HUGO ID Detailed Result 11180

PMID	Match String	Actual String	Score	Flanking text	Edited by	Edit
10671549	Mn-SOD	Mn-SOD	1.9	Transfected cells had the same antioxidant pattern such as of Mn-SOD as SH-SY5Y cells
10671549	Mn-SOD	Mn-SOD	1.9	Under these conditions the activity of Mn-SOD is almost fully inhibited ( 33
10742195	SOD2	SOD2	0.9	A manganese SOD SOD2 is the mitochondrial equivalent of SOD1 preventing O 2 _amp_#x2212
10742195	SOD2	SOD2	0.9	Knockout mice for SOD2 die within the first week of life from heart failure
10742195	SOD2	SOD2	0.9	the heart failure and subsequent early neonatal death of the SOD2 knockout mice the ROS produced within the developing brain reach
10742195	SOD2	SOD2	0.9	By two weeks the SOD2 mutant mice develop a profound spongiform encephalopathy accompanied by gliosis
10930589	MnSOD	MnSOD	1.9	Cyanide (3 3 mM was used to distinguish between resistant MnSOD and the sensitive CuZnSOD
11050436	MnSOD	MnSOD-depleted	1.9	inhibitors on superoxide production in isolated whole mitochondria compared with MnSOD-depleted submitochondrial particles also suggests that there is a sidedness to
11050436	MnSOD	MnSOD	1.9	is likewise suggested by the presence of appreciable levels of MnSOD in the mitochondrial matrix and the comparatively low levels of
11050436	MnSOD	MnSOD	1.9	comparatively low levels of superoxide production by whole mitochondria containing MnSOD ( Ref 23
11050436	MnSOD	MnSOD	1.9	also have important functional iron-sulphur centres becomes very pronounced in MnSOD knockout mice where superoxide produced in the mitochondria is not
11050436	MnSOD	MnSOD	1.9	birth with the severe phenotypic changes evident in mice lacking MnSOD which suggests that either the mitochondria are more susceptible to
11050436	MnSOD	MnSOD	1.9	from patients with complex I deficiency displayed significant elevations of MnSOD sometimes two- to threefold whereas patients with defects in complex
11050436	MnSOD	MnSOD	1.9	symptoms (EI EI and CD were less likely to induce MnSOD above the basal levels normally seen in fibroblasts whereas patients
11050436	MnSOD	MnSOD	1.9	LD FILA which were usually fatal always had elevations of MnSOD ( 20 and 27
11050436	MnSOD	MnSOD	1.9	increased superoxide production from complex I with no increase in MnSOD ( 26
11050436	MnSOD	MnSOD	1.9	The correlation of increased levels of expression of MnSOD with a poor prognosis in complex I deficiency suggests that
11050436	MnSOD	MnSOD	1.9	deficiency suggests that responding to the increased superoxide by inducing MnSOD could itself be detrimental in the long term because of
11050436	MnSOD	MnSOD	1.9	radical were demonstrated in cell lines with increased induction of MnSOD ( 28
11050436	MnSOD	MnSOD	1.9	to form increased amounts of superoxide (iv) iv induction of MnSOD (v) v increased formation of hydrogen peroxide from superoxide via
11050436	MnSOD	MnSOD	1.9	(v) v increased formation of hydrogen peroxide from superoxide via MnSOD or (vi) vi transformation of hydrogen peroxide to hydroxyl radicals
11050436	MnSOD	MnSOD	1.9	The overexpression of MnSOD in cultured rat glioma cells made those cells more sensitive
11050436	MnSOD	MnSOD	1.9	to damage by radiation and carcinogens 45 and 46 whereas MnSOD overexpression in mouse heart is protective against adriamycin-induced cardiotoxicity 47
11050436	MnSOD	MnSOD	1.9	O 2 by CuZnSOD if in the matrix space by MnSOD
11328670	MnSOD	MnSOD	2.9	Manganese superoxide dismutase (MnSOD) MnSOD is essential for life as dramatically illustrated by the neonatal
11328670	MnSOD	MnSOD	2.9	by the neonatal lethality of mice that are deficient in MnSOD
11328670	MnSOD	MnSOD	2.9	addition mice expressing only 50% of the normal compliment of MnSOD demonstrate increased susceptibility to oxidative stress and severe mitochondrial dysfunction
11328670	MnSOD	MnSOD	2.9	Thus it is important to know the status of both MnSOD protein levels and activity in order to assess its role
11328670	MnSOD	MnSOD	2.9	Numerous studies have shown that MnSOD can be induced to protect against pro-oxidant insults resulting from
11328670	MnSOD	MnSOD	2.9	In addition overexpression of MnSOD has been shown to protect against pro-apoptotic stimuli as well
11328670	MnSOD	MnSOD	2.9	Conversely several studies have reported declines in MnSOD activity during diseases including cancer aging progeria asthma and transplant
11328670	MnSOD	MnSOD	2.9	Certainly MnSOD gene expression or other defects could play a role in
11328670	MnSOD	MnSOD	2.9	However based on recent findings regarding the susceptibility of MnSOD to oxidative inactivation it is equally likely that post-translational modification
11328670	MnSOD	MnSOD	2.9	oxidative inactivation it is equally likely that post-translational modification of MnSOD may account for the loss of activity
11328670	MnSOD	MnSOD	2.9	Our laboratory has recently demonstrated that MnSOD is tyrosine nitrated and inactivated during human kidney allograft rejection
11328670	MnSOD	MnSOD	2.9	nitrate critical tyrosine residues and to induce dityrosine formation in MnSOD
11328670	MnSOD	MnSOD	2.9	Tyrosine nitration and inactivation of MnSOD would lead to increased levels of superoxide and concomitant increases
11328670	MnSOD	MnSOD	2.9	This article assesses the important role of MnSOD activity in various pathological states in light of this potentially
11679167	MnSOD	MnSOD	2.4	superoxide dismutases (either either the cytosolic CuZnSOD or the mitochondrial MnSOD or both ( Srinivasan et al. 2000 De Freitas et
11679167	MnSOD	MnSOD	2.4	such as the increase of the mitochondrial superoxide dismutase (MnSOD) MnSOD activity by ethanol the high ethanol sensitivity of S cerevisiae
11679167	MnSOD	MnSOD	2.4	the high ethanol sensitivity of S cerevisiae cells deficient in MnSOD ( Costa and Costa and the induction of CTT1 gene
11679167	SOD2	SOD2	2.7	in oxidative stress only two genes are under Hap1p regulation SOD2 and CTT1
11679167	SOD2	SOD2	2.7	Hap1p is a positive regulator of SOD2 promoter in glucose growing cells ensuring a basel level of
11679167	SOD2	SOD2	2.7	regulates the transcriptional activation of the antioxidant genes such as SOD2 (mitochondrial mitochondrial superoxide dismutase CTA1 (peroxisomal peroxisomal catalase CTT1 (cytosolic
11679167	SOD2	SOD2	2.7	induction of several genes important for respiration as well as SOD2 and UBI4 ( Pinkham et al. 1997
11679167	SOD2	SOD2	2.7	growth in a non-fermentable carbon source the transcriptional activation of SOD2 and CTT1 genes is also regulated by Msn2p and Msn4p
11905995	MnSOD	MnSOD	2.2	Similarly overexpression of mitochondrial antioxidative genes MnSOD and GPX4 by stable transfection significantly increased NSC-34 motor neuron-like
12392777	SOD2	SOD-2	1.2	Zn superoxide dismutase (SOD-1) SOD-1 and Mn superoxide dismutase (SOD-2) SOD-2 which catalyze the conversion of O 2 _amp_#x221a _amp_#x2212 to
12392777	SOD2	SOD-2	1.2	influence the expression of a large number of genes including SOD-2 50 179 and 180
14648077	SOD2	SOD2	0.9	superoxide dismutase (SOD) SOD EC 1.15.1.1 have been identified SOD1 SOD2 and SOD3 9
14739060	MnSOD	MnSOD	1.8	Tat protein decreases GSH and down regulate MnSOD gene expression leading to oxidative stress 16
15850589	MnSOD	MnSOD	1.9	In agreement with this overexpression of MnSOD attenuates neuronal death in cellular models of FALS 12 and
15896810	MnSOD	MnSOD	1.9	Up-regulation of protein manganese superoxide dismutase (MnSOD) MnSOD fails to occur in FRDA fibroblasts exposed to iron 25
15896810	MnSOD	MnSOD	1.9	free radical signaling is responsible for the reduced induction of MnSOD 26
16227974	SOD2	Sod2	1.7	Superoxide dismutase-2 - Sod2 - mice which lack one copy of this mitochondrial antioxidant
16227974	SOD2	Sod2	1.7	protein peroxiredoxin-I (Ref Ref 32 or are heterozygous deleted for Sod2 (Ref Ref 33 have increased spontaneous tumour formation
16227974	SOD2	Sod2	1.7	Sod2
17099894	SOD2	SOD2	0.9	cytochrome c oxidase subunit-I and alpha-synuclein as well as nitrated SOD2 accumulate in mSOD1 mouse spinal cord
17174478	MnSOD	MnSOD	1.9	Fig 1 The Human MnSOD active site
17174478	MnSOD	MnSOD	1.9	In the wild type MnSOD structure (PDB PDB code 1N0J the His26 His74 His163 and
17174478	MnSOD	MnSOD	1.9	inactivation of the mitochondrial form of SOD manganese SOD (MnSOD), MnSOD in mice
17174478	MnSOD	MnSOD	1.9	Treatment with an SOD mimetic MnTBAP rescued the MnSOD _amp_#x02212;/_amp_#x02212; _amp_#x02212 _amp_#x02212 mutant mice from this systemic pathology and
17174478	MnSOD	MnSOD	1.9	of ROS ( Melov et al. 1998 normally removed by MnSOD
17174478	MnSOD	MnSOD	1.9	To define how MnSOD controls ROS levels in the cell the molecular mechanism of
17174478	MnSOD	MnSOD	1.9	controls ROS levels in the cell the molecular mechanism of MnSOD has been extensively characterized through combined structural and biochemical studies
17174478	MnSOD	MnSOD	1.9	The crystal structure of human MnSOD revealed that the enzyme forms a homotetramer ( Borgstahl et
17174478	MnSOD	MnSOD	1.9	suggests that maintenance of the correct hydrogen bond partners in MnSOD is essential for the highly tuned reactivity of the active
17174478	MnSOD	MnSOD	1.9	dismutase (Cu,Zn Cu Zn SOD which similar to the mitochondrial MnSOD is responsible for the disproportionation of harmful superoxide radicals to
17191135	Mn-SOD	Mn-SOD	1.9	genes such as heme oxygenase thioredoxin and detoxificant enzymes (Mn-SOD, Mn-SOD glutathione S-transferase NADPH quinone reductase cytokine immunoreceptors and growth factors
17191135	Mn-SOD	Mn-SOD	1.9	of stress-inducible genes 107 -124 such as HO-1 G-glutamylcysteine synthetase Mn-SOD and glutathione S-transferase
17496232	MnSOD	MnSOD	1.9	MW molecular weight MnSOD manganese superoxide dismutase 2D two dimensional
17496232	MnSOD	MnSOD	1.9	In the presence of mitochondrial manganese superoxide dismutase (MnSOD), MnSOD most of O 2 is dismutated to H 2 O
17496232	MnSOD	MnSOD	1.9	dismutates to H 2 O 2 a reaction catalized by MnSOD ( reactions 4 and 5
17496232	MnSOD	MnSOD	1.9	in mitochondrial metabolism will depend on NO concentration and on MnSOD level
17496232	MnSOD	MnSOD	1.9	decays by reaction 4 and 2 depending on NO and MnSOD concentrations mitochondrial utilization of NO involves the formation of H
17496232	MnSOD	MnSOD	1.9	As described in cell transformation ( 71 concomitant changes in MnSOD have two effects to increase cytosolic H 2 O 2
17496232	MnSOD	MnSOD	1.9	Cu ZnSOD whereas in mitochondria the reaction is catalyzed by MnSOD
17496232	MnSOD	MnSOD	1.9	the concentration and activities of mtNOS cytosolic classic NOS isoforms MnSOD catalase and peroxidases
17496232	MnSOD	MnSOD	1.9	The main mitochondrial antioxidant defense is MnSOD
9462746	manganese superoxide dismutase	manganese superoxide dismutase	1.0	a novel neurological phenotype in mice lacking mitochondrial manganese superoxide dismutase.
10671549	mn sod	mn sod	1.0	transfected cells had the same antioxidant pattern such as of mn sod as sh sy5y cells.
10671549	mn sod	mn sod	1.0	under these conditions the activity of mn sod is almost fully inhibited 33 .
11328670	manganese superoxide dismutase	manganese superoxide dismutase	1.0	invited review: manganese superoxide dismutase in disease.
11328670	manganese superoxide dismutase	manganese superoxide dismutase	1.0	manganese superoxide dismutase mnsod is essential for life as dramatically illustrated by the neonatal lethality of mice that are deficient in mnsod.
11679167	mn superoxide dismutase	mn superoxide dismutase	1.0	ted to respiratory growth conditions which display high levels of antioxidant defences maclean et al. 2001 and by the decreased life span observed in mutants deficient in cuzn superoxide dismutase or mn superoxide dismutase longo et al. 1999 .
11679167	mn superoxide dismutase	mn superoxide dismutase	1.0	the deficiency in mn superoxide dismutase leads to the accumulation of superoxide radicals which destroy the 4fe_amp_#x2013;4s clusters of mitochondrial enzymes e.g. aconitase leading to an impaired respiratory activity.
11978481	manganese superoxide dismutase	manganese superoxide dismutase	1.0	one protein was manganese superoxide dismutase which was previously shown to be selectively nitrated at tyr 34 and inactivated [ 22 ].
11978481	manganese superoxide dismutase	manganese superoxide dismutase	1.0	a 6 fold increase in 3 nitrotyrosine concentrations was detected in ad cerebrospinal fluid as compared to age matched controls [ 41 ] and an increase in nitrated manganese superoxide dismutase was also reported [ 42 ].
11978481	manganese superoxide dismutase	manganese superoxide dismutase	1.0	an increase in nitrated manganese superoxide dismutase was found in cerebrospinal fluid [ 42 ].
11978481	manganese superoxide dismutase	manganese superoxide dismutase	1.0	other groups reported marked increases of both free 3 nitrotyrosine and nitrated manganese superoxide dismutase in the cerebrospinal fluid of sporadic als patients [ 42 and 62 ].
12392777	mn superoxide dismutase	mn superoxide dismutase	1.0	the antioxidant enzymes in the brain include cu/zn superoxide dismutase sod 1 and mn superoxide dismutase sod 2 which catalyze the conversion of o 2 _amp_#x221a; _amp_#x2212; to h 2 o 2 [ 73 ].
15896810	manganese superoxide dismutase	manganese superoxide dismutase	1.0	up regulation of protein manganese superoxide dismutase mnsod fails to occur in frda fibroblasts exposed to iron [25] .
15896810	manganese superoxide dismutase	manganese superoxide dismutase	1.0	the factors responsible for this include the inner mitochondrial membrane lipid composition and/or the oxidant/antioxidant balance particularly manganese superoxide dismutase and/or heat shock protein activity and expressions as well as the glutathione status.
16227974	superoxide dismutase 2	superoxide dismutase 2	1.0	superoxide dismutase 2 +/ sod2 +/ mice which lack one copy of this mitochondrial antioxidant protein show an increased rate of atherosclerotic plaque formation 26 .
17174478	manganese superoxide dismutase	manganese superoxide dismutase	1.0	ros removal by manganese superoxide dismutase
17174478	manganese superoxide dismutase	manganese superoxide dismutase	1.0	ros removal by manganese superoxide dismutase
17191135	mn sod	mn sod	1.0	in eukaryotes typical examples are genes such as heme oxygenase thioredoxin and detoxificant enzymes mn sod glutathione s transferase nadph: quinone reductase cytokine immunoreceptors and growth factors.
17191135	mn sod	mn sod	1.0	e alone in unstressed conditions by promoting acetylation of dna binding proteins may modulate are mediated expression of stress inducible genes [ 107 124 ] such as ho 1 g glutamylcysteine synthetase mn sod and glutathione s transferase.
17496232	manganese superoxide dismutase	manganese superoxide dismutase	1.0	mw molecular weight; mnsod manganese superoxide dismutase; 2d two dimensional.
17496232	manganese superoxide dismutase	manganese superoxide dismutase	1.0	in the presence of mitochondrial manganese superoxide dismutase mnsod most of o 2 is dismutated to h 2 o 2 which is freely diffusible to cytosol.