with bacteria Vibrio anguillarum, highest level at 12 h post-injection and return to normal between 24 h and 48 h post-injection
the activity of superoxide dismutase is not altered in response to any treatment of methyl jasmonate (0.0001 mM, 0.01 mM and 0.1 mM) or salicylic acid (1 mM, 5 mM and 10 mM)
-
the Arabidopsis thaliana Fe-SOD gene promoter containing the GTACT motif is repressed by Cu2+. Molecular mechanisms of GTACT motif-dependent transcriptional suppression by Cu2+ are conserved in land plants
the enzyme Fe-SOD is induced after exposure to toxic metal ions
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the enzyme is downregulated by UV-B radiation
-
the enzyme is induced by Cd2+
-
the expression of the enzyme is increased in plerocercoid larvae after treated with paraquat and significantly induced under oxidative stress
the FeSOD gene is expressed at low levels in Rhodobacter capsulatus cells grown under anaerobic or semiaerobic conditions, but expression is strongly induced upon exposure of the bacteria to air
the mRNA levels of Cu/Zn-SOD is increased in general during the metal (copper, zinc and cadmium) or thermal treatments
-
the mRNA levels of Mn-SOD is increased in general during the metal (copper, zinc and cadmium) or thermal treatments
-
the transcriptional profile and temporal assessment of Of-cCu/ZnSOD transcripts in animals under pathological (bacteriaor viral-induced) and physiological (H2O2-induced oxidative) stress conditions using quantitative PCR expression analysis, in which the enzyme expression exhibits significantly upregulated levels. Lipopolysaccharide induces the enzyme expression, and H2O2 causes a transient increase in Of-cCu/ZnSOD transcription
transgenic Nicotiana tabacum plants that overexpress a group IIe WRKY gene designated as BdWRKY36 from Brachypodium distachyon show higher SOD, POX, and CAT activity than the wild-type under drought stress. This implies that ROSscavenging systems might be more effective in transgenic than in wild-type plants. Overexpression of the BdWRKY36 gene may function in activation of the antioxidant defense system, which results in transgenic plants suffering less ROS-mediated injury under drought stress
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treatment with CuSO4 inhibits expression of SOD protein, addition of Mn2+ to the medium reduces the enzyme expressions
under 0.25 M and 0.5 M salt stress, the expression of SaCSD1 is downregulated in roots, but upregulated in leaves
up-regulation of SOD mRNA with low salinity stress, increase levels of Sod mRNA by thermal and osmotic stresses
-
UV-irradiation induces the enzyme
-