PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
21593737-3	2011	Cellular defenses against ROS include the enzymes manganese superoxide dismutase (MnSOD), catalase (CAT) and glutathione peroxidase type-1 (GPx-1).	Reactive Oxygen Species	26-29	superoxide dismutase 2	Homo sapiens	50-80
21593737-3	2011	Cellular defenses against ROS include the enzymes manganese superoxide dismutase (MnSOD), catalase (CAT) and glutathione peroxidase type-1 (GPx-1).	Reactive Oxygen Species	26-29	superoxide dismutase 2	Homo sapiens	82-87
21543431-11	2011	However, when histone acetylation was induced by histone deacetylase inhibitors, progesterone inhibited the TNFalpha-induced NF-kappaB binding to the Mn-SOD enhancer.	Progesterone	81-93	superoxide dismutase 2	Homo sapiens	150-156
21576359-7	2011	Overexpression of MnSOD inhibited IFN-gamma-mediated ROS accumulation and partially rescued RelA-deficient cells from necroptosis, while RNA interference (RNAi)-mediated silencing of sod2 expression increased susceptibility to IFN-gamma-induced cell death.	Reactive Oxygen Species	53-56	superoxide dismutase 2	Homo sapiens	18-23
21352821-7	2011	All the agents, except catechin, tended to reduce the expression of SOD2 induced by ethanol.	Catechin	23-31	superoxide dismutase 2	Homo sapiens	68-72
21045076-7	2011	Differentiated HL60 cells were stimulated with phorbol-12-myristate-7-acetate (PMA) after inhibition of SOD2 by small interfering RNA followed by respiratory burst assessment using flow cytometry.	phorbol-12-myristate-7-acetate	47-77	superoxide dismutase 2	Homo sapiens	104-108
21045076-7	2011	Differentiated HL60 cells were stimulated with phorbol-12-myristate-7-acetate (PMA) after inhibition of SOD2 by small interfering RNA followed by respiratory burst assessment using flow cytometry.	Tetradecanoylphorbol Acetate	79-82	superoxide dismutase 2	Homo sapiens	104-108
21045076-10	2011	Inhibition of SOD2 reduced the PMA-induced respiratory burst and IL1A, IL-1R1, IL-1R2 and IL8RA gene expression in neutrophil-differentiated HL60 cells.	Tetradecanoylphorbol Acetate	31-34	superoxide dismutase 2	Homo sapiens	14-18
21045076-11	2011	CONCLUSIONS: Because of the critical role of SOD2 in the generation of hydrogen peroxide during phagocytosis, downregulation of SOD2 gene expression after LPS stimulation in neutrophils from patients with CKD indicates a potential mechanism for neutrophil dysfunction and cytokine dysregulation in these patients.	Hydrogen Peroxide	71-88	superoxide dismutase 2	Homo sapiens	45-49
21045076-11	2011	CONCLUSIONS: Because of the critical role of SOD2 in the generation of hydrogen peroxide during phagocytosis, downregulation of SOD2 gene expression after LPS stimulation in neutrophils from patients with CKD indicates a potential mechanism for neutrophil dysfunction and cytokine dysregulation in these patients.	Hydrogen Peroxide	71-88	superoxide dismutase 2	Homo sapiens	128-132
21537499-0	2011	Manganese(II) complexes of scorpiand-like azamacrocycles as MnSOD mimics.	Manganese(2+)	0-13	superoxide dismutase 2	Homo sapiens	60-65
21537499-0	2011	Manganese(II) complexes of scorpiand-like azamacrocycles as MnSOD mimics.	azamacrocycles	42-56	superoxide dismutase 2	Homo sapiens	60-65
21537499-1	2011	Mn(II) complexes of scorpiand-type azamacrocycles constituted by a tretrazapyridinophane core appended with an ethylamino tail including 2- or 4-quinoline functionalities show very appealing in vitro SOD activity.	Manganese(2+)	0-6	superoxide dismutase 2	Homo sapiens	200-203
21537499-1	2011	Mn(II) complexes of scorpiand-type azamacrocycles constituted by a tretrazapyridinophane core appended with an ethylamino tail including 2- or 4-quinoline functionalities show very appealing in vitro SOD activity.	azamacrocycles	35-49	superoxide dismutase 2	Homo sapiens	200-203
21537499-1	2011	Mn(II) complexes of scorpiand-type azamacrocycles constituted by a tretrazapyridinophane core appended with an ethylamino tail including 2- or 4-quinoline functionalities show very appealing in vitro SOD activity.	tretrazapyridinophane	67-88	superoxide dismutase 2	Homo sapiens	200-203
21537499-1	2011	Mn(II) complexes of scorpiand-type azamacrocycles constituted by a tretrazapyridinophane core appended with an ethylamino tail including 2- or 4-quinoline functionalities show very appealing in vitro SOD activity.	Ethanamine-N,2-diylradical	111-121	superoxide dismutase 2	Homo sapiens	200-203
21537499-1	2011	Mn(II) complexes of scorpiand-type azamacrocycles constituted by a tretrazapyridinophane core appended with an ethylamino tail including 2- or 4-quinoline functionalities show very appealing in vitro SOD activity.	2- or 4-quinoline	137-154	superoxide dismutase 2	Homo sapiens	200-203
21566644-3	2011	Here, we report that SOD2 is acetylated at Lys 68 and that this acetylation decreases SOD2 activity.	Lysine	43-46	superoxide dismutase 2	Homo sapiens	21-25
21566644-3	2011	Here, we report that SOD2 is acetylated at Lys 68 and that this acetylation decreases SOD2 activity.	Lysine	43-46	superoxide dismutase 2	Homo sapiens	86-90
21566644-5	2011	Increase of reactive oxygen species (ROS) levels stimulates SIRT3 transcription, leading to SOD2 deacetylation and activation.	Reactive Oxygen Species	12-35	superoxide dismutase 2	Homo sapiens	92-96
21566644-5	2011	Increase of reactive oxygen species (ROS) levels stimulates SIRT3 transcription, leading to SOD2 deacetylation and activation.	Reactive Oxygen Species	37-40	superoxide dismutase 2	Homo sapiens	92-96
21566644-6	2011	SOD2-mediated ROS reduction is synergistically increased by SIRT3 co-expression, but is cancelled by SIRT3 depletion.	Reactive Oxygen Species	14-17	superoxide dismutase 2	Homo sapiens	0-4
21352821-7	2011	All the agents, except catechin, tended to reduce the expression of SOD2 induced by ethanol.	Ethanol	84-91	superoxide dismutase 2	Homo sapiens	68-72
21893688-9	2011	Hypoxia-induced ROS generation was significantly inhibited by CF, through the up-regulated expression of MnSOD, an anti-oxidant responsible for mitochondrial function preservation.	Reactive Oxygen Species	16-19	superoxide dismutase 2	Homo sapiens	105-110
21354306-13	2011	Thus, overexpression of both IRS-1 and IRS-2 induces complete resistance to glucose-induced caspase-3 activation via PI3-kinase mediated BAD phosphorylation and MnSOD expression independent of FoxO1.	Glucose	76-83	superoxide dismutase 2	Homo sapiens	161-166
21384159-4	2011	Mn-SOD and Catalase, and release of cytochrome c into the cytosol, were observed in time-dependent manner when cells were irradiated (5 Gy) in presence of Hoechst 33342.	bisbenzimide ethoxide trihydrochloride	155-168	superoxide dismutase 2	Homo sapiens	0-19
21384159-6	2011	Treatment with antioxidants PEG-MnSOD and PEG-catalase inhibited the increase in ROS and loss of cell survival, suggesting the involvement of ROS in the Hoechst 33342-induced cell death.	Reactive Oxygen Species	81-84	superoxide dismutase 2	Homo sapiens	32-37
21384159-6	2011	Treatment with antioxidants PEG-MnSOD and PEG-catalase inhibited the increase in ROS and loss of cell survival, suggesting the involvement of ROS in the Hoechst 33342-induced cell death.	Reactive Oxygen Species	142-145	superoxide dismutase 2	Homo sapiens	32-37
21384159-6	2011	Treatment with antioxidants PEG-MnSOD and PEG-catalase inhibited the increase in ROS and loss of cell survival, suggesting the involvement of ROS in the Hoechst 33342-induced cell death.	bisbenzimide ethoxide trihydrochloride	153-166	superoxide dismutase 2	Homo sapiens	32-37
21574139-0	2011	Ala-9Val polymorphism of Mn-SOD gene in sickle cell anemia.	ala-9val	0-8	superoxide dismutase 2	Homo sapiens	25-31
21574139-2	2011	We looked for a possible genetic association between the functional polymorphism Ala-9Val in the human Mn-SOD gene and sickle cell anemia.	ala-9val	81-89	superoxide dismutase 2	Homo sapiens	103-109
21574139-4	2011	Alanine versus valine polymorphism in the signal peptide of the Mn-SOD gene was evaluated using a primer pair to amplify a 107-bp fragment followed by digestion with the restriction enzyme NgoMIV.	Alanine	0-7	superoxide dismutase 2	Homo sapiens	64-70
21574139-4	2011	Alanine versus valine polymorphism in the signal peptide of the Mn-SOD gene was evaluated using a primer pair to amplify a 107-bp fragment followed by digestion with the restriction enzyme NgoMIV.	Valine	15-21	superoxide dismutase 2	Homo sapiens	64-70
21445095-10	2011	From these results, we conclude that complex I-derived O(2) (-), produced through reverse electron transport due to enhanced metabolism and a high activity of complex I, was dismutated into H(2)O(2) by MnSOD induced via NF-kappaB activation and that the dismutated mH(2)O(2) stimulated muscle differentiation as a signaling messenger.	o(2)	55-59	superoxide dismutase 2	Homo sapiens	202-207
21445095-10	2011	From these results, we conclude that complex I-derived O(2) (-), produced through reverse electron transport due to enhanced metabolism and a high activity of complex I, was dismutated into H(2)O(2) by MnSOD induced via NF-kappaB activation and that the dismutated mH(2)O(2) stimulated muscle differentiation as a signaling messenger.	Water	190-195	superoxide dismutase 2	Homo sapiens	202-207
21445095-10	2011	From these results, we conclude that complex I-derived O(2) (-), produced through reverse electron transport due to enhanced metabolism and a high activity of complex I, was dismutated into H(2)O(2) by MnSOD induced via NF-kappaB activation and that the dismutated mH(2)O(2) stimulated muscle differentiation as a signaling messenger.	mh(2)o	265-271	superoxide dismutase 2	Homo sapiens	202-207
21528488-11	2011	An increased staining of SOD2 was observed in SKOV3.ip1 over that of SKOV3 in IHC analysis.	Isopenicillin N	52-55	superoxide dismutase 2	Homo sapiens	25-29
20617513-3	2011	Here, we report that manganese-enhanced magnetic resonance imaging (MEMRI) represents a promising approach for a more selective mesothelioma imaging by monitoring a high-level expression of manganese-superoxide dismutase (Mn-SOD), which is observed in many MM.	Manganese	21-30	superoxide dismutase 2	Homo sapiens	190-220
20617513-4	2011	We found that most human MM cells overexpressed Mn-SOD protein compared with human mesothelial cells and that NCI-H226 human MM cells highly expressed Mn-SOD and augmented Mn accumulation when loaded with manganese chloride (MnCl(2)).	manganese chloride	205-223	superoxide dismutase 2	Homo sapiens	151-157
21130430-8	2011	The SOD2 Ala allele frequency was 49% both in controls and IVF patients.	Alanine	9-12	superoxide dismutase 2	Homo sapiens	4-8
21053390-0	2011	Glabridin, a phytoestrogen from licorice root, up-regulates manganese superoxide dismutase, catalase and paraoxonase 2 under glucose stress.	Glucose	125-132	superoxide dismutase 2	Homo sapiens	60-90
21236335-5	2011	Basal levels of mitochondrial O(2)( -) or manganese superoxide dismutase (MnSOD) strictly correlated with the IC(50) for GEM or the percentage of synergism.	gemcitabine	121-124	superoxide dismutase 2	Homo sapiens	42-72
21236335-5	2011	Basal levels of mitochondrial O(2)( -) or manganese superoxide dismutase (MnSOD) strictly correlated with the IC(50) for GEM or the percentage of synergism.	gemcitabine	121-124	superoxide dismutase 2	Homo sapiens	74-79
21172440-1	2011	Manganese superoxide dismutase (Mn-SOD) is one of the major enzymes responsible for the defense against oxidative damage due to reactive oxygen species (ROS) in the mitochondria.	Reactive Oxygen Species	128-151	superoxide dismutase 2	Homo sapiens	0-30
21172440-1	2011	Manganese superoxide dismutase (Mn-SOD) is one of the major enzymes responsible for the defense against oxidative damage due to reactive oxygen species (ROS) in the mitochondria.	Reactive Oxygen Species	153-156	superoxide dismutase 2	Homo sapiens	0-30
21062213-8	2011	Distribution of MnSOD genotypes was 47% Val/Val-variant, 29.5% Ala/Val and 23.5% Ala/Ala-variants.	Valine	40-43	superoxide dismutase 2	Homo sapiens	16-21
21235219-8	2011	Expressions of DNA repair genes ERCC6, XPC, OGG1, and reactive oxygen species (ROS) scavenger MnSOD was also altered in arsenic-exposed cells.	Reactive Oxygen Species	54-77	superoxide dismutase 2	Homo sapiens	94-99
21062213-8	2011	Distribution of MnSOD genotypes was 47% Val/Val-variant, 29.5% Ala/Val and 23.5% Ala/Ala-variants.	Alanine	63-66	superoxide dismutase 2	Homo sapiens	16-21
21062213-8	2011	Distribution of MnSOD genotypes was 47% Val/Val-variant, 29.5% Ala/Val and 23.5% Ala/Ala-variants.	Alanine	81-84	superoxide dismutase 2	Homo sapiens	16-21
21062213-8	2011	Distribution of MnSOD genotypes was 47% Val/Val-variant, 29.5% Ala/Val and 23.5% Ala/Ala-variants.	Alanine	81-84	superoxide dismutase 2	Homo sapiens	16-21
21215799-0	2011	Resveratrol interacts with estrogen receptor-beta to inhibit cell replicative growth and enhance stress resistance by upregulating mitochondrial superoxide dismutase.	Resveratrol	0-11	superoxide dismutase 2	Homo sapiens	131-165
21215799-5	2011	When small interfering RNA was used to prevent induction of MnSOD expression, the effects of RES on population doubling time of cells in culture, and resistance to cell death after exposure to hydrogen peroxide or paraquat, were abolished.	Hydrogen Peroxide	193-210	superoxide dismutase 2	Homo sapiens	60-65
21352808-4	2011	Notably, GW501516 up-regulated the expression of antioxidant genes, such as glutathione peroxidase 1, thioredoxin 1, manganese superoxide dismutase and heme oxygenase 1.	GW 501516	9-17	superoxide dismutase 2	Homo sapiens	117-147
21235219-8	2011	Expressions of DNA repair genes ERCC6, XPC, OGG1, and reactive oxygen species (ROS) scavenger MnSOD was also altered in arsenic-exposed cells.	Reactive Oxygen Species	79-82	superoxide dismutase 2	Homo sapiens	94-99
21235219-8	2011	Expressions of DNA repair genes ERCC6, XPC, OGG1, and reactive oxygen species (ROS) scavenger MnSOD was also altered in arsenic-exposed cells.	Arsenic	120-127	superoxide dismutase 2	Homo sapiens	94-99
21167124-0	2011	Exploring the molecular basis of human manganese superoxide dismutase inactivation mediated by tyrosine 34 nitration.	Tyrosine	95-103	superoxide dismutase 2	Homo sapiens	39-69
21167124-1	2011	Manganese Superoxide Dismutase (MnSOD) is an essential mitochondrial antioxidant enzyme that protects organisms against oxidative damage, dismutating superoxide radical (O2(.	Superoxides	150-168	superoxide dismutase 2	Homo sapiens	0-30
21167124-1	2011	Manganese Superoxide Dismutase (MnSOD) is an essential mitochondrial antioxidant enzyme that protects organisms against oxidative damage, dismutating superoxide radical (O2(.	Superoxides	150-168	superoxide dismutase 2	Homo sapiens	32-37
21167124-1	2011	Manganese Superoxide Dismutase (MnSOD) is an essential mitochondrial antioxidant enzyme that protects organisms against oxidative damage, dismutating superoxide radical (O2(.	Superoxides	170-172	superoxide dismutase 2	Homo sapiens	0-30
21167124-1	2011	Manganese Superoxide Dismutase (MnSOD) is an essential mitochondrial antioxidant enzyme that protects organisms against oxidative damage, dismutating superoxide radical (O2(.	Superoxides	170-172	superoxide dismutase 2	Homo sapiens	32-37
21167124-6	2011	However, the molecular basis about MnSOD tyrosine nitration affects the protein catalytic function is mostly unknown.	Tyrosine	41-49	superoxide dismutase 2	Homo sapiens	35-40
21386137-3	2011	Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases.	Water	172-177	superoxide dismutase 2	Homo sapiens	0-30
20615501-9	2011	In parallel, rhCG augmented the expression of the forkhead transcription factor FOXO1 and its downstream target, the ROS scavenger SOD2.	Reactive Oxygen Species	117-120	superoxide dismutase 2	Homo sapiens	131-135
21150282-9	2011	In direct support of these findings, the tumor promoting effects of Cav-1 deficient fibroblasts could be functionally suppressed (nearly 2-fold) by the recombinant over-expression of SOD2 (superoxide dismutase 2), a known mitochondrial enzyme that de-activates superoxide, thereby reducing mitochondrial oxidative stress.	Superoxides	189-199	superoxide dismutase 2	Homo sapiens	183-187
21056653-6	2011	Both MnSOD clones exhibit lower superoxide levels and higher H(2)O(2) levels.	Superoxides	32-42	superoxide dismutase 2	Homo sapiens	5-10
21056653-7	2011	MnSOD-overexpressing cells show higher proliferation rates in complete medium, but in steroid-free medium MnSOD-S12 cells are still capable of proliferation.	Steroids	86-93	superoxide dismutase 2	Homo sapiens	106-111
21056653-9	2011	MnSOD also induces up-regulation of Bcl-2 and prevents docetaxel-, etoposide-, or TNF-induced cell death.	Docetaxel	55-64	superoxide dismutase 2	Homo sapiens	0-5
21056653-9	2011	MnSOD also induces up-regulation of Bcl-2 and prevents docetaxel-, etoposide-, or TNF-induced cell death.	Etoposide	67-76	superoxide dismutase 2	Homo sapiens	0-5
21386137-3	2011	Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases.	Reactive Oxygen Species	68-71	superoxide dismutase 2	Homo sapiens	0-30
21386137-3	2011	Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases.	Reactive Oxygen Species	68-71	superoxide dismutase 2	Homo sapiens	32-37
21386137-3	2011	Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
21386137-3	2011	Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases.	Hydrogen Peroxide	118-135	superoxide dismutase 2	Homo sapiens	0-30
21386137-3	2011	Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases.	Hydrogen Peroxide	118-135	superoxide dismutase 2	Homo sapiens	32-37
21386137-3	2011	Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases.	Water	172-177	superoxide dismutase 2	Homo sapiens	32-37
21386137-4	2011	It has recently been shown that MnSOD enzymatic activity is regulated by the reversible acetylation of specific, evolutionarily conserved lysine(s) in the protein.	Lysine	138-144	superoxide dismutase 2	Homo sapiens	32-37
21386137-5	2011	These results, suggest for the first time, that the mitochondria contain bidirectional post-translational signaling networks, similar to that observed in the cytoplasm and nucleus, and that changes in lysine acetylation alter MnSOD enzymatic activity.	Lysine	201-207	superoxide dismutase 2	Homo sapiens	226-231
21386137-6	2011	In addition, these new results demonstrate that the mitochondrial anti-aging or fidelity / sensing protein, SIRT3, responds to changes in mitochondrial nutrient and/or redox status to alter the enzymatic activity of specific downstream targets, including MnSOD that adjusts and/or maintains ROS levels as well as metabolic homeostatic poise.	Reactive Oxygen Species	291-294	superoxide dismutase 2	Homo sapiens	255-260
21291402-0	2011	Does more MnSOD mean more hydrogen peroxide?	Hydrogen Peroxide	26-43	superoxide dismutase 2	Homo sapiens	10-15
21131394-1	2011	Reactive oxygen species (ROS) are generated as a result of normal cellular metabolism, mainly through the mitochondria and peroxisomes, but their release is enhanced by the activation of oxidant enzymes such as NADPH oxidases or downregulation of endogenous antioxidant enzymes such as manganese-superoxide dismutase (MnSOD) and catalase.	Reactive Oxygen Species	0-23	superoxide dismutase 2	Homo sapiens	286-316
21131394-1	2011	Reactive oxygen species (ROS) are generated as a result of normal cellular metabolism, mainly through the mitochondria and peroxisomes, but their release is enhanced by the activation of oxidant enzymes such as NADPH oxidases or downregulation of endogenous antioxidant enzymes such as manganese-superoxide dismutase (MnSOD) and catalase.	Reactive Oxygen Species	0-23	superoxide dismutase 2	Homo sapiens	318-323
21131394-1	2011	Reactive oxygen species (ROS) are generated as a result of normal cellular metabolism, mainly through the mitochondria and peroxisomes, but their release is enhanced by the activation of oxidant enzymes such as NADPH oxidases or downregulation of endogenous antioxidant enzymes such as manganese-superoxide dismutase (MnSOD) and catalase.	Reactive Oxygen Species	25-28	superoxide dismutase 2	Homo sapiens	286-316
21131394-1	2011	Reactive oxygen species (ROS) are generated as a result of normal cellular metabolism, mainly through the mitochondria and peroxisomes, but their release is enhanced by the activation of oxidant enzymes such as NADPH oxidases or downregulation of endogenous antioxidant enzymes such as manganese-superoxide dismutase (MnSOD) and catalase.	Reactive Oxygen Species	25-28	superoxide dismutase 2	Homo sapiens	318-323
21291402-3	2011	A common misconception is that the increased MnSOD levels will result in increased hydrogen peroxide levels.	Hydrogen Peroxide	83-100	superoxide dismutase 2	Homo sapiens	45-50
21291402-5	2011	Data are offered that demonstrate the ability of MnSOD, in the presence of nitric oxide, to utilize hydrogen peroxide to produce superoxide and the more toxic oxidant, peroxynitrite.	Nitric Oxide	75-87	superoxide dismutase 2	Homo sapiens	49-54
21434856-3	2011	It is now commonly held that loss of Sod2 expression is likely an early event in tumor progression allowing for further propagation of the tumorigenic phenotype resulting from steady state increases in free radical production.	Free Radicals	202-214	superoxide dismutase 2	Homo sapiens	37-41
21291402-5	2011	Data are offered that demonstrate the ability of MnSOD, in the presence of nitric oxide, to utilize hydrogen peroxide to produce superoxide and the more toxic oxidant, peroxynitrite.	Hydrogen Peroxide	100-117	superoxide dismutase 2	Homo sapiens	49-54
21434856-6	2011	Sod2 overexpression in many instances enhances the metastatic phenotype that is reversed by efficient H(2)O(2) scavenging.	Hydrogen Peroxide	102-110	superoxide dismutase 2	Homo sapiens	0-4
21291402-5	2011	Data are offered that demonstrate the ability of MnSOD, in the presence of nitric oxide, to utilize hydrogen peroxide to produce superoxide and the more toxic oxidant, peroxynitrite.	Superoxides	129-139	superoxide dismutase 2	Homo sapiens	49-54
21291402-5	2011	Data are offered that demonstrate the ability of MnSOD, in the presence of nitric oxide, to utilize hydrogen peroxide to produce superoxide and the more toxic oxidant, peroxynitrite.	Peroxynitrous Acid	168-181	superoxide dismutase 2	Homo sapiens	49-54
21355846-1	2011	Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)( -)), the first member in a plethora of mitochondrial reactive oxygen species (ROS).	Superoxides	75-93	superoxide dismutase 2	Homo sapiens	0-34
21355846-1	2011	Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)( -)), the first member in a plethora of mitochondrial reactive oxygen species (ROS).	Superoxides	75-93	superoxide dismutase 2	Homo sapiens	36-41
21355846-1	2011	Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)( -)), the first member in a plethora of mitochondrial reactive oxygen species (ROS).	Superoxides	95-99	superoxide dismutase 2	Homo sapiens	0-34
21355846-1	2011	Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)( -)), the first member in a plethora of mitochondrial reactive oxygen species (ROS).	Superoxides	95-99	superoxide dismutase 2	Homo sapiens	36-41
21355846-1	2011	Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)( -)), the first member in a plethora of mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	154-177	superoxide dismutase 2	Homo sapiens	0-34
21355846-1	2011	Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)( -)), the first member in a plethora of mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	154-177	superoxide dismutase 2	Homo sapiens	36-41
21355846-1	2011	Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)( -)), the first member in a plethora of mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	179-182	superoxide dismutase 2	Homo sapiens	0-34
21355846-1	2011	Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)( -)), the first member in a plethora of mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	179-182	superoxide dismutase 2	Homo sapiens	36-41
21619840-6	2011	RESULTS: MTT method showed the transfection of SOD2 gene and empty plasmid did not affect the proliferation capacity.	monooxyethylene trimethylolpropane tristearate	9-12	superoxide dismutase 2	Homo sapiens	47-51
21035442-0	2011	Elevated free fatty acids and impaired adiponectin bioactivity contribute to reduced SOD2 protein in monocytes of type 2 diabetes patients.	Fatty Acids, Nonesterified	9-25	superoxide dismutase 2	Homo sapiens	85-89
21035442-2	2011	Monocytes are critically important in the pathogenesis of CVD and antioxidant enzymes like superoxide dismutase (SOD2) protect these cells from excessive reactive oxygen species (ROS).	Reactive Oxygen Species	154-177	superoxide dismutase 2	Homo sapiens	113-117
21035442-2	2011	Monocytes are critically important in the pathogenesis of CVD and antioxidant enzymes like superoxide dismutase (SOD2) protect these cells from excessive reactive oxygen species (ROS).	Reactive Oxygen Species	179-182	superoxide dismutase 2	Homo sapiens	113-117
21035442-5	2011	Elevated systemic free fatty acids (FFA) are commonly found in T2D patients and palmitic acid as well as oleic acid reduced monocyte SOD2 protein.	Oleic Acid	105-115	superoxide dismutase 2	Homo sapiens	133-137
21035442-9	2011	In summary this study indicates that elevated systemic free fatty acids and impaired adiponectin activity contribute to reduced SOD2 and most likely increased oxidative stress in T2D monocytes.	Fatty Acids, Nonesterified	55-71	superoxide dismutase 2	Homo sapiens	128-132
21619840-7	2011	SOD2 vitality in Ala(16) and Val(16) SOD2 transfected cells increased 2.51 and 2.71 times respectively (P < 0.01), but the difference between the two transfection groups was not statistically significant (P > 0.05).	Alanine	17-20	superoxide dismutase 2	Homo sapiens	0-4
21619840-7	2011	SOD2 vitality in Ala(16) and Val(16) SOD2 transfected cells increased 2.51 and 2.71 times respectively (P < 0.01), but the difference between the two transfection groups was not statistically significant (P > 0.05).	Valine	29-32	superoxide dismutase 2	Homo sapiens	0-4
21619840-7	2011	SOD2 vitality in Ala(16) and Val(16) SOD2 transfected cells increased 2.51 and 2.71 times respectively (P < 0.01), but the difference between the two transfection groups was not statistically significant (P > 0.05).	Valine	29-32	superoxide dismutase 2	Homo sapiens	37-41
21619840-8	2011	After exposed to t-BHP, the majority of the untransfected and empty plasmid transfected cells sent "++" class bright fluorescence, while in Ala(16) and Val(16) SOD2 transfected groups, only about half cells sent "+-" ~ "+" level fuzzy fluorescence.	Valine	152-155	superoxide dismutase 2	Homo sapiens	160-164
21619840-10	2011	CONCLUSION: High expression of SOD2 below 3.71 times can reduce intracellular ROS level in HEI-OC1 cells, while SOD2 C47T mutation had no effect on them.	ros	78-81	superoxide dismutase 2	Homo sapiens	31-35
20567899-0	2011	Possible risk modifications in the association between MnSOD Ala-9Val polymorphism and breast cancer risk: subgroup analysis and evidence-based sample size calculation for a future trial.	ala-9val	61-69	superoxide dismutase 2	Homo sapiens	55-60
20477822-2	2011	We previously reported a statistically significant interaction between circulating selenium levels, variants in the superoxide dismutase 2 gene (SOD2; rs4880), and risk of developing prostate cancer and presenting with aggressive prostate cancer.	Selenium	83-91	superoxide dismutase 2	Homo sapiens	145-149
20309937-1	2011	MnSOD as molecular carrier which delivers high amounts of Cisplatin into tumor cells inducing a fast apoptosis in vitro.	Cisplatin	58-67	superoxide dismutase 2	Homo sapiens	0-5
20567899-1	2011	Manganese superoxide dismutase (MnSOD) has been identified as an important scavenger of reactive oxygen species (ROS), which can cause oxidative stress followed by breast cancer.	Reactive Oxygen Species	88-111	superoxide dismutase 2	Homo sapiens	0-30
20567899-1	2011	Manganese superoxide dismutase (MnSOD) has been identified as an important scavenger of reactive oxygen species (ROS), which can cause oxidative stress followed by breast cancer.	Reactive Oxygen Species	88-111	superoxide dismutase 2	Homo sapiens	32-37
20567899-1	2011	Manganese superoxide dismutase (MnSOD) has been identified as an important scavenger of reactive oxygen species (ROS), which can cause oxidative stress followed by breast cancer.	Reactive Oxygen Species	113-116	superoxide dismutase 2	Homo sapiens	0-30
20567899-1	2011	Manganese superoxide dismutase (MnSOD) has been identified as an important scavenger of reactive oxygen species (ROS), which can cause oxidative stress followed by breast cancer.	Reactive Oxygen Species	113-116	superoxide dismutase 2	Homo sapiens	32-37
20567899-2	2011	A number of subsequent population-based studies have investigated the association between MnSOD Ala-9Val polymorphism and the risk of breast cancer.	ala-9val	96-104	superoxide dismutase 2	Homo sapiens	90-95
20567899-4	2011	This fact implies that the effect of MnSOD Ala-9Val polymorphism on the susceptibility to breast cancer may be modified by other risk factors.	ala-9val	43-51	superoxide dismutase 2	Homo sapiens	37-42
21787690-0	2011	Mitochondria protection of baicalein against oxidative damage via induction of manganese superoxide dismutase.	baicalein	27-36	superoxide dismutase 2	Homo sapiens	79-109
21687640-2	2011	We studied the inhibitory effects of Al(3+) on the activity and conformation of manganese-containing SOD (Mn-SOD).	ALUMINUM ION	37-43	superoxide dismutase 2	Homo sapiens	80-104
21687640-3	2011	Mn-SOD was significantly inactivated by Al(3+) in a dose-dependent manner.	ALUMINUM ION	40-46	superoxide dismutase 2	Homo sapiens	0-6
20598578-2	2011	Using the nitrite method, we investigated sequential changes in CuZn and Mn SOD activity in the cerebrospinal fluid (CSF) of 8 patients with acute ischemic stroke.	Nitrites	10-17	superoxide dismutase 2	Homo sapiens	73-79
21687640-4	2011	The kinetic studies showed that Al(3+) inactivated Mn-SOD follows the first-order reaction.	ALUMINUM ION	32-38	superoxide dismutase 2	Homo sapiens	51-57
21687640-5	2011	Al(3+) increased the degree of secondary structure of Mn-SOD and also disrupted the tertiary structure of Mn-SOD, which directly resulted in enzyme inactivation.	ALUMINUM ION	0-6	superoxide dismutase 2	Homo sapiens	54-60
21687640-5	2011	Al(3+) increased the degree of secondary structure of Mn-SOD and also disrupted the tertiary structure of Mn-SOD, which directly resulted in enzyme inactivation.	ALUMINUM ION	0-6	superoxide dismutase 2	Homo sapiens	106-112
21687640-6	2011	We further simulated the docking between Mn-SOD and Al(3+) (binding energy for Dock 6.3: -14.07 kcal/mol) and suggested that ASP152 and GLU157 residues were predicted to interact with Al(3+), which are not located in the Mn-contained active site.	Aluminum	52-54	superoxide dismutase 2	Homo sapiens	41-47
21687640-7	2011	Our results provide insight into the inactivation of Mn-SOD during unfolding in the presence of Al(3+) and allow us to describe a ligand binding via inhibition kinetics combined with the computational prediction.	ALUMINUM ION	96-102	superoxide dismutase 2	Homo sapiens	53-59
22072939-4	2011	The cell is equipped with myriad antioxidant enzyme systems to combat deleterious ROS production in mitochondria, with the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) acting as the chief ROS scavenging enzyme in the cell.	Reactive Oxygen Species	82-85	superoxide dismutase 2	Homo sapiens	156-186
22072939-4	2011	The cell is equipped with myriad antioxidant enzyme systems to combat deleterious ROS production in mitochondria, with the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) acting as the chief ROS scavenging enzyme in the cell.	Reactive Oxygen Species	82-85	superoxide dismutase 2	Homo sapiens	188-193
22072939-4	2011	The cell is equipped with myriad antioxidant enzyme systems to combat deleterious ROS production in mitochondria, with the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) acting as the chief ROS scavenging enzyme in the cell.	Reactive Oxygen Species	215-218	superoxide dismutase 2	Homo sapiens	156-186
22072939-4	2011	The cell is equipped with myriad antioxidant enzyme systems to combat deleterious ROS production in mitochondria, with the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) acting as the chief ROS scavenging enzyme in the cell.	Reactive Oxygen Species	215-218	superoxide dismutase 2	Homo sapiens	188-193
22072939-6	2011	A better understanding of the mechanisms by which MnSOD protects cells from the harmful effects of overproduction of ROS, in particular, the effects of ROS on mitochondrial metabolic enzymes, may contribute to the development of novel treatments for various diseases in which ROS are an important component.	Reactive Oxygen Species	117-120	superoxide dismutase 2	Homo sapiens	50-55
22072939-6	2011	A better understanding of the mechanisms by which MnSOD protects cells from the harmful effects of overproduction of ROS, in particular, the effects of ROS on mitochondrial metabolic enzymes, may contribute to the development of novel treatments for various diseases in which ROS are an important component.	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	50-55
22072939-6	2011	A better understanding of the mechanisms by which MnSOD protects cells from the harmful effects of overproduction of ROS, in particular, the effects of ROS on mitochondrial metabolic enzymes, may contribute to the development of novel treatments for various diseases in which ROS are an important component.	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	50-55
21077177-4	2011	Recently, the reduction of Cu/Zn-SOD and the induction of Mn-SOD by TPA in leukemic cells have been reported; however, the regulation of EC-SOD by TPA remains poorly understood.	Tetradecanoylphorbol Acetate	68-71	superoxide dismutase 2	Homo sapiens	58-64
21175348-9	2011	SOD2 played an important role in the adaptive/delayed radioprotective response by inhibiting the initiation of a superoxide anion-induced ROS cascade leading to enhanced mitochondrial and nuclear damages.	Superoxides	113-129	superoxide dismutase 2	Homo sapiens	0-4
19949914-5	2011	Furthermore, CSC exposure caused a reduction of the gene expression of the antioxidant enzymes SOD1, SOD2, GPx, and CAT that was counteracted by Vitamin E (50 muM).	Vitamin E	145-154	superoxide dismutase 2	Homo sapiens	101-105
19949914-7	2011	In fact the scavenger vitamin E can block both cell injury and inhibition of SOD1, SOD2, GPx, and CAT induced by CSC exposure.	Vitamin E	22-31	superoxide dismutase 2	Homo sapiens	83-87
21175348-9	2011	SOD2 played an important role in the adaptive/delayed radioprotective response by inhibiting the initiation of a superoxide anion-induced ROS cascade leading to enhanced mitochondrial and nuclear damages.	ros	138-141	superoxide dismutase 2	Homo sapiens	0-4
20473639-7	2010	Manganese-containing superoxide dismutase (MnSOD) activity was unaffected by oxygen tension, but was elevated in young confluent cultures as compared with cultures in log-phase growth.	Oxygen	77-83	superoxide dismutase 2	Homo sapiens	43-48
21080654-0	2010	Peroxynitrite mediates active site tyrosine nitration in manganese superoxide dismutase.	Peroxynitrous Acid	0-13	superoxide dismutase 2	Homo sapiens	57-87
21080654-0	2010	Peroxynitrite mediates active site tyrosine nitration in manganese superoxide dismutase.	Tyrosine	35-43	superoxide dismutase 2	Homo sapiens	57-87
21080654-6	2010	Manganese superoxide dismutase (MnSOD), which plays a critical role in cellular defense against oxidative stress by decomposing superoxide within mitochondria, is nitrated and inactivated under pathological conditions.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
21080654-7	2010	In this study, MnSOD is shown to catalyze PN-mediated self-nitration.	Peroxynitrous Acid	42-44	superoxide dismutase 2	Homo sapiens	15-20
21080654-9	2010	Distinctive patterns of tyrosine nitration within MnSOD by various reagents were revealed and quantified by MS/MS analysis of MnSOD trypsin digest peptides.	Tyrosine	24-32	superoxide dismutase 2	Homo sapiens	50-55
21080654-9	2010	Distinctive patterns of tyrosine nitration within MnSOD by various reagents were revealed and quantified by MS/MS analysis of MnSOD trypsin digest peptides.	Tyrosine	24-32	superoxide dismutase 2	Homo sapiens	126-131
21080654-10	2010	These analyses showed that three of the seven tyrosine residues of MnSOD (Tyr34, Tyr9, and Tyr11) were the most susceptible to nitration and that the relative amounts of nitration of these residues varied widely depending upon the nature of the nitrating agent.	Tyrosine	46-54	superoxide dismutase 2	Homo sapiens	67-72
21080654-13	2010	These kinetics and the 20-fold increase in the efficiency of tyrosine nitration in the presence of CO2 suggest a specific role for the carbonate radical anion ( CO3(-)) in MnSOD nitration by PN.	Tyrosine	61-69	superoxide dismutase 2	Homo sapiens	172-177
21080654-13	2010	These kinetics and the 20-fold increase in the efficiency of tyrosine nitration in the presence of CO2 suggest a specific role for the carbonate radical anion ( CO3(-)) in MnSOD nitration by PN.	carbonate radical	135-152	superoxide dismutase 2	Homo sapiens	172-177
21080654-13	2010	These kinetics and the 20-fold increase in the efficiency of tyrosine nitration in the presence of CO2 suggest a specific role for the carbonate radical anion ( CO3(-)) in MnSOD nitration by PN.	co3(-)	161-167	superoxide dismutase 2	Homo sapiens	172-177
21080654-15	2010	The loss of MnSOD activity upon Tyr34 nitration implies that the responsible reagent in vivo is peroxynitrite, acting either directly or through the action of  CO3(-).	Peroxynitrous Acid	96-109	superoxide dismutase 2	Homo sapiens	12-17
21080654-15	2010	The loss of MnSOD activity upon Tyr34 nitration implies that the responsible reagent in vivo is peroxynitrite, acting either directly or through the action of  CO3(-).	co3(-)	160-166	superoxide dismutase 2	Homo sapiens	12-17
20473639-8	2010	MnSOD activity was significantly higher in senescent cultures than in early passage cultures and was also responsive to increased oxygen tension in senescent cultures.	Oxygen	130-136	superoxide dismutase 2	Homo sapiens	0-5
21042727-7	2010	Importantly, 2DG selectively induces the expression of the antioxidant enzymes manganese superoxide dismutase (MnSOD) and glutathione peroxidase 1 (GPx1) in a p53-dependent manner.	Deoxyglucose	13-16	superoxide dismutase 2	Homo sapiens	79-109
21042727-7	2010	Importantly, 2DG selectively induces the expression of the antioxidant enzymes manganese superoxide dismutase (MnSOD) and glutathione peroxidase 1 (GPx1) in a p53-dependent manner.	Deoxyglucose	13-16	superoxide dismutase 2	Homo sapiens	111-116
20926681-5	2010	Laser capture microdissection demonstrated endogenous c-jun inhibits expression of apoptosis inducing genes and reactive oxygen species (ROS)-reducing genes (MnSOD, catalase).	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	158-163
20656555-4	2010	This indicates that the bifunctional protein possesses a greater antioxidant capability, which is possibly due to the close proximity between the active site of MnSOD and the heme moiety of VHb.	Heme	175-179	superoxide dismutase 2	Homo sapiens	161-166
20706703-4	2010	We examined the expression of the ROS-detoxifying enzymes superoxide dismutase 1 and 2 (SOD1, SOD2), catalase, and glutathione reductase.	Reactive Oxygen Species	34-37	superoxide dismutase 2	Homo sapiens	94-98
20926681-5	2010	Laser capture microdissection demonstrated endogenous c-jun inhibits expression of apoptosis inducing genes and reactive oxygen species (ROS)-reducing genes (MnSOD, catalase).	Reactive Oxygen Species	137-140	superoxide dismutase 2	Homo sapiens	158-163
20926681-6	2010	ROS have been implicated in apoptosis and undergo enzymatic elimination via MnSOD and CuZnSOD with further detoxification via catalase.	Reactive Oxygen Species	0-3	superoxide dismutase 2	Homo sapiens	76-81
20163859-4	2010	4-Cl-BQ decreased manganese superoxide dismutase (MnSOD) activity, protein, and mRNA levels.	4-cl-bq	0-7	superoxide dismutase 2	Homo sapiens	18-48
20797432-0	2010	Carbon monoxide-releasing molecule CORM-3 suppresses vascular endothelial cell SOD-1/SOD-2 activity while up-regulating the cell surface levels of SOD-3 in a heparin-dependent manner.	Carbon Monoxide	0-15	superoxide dismutase 2	Homo sapiens	85-90
21053180-6	2010	However, a possible association with Hp1-1 and MnSOD Val/Ala genotypes suggests that, at least for the Brazilian population, polymorphisms related to oxidative stress should be more deeply investigated.	Valine	53-56	superoxide dismutase 2	Homo sapiens	47-52
20163859-4	2010	4-Cl-BQ decreased manganese superoxide dismutase (MnSOD) activity, protein, and mRNA levels.	4-cl-bq	0-7	superoxide dismutase 2	Homo sapiens	50-55
20163859-9	2010	These results demonstrate that MnSOD activity and ROS-signaling perturb proliferation in 4-Cl-BQ treated in vitro cultures of human prostate cells.	4-cl-bq	89-96	superoxide dismutase 2	Homo sapiens	31-36
20637262-2	2010	We have recently reported that nitration and inactivation of spinal mitochondrial superoxide dismutase (MnSOD) provides a critical source of these reactive oxygen and nitrogen species during central sensitization associated with the development of morphine-induced hyperalgesia and antinociceptive tolerance.	reactive oxygen and nitrogen species	147-183	superoxide dismutase 2	Homo sapiens	104-109
20864405-11	2010	In late-onset bortezomib-induced peripheral neuropathy, the significant genes were SOD2 (upregulated by 1 18 times; p=9 6x10(-3)) and MYO5A (1 93 times; p=3 2x10(-2)), involved in development and function of the nervous system.	Bortezomib	14-24	superoxide dismutase 2	Homo sapiens	83-87
20685861-0	2010	Progesterone increases manganese superoxide dismutase expression via a cAMP-dependent signaling mediated by noncanonical Wnt5a pathway in human endometrial stromal cells.	Progesterone	0-12	superoxide dismutase 2	Homo sapiens	23-53
20685861-0	2010	Progesterone increases manganese superoxide dismutase expression via a cAMP-dependent signaling mediated by noncanonical Wnt5a pathway in human endometrial stromal cells.	Cyclic AMP	71-75	superoxide dismutase 2	Homo sapiens	23-53
20685861-1	2010	CONTEXT: Manganese superoxide dismutase (Mn-SOD), an antioxidant enzyme in the mitochondria, protects cells by scavenging superoxide radicals in human endometrial stromal cells (ESCs).	Superoxides	19-29	superoxide dismutase 2	Homo sapiens	41-47
20685861-2	2010	Mn-SOD increases in ESCs during decidualization induced by progesterone.	Progesterone	59-71	superoxide dismutase 2	Homo sapiens	0-6
20685861-3	2010	OBJECTIVE: The present study investigated the molecular mechanism for Mn-SOD expression induced by progesterone in human ESCs.	Progesterone	99-111	superoxide dismutase 2	Homo sapiens	70-76
20685861-9	2010	The increase in Mn-SOD mRNA levels by MPA or dibutyryl-cAMP was completely inhibited by H89.	Cyclic AMP	55-59	superoxide dismutase 2	Homo sapiens	16-22
20685861-10	2010	The chromatin immunoprecipitation assay revealed that MPA induced cAMP-binding protein binding with cAMP-response element on the Mn-SOD gene promoter.	Cyclic AMP	66-70	superoxide dismutase 2	Homo sapiens	129-135
20685861-10	2010	The chromatin immunoprecipitation assay revealed that MPA induced cAMP-binding protein binding with cAMP-response element on the Mn-SOD gene promoter.	Cyclic AMP	100-104	superoxide dismutase 2	Homo sapiens	129-135
20685861-13	2010	CONCLUSIONS: Progesterone increased Mn-SOD expression via a cAMP-dependent pathway in ESCs during decidualization.	Cyclic AMP	60-64	superoxide dismutase 2	Homo sapiens	36-42
20601193-0	2010	Manganese superoxide dismutase vs. p53: regulation of mitochondrial ROS.	Reactive Oxygen Species	68-71	superoxide dismutase 2	Homo sapiens	0-30
20601193-3	2010	p53 affect mitochondrial ROS production, in part, by regulating the expression of the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	25-28	superoxide dismutase 2	Homo sapiens	119-149
20601193-3	2010	p53 affect mitochondrial ROS production, in part, by regulating the expression of the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	25-28	superoxide dismutase 2	Homo sapiens	151-156
19084291-4	2010	8-OHdG co-localized with the mitochondrial enzyme superoxide dismutase (MnSOD), suggesting damage to mtDNA.	8-ohdg	0-6	superoxide dismutase 2	Homo sapiens	29-70
19084291-4	2010	8-OHdG co-localized with the mitochondrial enzyme superoxide dismutase (MnSOD), suggesting damage to mtDNA.	8-ohdg	0-6	superoxide dismutase 2	Homo sapiens	72-77
20637262-2	2010	We have recently reported that nitration and inactivation of spinal mitochondrial superoxide dismutase (MnSOD) provides a critical source of these reactive oxygen and nitrogen species during central sensitization associated with the development of morphine-induced hyperalgesia and antinociceptive tolerance.	Morphine	248-256	superoxide dismutase 2	Homo sapiens	104-109
20172051-0	2010	Cerium oxide nanoparticles protect gastrointestinal epithelium from radiation-induced damage by reduction of reactive oxygen species and upregulation of superoxide dismutase 2.	ceric oxide	0-12	superoxide dismutase 2	Homo sapiens	153-175
20610621-9	2010	Treatment of human endothelial cells with resveratrol led to an up-regulation of SOD1, SOD2, SOD3, GPx1, catalase, and GCH1.	Resveratrol	42-53	superoxide dismutase 2	Homo sapiens	87-91
21056286-7	2010	SOD2 CT or CC genotype was associated with lower risk (odds ratio, 0.53; 95% confidence interval, 0.30-0.93; P for interaction = .025) in subjects with low plasma gamma-tocopherol concentration.	gamma-Tocopherol	163-179	superoxide dismutase 2	Homo sapiens	0-4
21056286-8	2010	Our findings suggest that the SOD2 Val16Ala variant is not related to the risk of breast cancer in Korean women; however, it may affect the association between plasma gamma-tocopherol levels and the risk of breast cancer.	gamma-Tocopherol	167-183	superoxide dismutase 2	Homo sapiens	30-34
20806431-8	2010	HET-1A cells exposed to bile acid yielded reduced expression of SOD-1 and SOD-2 genes with the exception that high dose deoxycholic acid at 200 mumol/L led to a 3-fold increase in SOD-2 expression.	Bile Acids and Salts	24-33	superoxide dismutase 2	Homo sapiens	74-79
20726524-1	2010	Manganese superoxide dismutase (MnSOD) from different species differs in its efficiency in removing high concentrations of superoxide (O(2)(-)), due to different levels of product inhibition.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
20726524-1	2010	Manganese superoxide dismutase (MnSOD) from different species differs in its efficiency in removing high concentrations of superoxide (O(2)(-)), due to different levels of product inhibition.	Superoxides	135-139	superoxide dismutase 2	Homo sapiens	0-30
20726524-1	2010	Manganese superoxide dismutase (MnSOD) from different species differs in its efficiency in removing high concentrations of superoxide (O(2)(-)), due to different levels of product inhibition.	Superoxides	135-139	superoxide dismutase 2	Homo sapiens	32-37
20600601-0	2010	Zonisamide reduces cell death in SH-SY5Y cells via an anti-apoptotic effect and by upregulating MnSOD.	Zonisamide	0-10	superoxide dismutase 2	Homo sapiens	96-101
20600601-3	2010	Here, we show that zonisamide increases cell viability in SH-SY5Y cells via an anti-apoptotic effect and by upregulating levels of manganese superoxide dismutase (MnSOD).	Zonisamide	19-29	superoxide dismutase 2	Homo sapiens	131-161
20806431-8	2010	HET-1A cells exposed to bile acid yielded reduced expression of SOD-1 and SOD-2 genes with the exception that high dose deoxycholic acid at 200 mumol/L led to a 3-fold increase in SOD-2 expression.	Deoxycholic Acid	120-136	superoxide dismutase 2	Homo sapiens	180-185
20600601-3	2010	Here, we show that zonisamide increases cell viability in SH-SY5Y cells via an anti-apoptotic effect and by upregulating levels of manganese superoxide dismutase (MnSOD).	Zonisamide	19-29	superoxide dismutase 2	Homo sapiens	163-168
20627099-5	2010	TBARS, carbonyl protein, thiols, CAT, and vitamin E were significantly higher in hypercholesterolemic subjects with VV genotype for MnSOD, while GSH, SOD, and vitamin C were lower in these subjects.	Thiobarbituric Acid Reactive Substances	0-5	superoxide dismutase 2	Homo sapiens	132-137
20473585-5	2010	The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment.	naaso	160-165	superoxide dismutase 2	Homo sapiens	13-35
20473585-5	2010	The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment.	naaso	160-165	superoxide dismutase 2	Homo sapiens	37-41
20473585-5	2010	The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment.	Arsenic	251-258	superoxide dismutase 2	Homo sapiens	13-35
20473585-5	2010	The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment.	Arsenic	251-258	superoxide dismutase 2	Homo sapiens	37-41
20473585-7	2010	The decrease in intracellular ROS and the increase in SOD2 and NQO1 expressions observed when HUVECs were treated with low concentration of NaAsO(2), suggest the role of the two enzymes in protecting HUVECs from injuries of arsenic exposure.	naaso	140-145	superoxide dismutase 2	Homo sapiens	54-58
20478627-3	2010	The study examined the relationship between MnSOD gene polymorphisms (Ala-9Val, Ile-58Thr) and DD in the Polish population.	Alanine	70-73	superoxide dismutase 2	Homo sapiens	44-49
20538313-3	2010	Our results show that within the initial 48 h of infection the expression of the mitochondrial superoxide dismutase (MnSOD) is significantly increased, which correlates with a decrease in reactive oxygen species production, and with a lack of cellular glutathione depletion.	Reactive Oxygen Species	188-211	superoxide dismutase 2	Homo sapiens	81-115
20538313-3	2010	Our results show that within the initial 48 h of infection the expression of the mitochondrial superoxide dismutase (MnSOD) is significantly increased, which correlates with a decrease in reactive oxygen species production, and with a lack of cellular glutathione depletion.	Reactive Oxygen Species	188-211	superoxide dismutase 2	Homo sapiens	117-122
20538313-3	2010	Our results show that within the initial 48 h of infection the expression of the mitochondrial superoxide dismutase (MnSOD) is significantly increased, which correlates with a decrease in reactive oxygen species production, and with a lack of cellular glutathione depletion.	Glutathione	252-263	superoxide dismutase 2	Homo sapiens	81-115
20543097-11	2010	Cardiac oxidative stress was attenuated and antioxidant capacity was enhanced by tadalafil possibly via up-regulation of mitochondrial superoxide dismutase (MnSOD).	Tadalafil	81-90	superoxide dismutase 2	Homo sapiens	157-162
20543097-14	2010	We conclude that tadalafil improved left ventricular function and prevented cardiomyocyte apoptosis in DOX-induced cardiomyopathy through mechanisms involving up-regulation of cGMP, PKG activity, and MnSOD level without interfering with the chemotherapeutic benefits of DOX.	Tadalafil	17-26	superoxide dismutase 2	Homo sapiens	200-205
20802415-2	2010	The first-line defense against oxidative stress is provided by the mitochondrial enzyme manganese superoxide dismutase (MnSOD), which is a superoxide anion scavenger.	Superoxides	139-155	superoxide dismutase 2	Homo sapiens	88-118
20802415-2	2010	The first-line defense against oxidative stress is provided by the mitochondrial enzyme manganese superoxide dismutase (MnSOD), which is a superoxide anion scavenger.	Superoxides	139-155	superoxide dismutase 2	Homo sapiens	120-125
20802415-11	2010	CONCLUSIONS: The presence of valine at position 9 of the MnSOD signal peptide encoded by exon 2 is a risk factor for the occurrence of respiratory failure in the course of COPD in the Polish population.	Valine	29-35	superoxide dismutase 2	Homo sapiens	57-62
20931825-18	2010	In the group of patients with COPD, Val/Val genotype at position 9 of MnSOD signal peptide is associated with more severe depression, anxiety as a trait and anxiety as a state in comparison with patients who have Val/Ala and Ala/Ala genotypes.	Valine	36-39	superoxide dismutase 2	Homo sapiens	70-75
20931825-18	2010	In the group of patients with COPD, Val/Val genotype at position 9 of MnSOD signal peptide is associated with more severe depression, anxiety as a trait and anxiety as a state in comparison with patients who have Val/Ala and Ala/Ala genotypes.	Valine	40-43	superoxide dismutase 2	Homo sapiens	70-75
20931825-18	2010	In the group of patients with COPD, Val/Val genotype at position 9 of MnSOD signal peptide is associated with more severe depression, anxiety as a trait and anxiety as a state in comparison with patients who have Val/Ala and Ala/Ala genotypes.	Valine	40-43	superoxide dismutase 2	Homo sapiens	70-75
20931825-18	2010	In the group of patients with COPD, Val/Val genotype at position 9 of MnSOD signal peptide is associated with more severe depression, anxiety as a trait and anxiety as a state in comparison with patients who have Val/Ala and Ala/Ala genotypes.	Alanine	217-220	superoxide dismutase 2	Homo sapiens	70-75
20931825-18	2010	In the group of patients with COPD, Val/Val genotype at position 9 of MnSOD signal peptide is associated with more severe depression, anxiety as a trait and anxiety as a state in comparison with patients who have Val/Ala and Ala/Ala genotypes.	Alanine	225-228	superoxide dismutase 2	Homo sapiens	70-75
20931825-18	2010	In the group of patients with COPD, Val/Val genotype at position 9 of MnSOD signal peptide is associated with more severe depression, anxiety as a trait and anxiety as a state in comparison with patients who have Val/Ala and Ala/Ala genotypes.	Alanine	225-228	superoxide dismutase 2	Homo sapiens	70-75
20511611-5	2010	The DNA methylation status of the SOD2 promoter was determined using bisulphite sequencing.	hydrogen sulfite	69-79	superoxide dismutase 2	Homo sapiens	34-38
20511611-6	2010	RNA interference was used to determine the consequence of SOD2 depletion on the levels of reactive oxygen species (ROS) using MitoSOX and collagenases, matrix metalloproteinase 1 (MMP-1) and MMP-13, gene expression.	Reactive Oxygen Species	90-113	superoxide dismutase 2	Homo sapiens	58-62
20511611-6	2010	RNA interference was used to determine the consequence of SOD2 depletion on the levels of reactive oxygen species (ROS) using MitoSOX and collagenases, matrix metalloproteinase 1 (MMP-1) and MMP-13, gene expression.	Reactive Oxygen Species	115-118	superoxide dismutase 2	Homo sapiens	58-62
20511611-10	2010	Depletion of SOD2 in chondrocytes increased ROS but decreased collagenase expression.	Reactive Oxygen Species	44-47	superoxide dismutase 2	Homo sapiens	13-17
20511611-12	2010	A decrease in SOD2 was found to be associated with an increase in ROS but a reduction of collagenase gene expression, demonstrating the complexities of ROS function.	Reactive Oxygen Species	66-69	superoxide dismutase 2	Homo sapiens	14-18
20511611-12	2010	A decrease in SOD2 was found to be associated with an increase in ROS but a reduction of collagenase gene expression, demonstrating the complexities of ROS function.	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	14-18
20712757-3	2010	METHODS: Four candidate genes were selected a priori from two different steps in the oxidative stress pathway, specifically the synthesis of glutathione [catalytic subunit of glutamate cysteine ligase (GCLC) and regulatory subunit of glutamate cysteine ligase (GCLM)] and the removal of reactive oxygen species [superoxide dismutase 2 (SOD2) and glutathione peroxidase 3 (GPX3)].	Glutathione	141-152	superoxide dismutase 2	Homo sapiens	312-334
20712757-3	2010	METHODS: Four candidate genes were selected a priori from two different steps in the oxidative stress pathway, specifically the synthesis of glutathione [catalytic subunit of glutamate cysteine ligase (GCLC) and regulatory subunit of glutamate cysteine ligase (GCLM)] and the removal of reactive oxygen species [superoxide dismutase 2 (SOD2) and glutathione peroxidase 3 (GPX3)].	Glutathione	141-152	superoxide dismutase 2	Homo sapiens	336-340
20578157-6	2010	The SOD2 Ala/Ala genotype was associated with cholestatic/mixed damage (OR = 2.3; 95% confidence interval [CI] = 1.4-3.8; corrected P [Pc] = 0.0058), whereas the GPX1 Leu/Leu genotype was associated with cholestatic injury (OR = 5.1; 95%CI = 1.6-16.0; Pc = 0.0112).	Alanine	9-12	superoxide dismutase 2	Homo sapiens	4-8
20501330-0	2010	Val-9Ala and Ile+58Thr polymorphism of MnSOD in Parkinson"s disease.	Valine	0-3	superoxide dismutase 2	Homo sapiens	39-44
20501330-1	2010	OBJECTIVES: To investigate the polymorphism distribution of Val-9Ala and Ile+58Thr of the Mn-superoxide dismutase (Mn-SOD) gene among subjects with Parkinson"s disease (PD) by analyses of genders and clinical severity.	Isoleucine	73-76	superoxide dismutase 2	Homo sapiens	90-113
20501330-1	2010	OBJECTIVES: To investigate the polymorphism distribution of Val-9Ala and Ile+58Thr of the Mn-superoxide dismutase (Mn-SOD) gene among subjects with Parkinson"s disease (PD) by analyses of genders and clinical severity.	Isoleucine	73-76	superoxide dismutase 2	Homo sapiens	115-121
20501330-6	2010	CONCLUSION: The higher Ala-allele carrier rate among PD subjects may suggest a possible higher amount of mitochondrial Mn-SOD rendering higher intracellular stress in PD.	Alanine	23-26	superoxide dismutase 2	Homo sapiens	119-125
20649542-7	2010	Manganese superoxide dismutase (MnSOD), a p53-regulated gene that is a vital antioxidant enzyme localized in the matrix of mitochondria, scavenges reactive oxygen species.	Reactive Oxygen Species	147-170	superoxide dismutase 2	Homo sapiens	0-30
20649542-7	2010	Manganese superoxide dismutase (MnSOD), a p53-regulated gene that is a vital antioxidant enzyme localized in the matrix of mitochondria, scavenges reactive oxygen species.	Reactive Oxygen Species	147-170	superoxide dismutase 2	Homo sapiens	32-37
20819578-12	2010	Real-time RT-PCR confirmed UA could up-regulate the mRNA expressions of GDF15, SOD2, ATF3 and down-regulate the mRAN expression of fos.	ursolic acid	27-29	superoxide dismutase 2	Homo sapiens	79-83
20307652-7	2010	Results from the mRNA turnover assay showed that the 4-Cl-BQ treatment selectively enhanced the degradation of the 4.2kb MnSOD transcript, while the half-life of the 1.5 kb transcript did not change.	4-cl-bq	53-60	superoxide dismutase 2	Homo sapiens	121-126
20673057-3	2010	Genistein significantly decreased reactive oxygen species levels and induced the expression of the antioxidant enzymes manganese (Mn) superoxide dismutase (SOD) and catalase, which were associated with AMP-activated protein kinase (AMPK) and phosphatase and tensin homolog deleted from chromosome 10 (PTEN) pathways.	Genistein	0-9	superoxide dismutase 2	Homo sapiens	156-159
20673057-4	2010	The induced expression of catalase, MnSOD, and PTEN were attenuated by pretreatment with a pharmacological inhibitor for AMPK, indicating the effects of genistein primarily depend on AMPK.	Genistein	153-162	superoxide dismutase 2	Homo sapiens	36-41
20668652-7	2010	Moreover, we show that the modulation of intracellular ROS levels by KRIT1 loss/restoration is strictly correlated with the modulation of the expression of the antioxidant protein SOD2 as well as of the transcriptional factor FoxO1, a master regulator of cell responses to oxidative stress and a modulator of SOD2 levels.	Reactive Oxygen Species	55-58	superoxide dismutase 2	Homo sapiens	180-184
20668652-7	2010	Moreover, we show that the modulation of intracellular ROS levels by KRIT1 loss/restoration is strictly correlated with the modulation of the expression of the antioxidant protein SOD2 as well as of the transcriptional factor FoxO1, a master regulator of cell responses to oxidative stress and a modulator of SOD2 levels.	Reactive Oxygen Species	55-58	superoxide dismutase 2	Homo sapiens	309-313
20668652-10	2010	Taken together, our results point to a new model where KRIT1 limits the accumulation of intracellular oxidants and prevents oxidative stress-mediated cellular dysfunction and DNA damage by enhancing the cell capacity to scavenge intracellular ROS through an antioxidant pathway involving FoxO1 and SOD2, thus providing novel and useful insights into the understanding of KRIT1 molecular and cellular functions.	Reactive Oxygen Species	243-246	superoxide dismutase 2	Homo sapiens	298-302
20578157-6	2010	The SOD2 Ala/Ala genotype was associated with cholestatic/mixed damage (OR = 2.3; 95% confidence interval [CI] = 1.4-3.8; corrected P [Pc] = 0.0058), whereas the GPX1 Leu/Leu genotype was associated with cholestatic injury (OR = 5.1; 95%CI = 1.6-16.0; Pc = 0.0112).	Alanine	13-16	superoxide dismutase 2	Homo sapiens	4-8
20578157-7	2010	The presence of two or more combined risk alleles (SOD2 Ala and GPX1 Leu) was more frequent in DILI patients (OR = 2.1; 95%CI = 1.4-3.0; Pc = 0.0006).	Alanine	56-59	superoxide dismutase 2	Homo sapiens	51-55
20578157-8	2010	Patients with cholestatic/mixed injury induced by mitochondria hazardous drugs were more prone to have the SOD2 Ala/Ala genotype (OR = 3.6; 95%CI = 1.4-9.3; Pc = 0.02).	Alanine	112-115	superoxide dismutase 2	Homo sapiens	107-111
20514394-5	2010	At the same time, ATR is activated, activating CHK1 that may phosphorylate P53 but also contribute to inhibition of MnSOD expression leading to accumulation of ROS (reactive oxygen species) and subsequent DNA injury, which in turn maintains ATR/CHK1 activated.	Reactive Oxygen Species	160-163	superoxide dismutase 2	Homo sapiens	116-121
20578157-8	2010	Patients with cholestatic/mixed injury induced by mitochondria hazardous drugs were more prone to have the SOD2 Ala/Ala genotype (OR = 3.6; 95%CI = 1.4-9.3; Pc = 0.02).	Alanine	116-119	superoxide dismutase 2	Homo sapiens	107-111
20514394-5	2010	At the same time, ATR is activated, activating CHK1 that may phosphorylate P53 but also contribute to inhibition of MnSOD expression leading to accumulation of ROS (reactive oxygen species) and subsequent DNA injury, which in turn maintains ATR/CHK1 activated.	Reactive Oxygen Species	165-188	superoxide dismutase 2	Homo sapiens	116-121
20514411-3	2010	Overexpression of CuZnSOD and MnSOD significantly suppressed the growth of A549 and MCF-7 MTS, supporting a critical role(s) of reactive oxygen species (ROS) in tumour growth.	Reactive Oxygen Species	128-151	superoxide dismutase 2	Homo sapiens	30-35
20578157-10	2010	CONCLUSION: Patients homozygous for the SOD2 Ala allele and the GPX1 Leu allele are at higher risk of developing cholestatic DILI.	Alanine	45-48	superoxide dismutase 2	Homo sapiens	40-44
20514411-3	2010	Overexpression of CuZnSOD and MnSOD significantly suppressed the growth of A549 and MCF-7 MTS, supporting a critical role(s) of reactive oxygen species (ROS) in tumour growth.	Reactive Oxygen Species	153-156	superoxide dismutase 2	Homo sapiens	30-35
20514411-5	2010	We observed that CuZnSOD and MnSOD overexpression prevents metabolic stress-induced necrosis and HMGB1 release by inhibiting mitochondrial ROS and intracellular O2- production in response to glucose depletion in two dimensional cell culture.	Reactive Oxygen Species	139-142	superoxide dismutase 2	Homo sapiens	29-34
20529999-2	2010	Expression and activity of mitochondrial superoxide dismutase-2 (SOD2), the major generator of H(2)O(2), is known to be reduced in PAH; however, the mechanism and therapeutic relevance of this are unknown.	Hydrogen Peroxide	95-103	superoxide dismutase 2	Homo sapiens	65-69
20514411-5	2010	We observed that CuZnSOD and MnSOD overexpression prevents metabolic stress-induced necrosis and HMGB1 release by inhibiting mitochondrial ROS and intracellular O2- production in response to glucose depletion in two dimensional cell culture.	Oxygen	161-163	superoxide dismutase 2	Homo sapiens	29-34
20514411-5	2010	We observed that CuZnSOD and MnSOD overexpression prevents metabolic stress-induced necrosis and HMGB1 release by inhibiting mitochondrial ROS and intracellular O2- production in response to glucose depletion in two dimensional cell culture.	Glucose	191-198	superoxide dismutase 2	Homo sapiens	29-34
20514411-8	2010	These results suggest that CuZnSOD and MnSOD may suppress tumour growth through inhibiting metabolic stress-induced necrosis and HMGB1 release via inhibiting metabolic stress-induced mitochondrial ROS production.	Reactive Oxygen Species	197-200	superoxide dismutase 2	Homo sapiens	39-44
20012093-10	2010	CONCLUSIONS: This meta-analysis suggests that the Ala allele of the MnSOD gene was a low-penetrance susceptible gene in PCA development, especially in Caucasians.	Alanine	50-53	superoxide dismutase 2	Homo sapiens	68-73
20529999-3	2010	METHODS AND RESULTS: SOD2 expression in PASMCs is decreased in PAH patients and FHRs with PAH.	pasmcs	40-46	superoxide dismutase 2	Homo sapiens	21-25
20529999-6	2010	Administration of SOD2 small interfering RNA to normal PASMCs recapitulates the FHR PAH phenotype, hyperpolarizing mitochondria, decreasing H(2)O(2), and inhibiting caspase activity.	pasmcs	55-61	superoxide dismutase 2	Homo sapiens	18-22
20529999-7	2010	Conversely, SOD2 overexpression in FHR PASMCs or therapy with the SOD-mimetic metalloporphyrin Mn(III)tetrakis (4-benzoic acid) porphyrin (MnTBAP) reverses the hyperproliferative PAH phenotype.	pasmcs	39-45	superoxide dismutase 2	Homo sapiens	12-16
20529999-7	2010	Conversely, SOD2 overexpression in FHR PASMCs or therapy with the SOD-mimetic metalloporphyrin Mn(III)tetrakis (4-benzoic acid) porphyrin (MnTBAP) reverses the hyperproliferative PAH phenotype.	pasmcs	39-45	superoxide dismutase 2	Homo sapiens	12-15
20529999-11	2010	Differential methylation occurs selectively in PAs versus aortic SMCs and is reversed by the DNA methyltransferase inhibitor 5-aza-2"-deoxycytidine, restoring both SOD2 expression and the ratio of proliferation to apoptosis.	Decitabine	125-147	superoxide dismutase 2	Homo sapiens	164-168
20188165-0	2010	Reactive oxygen species produced by the knockdown of manganese-superoxide dismutase up-regulate hypoxia-inducible factor-1alpha expression in oral squamous cell carcinoma cells.	Reactive Oxygen Species	0-23	superoxide dismutase 2	Homo sapiens	53-83
20606706-10	2010	Mn-superoxide dismutase (MnSOD) was quantified in the long-red channel using an anti-MnSOD antibody and an Alexa Fluor 647-labeled secondary antibody.	Alexa Fluor 647	107-122	superoxide dismutase 2	Homo sapiens	0-23
20606706-10	2010	Mn-superoxide dismutase (MnSOD) was quantified in the long-red channel using an anti-MnSOD antibody and an Alexa Fluor 647-labeled secondary antibody.	Alexa Fluor 647	107-122	superoxide dismutase 2	Homo sapiens	25-30
20361947-6	2010	Protein levels of copper, zinc-superoxide dismutase (CuZnSOD), manganese-superoxide dismutase (MnSOD), catalase, and glutathione peroxidases 1/2 were also found to increase with DHA exposure.	artenimol	178-181	superoxide dismutase 2	Homo sapiens	63-93
20361947-7	2010	4-hydroxy-tempol (TEMPOL) and DF-Mn, MnSOD mimetics, could significantly inhibit ROS generation and reduce cell death.	df-mn	30-35	superoxide dismutase 2	Homo sapiens	37-42
20361947-7	2010	4-hydroxy-tempol (TEMPOL) and DF-Mn, MnSOD mimetics, could significantly inhibit ROS generation and reduce cell death.	Reactive Oxygen Species	81-84	superoxide dismutase 2	Homo sapiens	37-42
20353787-0	2010	ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite-induced apoptosis of NB4 cells.	Reactive Oxygen Species	0-3	superoxide dismutase 2	Homo sapiens	13-18
20536280-3	2010	Manganese superoxide dismutase (MnSOD) is an ROS scavenger, and myeloperoxidase (MPO) can convert hydrogen peroxide into hypochlorous acid; thus, they are considered to be involved in inflammatory defense.	Reactive Oxygen Species	45-48	superoxide dismutase 2	Homo sapiens	0-30
20536280-3	2010	Manganese superoxide dismutase (MnSOD) is an ROS scavenger, and myeloperoxidase (MPO) can convert hydrogen peroxide into hypochlorous acid; thus, they are considered to be involved in inflammatory defense.	Reactive Oxygen Species	45-48	superoxide dismutase 2	Homo sapiens	32-37
20536280-3	2010	Manganese superoxide dismutase (MnSOD) is an ROS scavenger, and myeloperoxidase (MPO) can convert hydrogen peroxide into hypochlorous acid; thus, they are considered to be involved in inflammatory defense.	Hydrogen Peroxide	98-115	superoxide dismutase 2	Homo sapiens	0-30
20536280-3	2010	Manganese superoxide dismutase (MnSOD) is an ROS scavenger, and myeloperoxidase (MPO) can convert hydrogen peroxide into hypochlorous acid; thus, they are considered to be involved in inflammatory defense.	Hydrogen Peroxide	98-115	superoxide dismutase 2	Homo sapiens	32-37
20536280-3	2010	Manganese superoxide dismutase (MnSOD) is an ROS scavenger, and myeloperoxidase (MPO) can convert hydrogen peroxide into hypochlorous acid; thus, they are considered to be involved in inflammatory defense.	Hypochlorous Acid	121-138	superoxide dismutase 2	Homo sapiens	0-30
20536280-3	2010	Manganese superoxide dismutase (MnSOD) is an ROS scavenger, and myeloperoxidase (MPO) can convert hydrogen peroxide into hypochlorous acid; thus, they are considered to be involved in inflammatory defense.	Hypochlorous Acid	121-138	superoxide dismutase 2	Homo sapiens	32-37
20536280-8	2010	RESULTS: A higher level of parental education, family history of asthma, incense burning at home, allergen-test positive, and the MnSOD Val-Ala/Ala-Ala genotypes (matched relative risk = 2.0; 95% confidence interval = 1.0-4.2) were significantly associated with childhood asthma.	H-VAL-ALA-OH	136-143	superoxide dismutase 2	Homo sapiens	130-135
20206302-8	2010	Overexpression of MnSOD decreased ROS levels, and preserved mitochondrial morphology in aged quiescent NHFs.	Reactive Oxygen Species	34-37	superoxide dismutase 2	Homo sapiens	18-23
20353787-0	2010	ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite-induced apoptosis of NB4 cells.	Selenious Acid	81-89	superoxide dismutase 2	Homo sapiens	13-18
20353787-1	2010	Following our previous finding that sodium selenite induces apoptosis in human leukemia NB4 cells, we now show that the expression of the critical antioxidant enzyme manganese superoxide dismutase (MnSOD) is remarkably elevated during this process.	Sodium Selenite	36-51	superoxide dismutase 2	Homo sapiens	166-196
20353787-1	2010	Following our previous finding that sodium selenite induces apoptosis in human leukemia NB4 cells, we now show that the expression of the critical antioxidant enzyme manganese superoxide dismutase (MnSOD) is remarkably elevated during this process.	Sodium Selenite	36-51	superoxide dismutase 2	Homo sapiens	198-203
20353787-2	2010	We further reveal that reactive oxygen species (ROS), especially superoxide radicals, play a crucial role in selenite-induced MnSOD upregulation, with extracellular regulated kinase (ERK) and p53 closely implicated.	Reactive Oxygen Species	23-46	superoxide dismutase 2	Homo sapiens	126-131
20353787-2	2010	We further reveal that reactive oxygen species (ROS), especially superoxide radicals, play a crucial role in selenite-induced MnSOD upregulation, with extracellular regulated kinase (ERK) and p53 closely implicated.	Reactive Oxygen Species	48-51	superoxide dismutase 2	Homo sapiens	126-131
20353787-2	2010	We further reveal that reactive oxygen species (ROS), especially superoxide radicals, play a crucial role in selenite-induced MnSOD upregulation, with extracellular regulated kinase (ERK) and p53 closely implicated.	Superoxides	65-84	superoxide dismutase 2	Homo sapiens	126-131
20012547-3	2010	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Superoxides	94-111	superoxide dismutase 2	Homo sapiens	23-53
20012547-3	2010	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Superoxides	94-111	superoxide dismutase 2	Homo sapiens	55-59
20012547-3	2010	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Hydrogen Peroxide	117-134	superoxide dismutase 2	Homo sapiens	23-53
20012547-3	2010	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Hydrogen Peroxide	117-134	superoxide dismutase 2	Homo sapiens	55-59
20346996-0	2010	Association of the manganese superoxide dismutase gene Ala-9Val polymorphism with clinical phenotypes and tardive dyskinesia in schizophrenic patients.	ala-9val	55-63	superoxide dismutase 2	Homo sapiens	19-49
20346996-1	2010	OBJECTIVE: Several recent studies that have investigated the genetic association between the manganese superoxide dismutase (MnSOD) gene Ala-9Val single-nucleotide polymorphism (SNP) and tardive dyskinesia (TD) have produced conflicting results.	ala-9val	137-145	superoxide dismutase 2	Homo sapiens	93-123
20346996-1	2010	OBJECTIVE: Several recent studies that have investigated the genetic association between the manganese superoxide dismutase (MnSOD) gene Ala-9Val single-nucleotide polymorphism (SNP) and tardive dyskinesia (TD) have produced conflicting results.	ala-9val	137-145	superoxide dismutase 2	Homo sapiens	125-130
20346996-3	2010	METHODS: Genotyping was performed for the MnSOD gene Ala-9Val SNP in Chinese schizophrenia patients with (n=176) and without TD (n=346).	Alanine	53-56	superoxide dismutase 2	Homo sapiens	42-47
20346996-3	2010	METHODS: Genotyping was performed for the MnSOD gene Ala-9Val SNP in Chinese schizophrenia patients with (n=176) and without TD (n=346).	9val	57-61	superoxide dismutase 2	Homo sapiens	42-47
20346996-8	2010	CONCLUSION: While the MnSOD gene Ala-9Val polymorphism did not play a major role in the susceptibility to TD in schizophrenic patients, it might be associated with negative symptoms of schizophrenia.	ala-9val	33-41	superoxide dismutase 2	Homo sapiens	22-27
20188165-8	2010	These results suggest that intracellular ROS produced by the knockdown of Mn-SOD enhance HIF-1alpha expression in OSCC cells through transcriptional, translational, and posttranslational regulation.	Reactive Oxygen Species	41-44	superoxide dismutase 2	Homo sapiens	74-80
20097730-7	2010	Moreover, the SOD2 -1221G>A AA genotype carriers had a significantly increased risk for pancreatic cancer among those with a low dietary vitamin E intake but decreased risk among those with a high vitamin E intake (P(interaction) = 0.002).	Vitamin E	140-149	superoxide dismutase 2	Homo sapiens	14-18
20144705-0	2010	Thiol-sensitive mutant forms of human SOD2, L60F, and I58T: the role of Cys140.	Sulfhydryl Compounds	0-5	superoxide dismutase 2	Homo sapiens	38-42
20144705-4	2010	Both mutant proteins display a weakened dimer-dimer interaction and thermal instability at 55 degrees C. Both I58T and L60F lose activity at 37 degrees C in the presence of 5 mM N-ethylmaleimide, whereas the wild-type SOD2 does not.	Ethylmaleimide	178-194	superoxide dismutase 2	Homo sapiens	218-222
20089930-5	2010	This response was significantly attenuated in neurons overexpressing the mitochondria-targeted O(2)(.-)-scavenging enzyme Mn-SOD.	Superoxides	95-101	superoxide dismutase 2	Homo sapiens	122-128
20097730-7	2010	Moreover, the SOD2 -1221G>A AA genotype carriers had a significantly increased risk for pancreatic cancer among those with a low dietary vitamin E intake but decreased risk among those with a high vitamin E intake (P(interaction) = 0.002).	Vitamin E	200-209	superoxide dismutase 2	Homo sapiens	14-18
20204285-4	2010	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Superoxides	94-111	superoxide dismutase 2	Homo sapiens	23-53
20043000-2	2010	The mitochondrial superoxide dismutase 2 (SOD2) enzyme is critical in the metabolism of superoxide.	Superoxides	18-28	superoxide dismutase 2	Homo sapiens	42-46
20079425-9	2010	We propose that hypoxia induces superoxide accumulation in pulmonary artery myocytes through inhibition of mitochondrial SOD2 activity, promoting peroxynitrite-induced generation of 8-isoprostane.	Superoxides	32-42	superoxide dismutase 2	Homo sapiens	121-125
20079425-9	2010	We propose that hypoxia induces superoxide accumulation in pulmonary artery myocytes through inhibition of mitochondrial SOD2 activity, promoting peroxynitrite-induced generation of 8-isoprostane.	Peroxynitrous Acid	146-159	superoxide dismutase 2	Homo sapiens	121-125
20144676-4	2010	UDP also causes mitochondrial damage through diffusion of cytochrome c in the cytoplasm, and stimulates caspase-3,7,8 activities, with extensive over-expression of manganese superoxide dismutase.	Uridine Diphosphate	0-3	superoxide dismutase 2	Homo sapiens	164-194
20204285-4	2010	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Superoxides	94-111	superoxide dismutase 2	Homo sapiens	55-59
20204285-4	2010	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Hydrogen Peroxide	117-134	superoxide dismutase 2	Homo sapiens	23-53
20204285-4	2010	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Hydrogen Peroxide	117-134	superoxide dismutase 2	Homo sapiens	55-59
20089851-7	2010	Nuclear but not cytoplasmic SIRT1-induced manganese superoxide dismutase (Mn-SOD), which was further enhanced by resveratrol, and increased the resistance of C2C12 myoblasts to oxidative stress.	Resveratrol	113-124	superoxide dismutase 2	Homo sapiens	42-72
20059731-5	2010	Superoxide radicals produced are quickly scavenged by superoxide dismutase (MnSOD), and the resulting H(2)O(2) is detoxified by peroxiredoxin-thioredoxin system or by the enzymes of ascorbate-glutathione cycle, found in the mitochondrial matrix.	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	76-81
20059731-5	2010	Superoxide radicals produced are quickly scavenged by superoxide dismutase (MnSOD), and the resulting H(2)O(2) is detoxified by peroxiredoxin-thioredoxin system or by the enzymes of ascorbate-glutathione cycle, found in the mitochondrial matrix.	Hydrogen Peroxide	102-110	superoxide dismutase 2	Homo sapiens	76-81
20059731-5	2010	Superoxide radicals produced are quickly scavenged by superoxide dismutase (MnSOD), and the resulting H(2)O(2) is detoxified by peroxiredoxin-thioredoxin system or by the enzymes of ascorbate-glutathione cycle, found in the mitochondrial matrix.	Ascorbic Acid	182-191	superoxide dismutase 2	Homo sapiens	76-81
20059731-5	2010	Superoxide radicals produced are quickly scavenged by superoxide dismutase (MnSOD), and the resulting H(2)O(2) is detoxified by peroxiredoxin-thioredoxin system or by the enzymes of ascorbate-glutathione cycle, found in the mitochondrial matrix.	Glutathione	192-203	superoxide dismutase 2	Homo sapiens	76-81
20018168-4	2010	Protein expression and enzymatic activity of MnSOD and catalase were increased in thermotolerant cells, as well as intracellular glutathione levels and gamma-glutamylcysteine synthetase expression.	Glutathione	129-140	superoxide dismutase 2	Homo sapiens	45-50
20089851-7	2010	Nuclear but not cytoplasmic SIRT1-induced manganese superoxide dismutase (Mn-SOD), which was further enhanced by resveratrol, and increased the resistance of C2C12 myoblasts to oxidative stress.	Resveratrol	113-124	superoxide dismutase 2	Homo sapiens	74-80
20089851-8	2010	Resveratrol"s enhancement of Mn-SOD levels depended on the level of nuclear SIRT1, and it suppressed the cell death induced by antimycin A or angiotensin II.	Resveratrol	0-11	superoxide dismutase 2	Homo sapiens	29-35
20089851-9	2010	The cell-protective effects of nuclear SIRT1 or resveratrol were canceled by the Mn-SOD small interfering RNA or SIRT1 small interfering RNA.	Resveratrol	48-59	superoxide dismutase 2	Homo sapiens	81-87
20089851-10	2010	The oral administration of resveratrol to TO-2 hamsters increased Mn-SOD levels in cardiomyocytes, suppressed fibrosis, preserved cardiac function, and significantly improved survival.	Resveratrol	27-38	superoxide dismutase 2	Homo sapiens	66-72
20089851-11	2010	Thus, Mn-SOD induced by resveratrol via nuclear SIRT1 reduced oxidative stress and participated in cardiomyocyte protection.	Resveratrol	24-35	superoxide dismutase 2	Homo sapiens	6-12
20110409-6	2010	MnSOD siRNA also reduced nitric oxide production in supernatants of IPAH-ECs.	Nitric Oxide	25-37	superoxide dismutase 2	Homo sapiens	0-5
20110409-6	2010	MnSOD siRNA also reduced nitric oxide production in supernatants of IPAH-ECs.	ipah-ecs	68-76	superoxide dismutase 2	Homo sapiens	0-5
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Valine	116-122	superoxide dismutase 2	Homo sapiens	24-29
20088710-1	2010	Retinal mitochondria become dysfunctional in diabetes and the production of superoxide radicals is increased; over-expression of MnSOD abrogates mitochondrial dysfunction and prevents the development of diabetic retinopathy.	Superoxides	76-86	superoxide dismutase 2	Homo sapiens	129-134
20088710-4	2010	The effect of MnSOD mimic, MnTBAP or over-expression of MnSOD on glucose-induced alterations in mtDNA homeostasis and its functional consequence was determined in retinal endothelial cells.	Glucose	65-72	superoxide dismutase 2	Homo sapiens	56-61
20088710-7	2010	Inhibition of superoxide radicals by either MnTBAP or by over-expression of MnSOD prevented mtDNA damage and protected mitochondrial-encoded genes.	Superoxides	14-24	superoxide dismutase 2	Homo sapiens	76-81
20088710-8	2010	Thus, the protection of mtDNA from glucose-induced oxidative damage is one of the plausible mechanisms by which MnSOD ameliorates the development of diabetic retinopathy.	Glucose	35-42	superoxide dismutase 2	Homo sapiens	112-117
20150532-7	2010	Preliminary in vitro experiments showed an increase of SOD2 expression on podocyte plasma membrane after treatment with hydrogen peroxide.	Hydrogen Peroxide	120-137	superoxide dismutase 2	Homo sapiens	55-59
20206073-3	2010	There are two genetic variants of MnSOD arising from a substitution of an alanine for a valine in the signal peptide.	Alanine	74-81	superoxide dismutase 2	Homo sapiens	34-39
20206073-3	2010	There are two genetic variants of MnSOD arising from a substitution of an alanine for a valine in the signal peptide.	Valine	88-94	superoxide dismutase 2	Homo sapiens	34-39
20206073-4	2010	We previously reported that the valine allele of MnSOD decreases the mitochondrial MnSOD (mtMnSOD) activity.	Valine	32-38	superoxide dismutase 2	Homo sapiens	49-54
20206073-4	2010	We previously reported that the valine allele of MnSOD decreases the mitochondrial MnSOD (mtMnSOD) activity.	Valine	32-38	superoxide dismutase 2	Homo sapiens	83-88
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Alanine	68-75	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Alanine	76-83	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Alanine	76-83	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Valine	98-104	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Valine	116-122	superoxide dismutase 2	Homo sapiens	24-29
20109103-4	2010	MnSOD significantly influenced results of CK and a possible association between Hp1F-1S and Hp1S-2 genotypes with a superior TBARS values was found.	Thiobarbituric Acid Reactive Substances	125-130	superoxide dismutase 2	Homo sapiens	0-5
20109103-5	2010	Higher or lower TBARS and CK values or DNA damage also depended on the interaction between Hp and ACE or GST genotypes, indicating that MnSOD and Hp polymorphisms can be determining factors in performance, at least for runners.	Thiobarbituric Acid Reactive Substances	16-21	superoxide dismutase 2	Homo sapiens	136-141
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Alanine	76-83	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Alanine	76-83	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Alanine	76-83	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Valine	116-122	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Valine	116-122	superoxide dismutase 2	Homo sapiens	24-29
20206073-9	2010	In healthy subjects the MnSOD genotype distribution was as follows: alanine/alanine 1.9%, alanine/valine 28.3%, and valine/valine 69.8%, and in VSA patients the prevalence was: alanine/alanine 1.3%, alanine/valine 19.3%, and valine/valine 79.4%.	Valine	116-122	superoxide dismutase 2	Homo sapiens	24-29
20206073-12	2010	CONCLUSION: The valine variant of MnSOD signal peptide increases the risk of VSA.	Valine	16-22	superoxide dismutase 2	Homo sapiens	34-39
20532186-2	2010	Recent work has shown that cancer cells can be sensitized to cell killing by raising peroxide levels through increased manganese superoxide dismutase (MnSOD) when combined with inhibition of peroxide removal.	Peroxides	85-93	superoxide dismutase 2	Homo sapiens	151-156
20532186-2	2010	Recent work has shown that cancer cells can be sensitized to cell killing by raising peroxide levels through increased manganese superoxide dismutase (MnSOD) when combined with inhibition of peroxide removal.	Peroxides	131-139	superoxide dismutase 2	Homo sapiens	151-156
20532186-4	2010	The purpose of this study was to determine if anticancer modalities known to produce superoxide radicals can increase the antitumor effect of MnSOD overexpression when combined with BCNU.	Superoxides	85-95	superoxide dismutase 2	Homo sapiens	142-147
19699328-0	2010	Metal uptake by manganese superoxide dismutase.	Metals	0-5	superoxide dismutase 2	Homo sapiens	16-46
19699328-1	2010	Manganese superoxide dismutase is an important antioxidant defense metalloenzyme that protects cells from damage by the toxic oxygen metabolite, superoxide free radical, formed as an unavoidable by-product of aerobic metabolism.	Oxygen	126-132	superoxide dismutase 2	Homo sapiens	0-30
19699328-1	2010	Manganese superoxide dismutase is an important antioxidant defense metalloenzyme that protects cells from damage by the toxic oxygen metabolite, superoxide free radical, formed as an unavoidable by-product of aerobic metabolism.	superoxide free radical	145-168	superoxide dismutase 2	Homo sapiens	0-30
19699328-4	2010	Recent work is beginning to provide insight into the mechanisms of metal delivery to manganese superoxide dismutase in vivo and in vitro.	Metals	67-72	superoxide dismutase 2	Homo sapiens	85-115
19756960-0	2010	Manganese superoxide dismutase: effect of the ala16val polymorphism on protein, activity, and mRNA levels in human breast cancer cell lines and stably transfected mouse embryonic fibroblasts.	ala16val	46-54	superoxide dismutase 2	Homo sapiens	0-30
19837190-6	2010	On the other hand, tyrosine 34 of human MnSOD was exclusively nitrated to 3-nitrotyrosine and almost completely inactivated by the reaction with peroxynitrite.	Tyrosine	19-27	superoxide dismutase 2	Homo sapiens	40-45
19837190-6	2010	On the other hand, tyrosine 34 of human MnSOD was exclusively nitrated to 3-nitrotyrosine and almost completely inactivated by the reaction with peroxynitrite.	3-nitrotyrosine	74-89	superoxide dismutase 2	Homo sapiens	40-45
19837190-6	2010	On the other hand, tyrosine 34 of human MnSOD was exclusively nitrated to 3-nitrotyrosine and almost completely inactivated by the reaction with peroxynitrite.	Peroxynitrous Acid	145-158	superoxide dismutase 2	Homo sapiens	40-45
19929244-2	2010	The aim of this study was to assess the role of common variation in three polymorphic genes (MnSOD Ala-9Val, GPX1 Pro198Leu and CAT -262 C > T) coding for antioxidant defence enzymes in modulating individual susceptibility to hepatocellular carcinoma (HCC) using a case-control study (cases = 96 and controls = 222).	ala-9val	99-107	superoxide dismutase 2	Homo sapiens	93-98
19929244-5	2010	The MnSOD Ala/Ala and CAT TT genotypes were more frequent in HCC than in control (p = 0.001 and p = 0.072, respectively).	Alanine	10-13	superoxide dismutase 2	Homo sapiens	4-9
19929244-5	2010	The MnSOD Ala/Ala and CAT TT genotypes were more frequent in HCC than in control (p = 0.001 and p = 0.072, respectively).	Alanine	14-17	superoxide dismutase 2	Homo sapiens	4-9
19929244-7	2010	Combined MnSOD Ala/Ala and GPx1 Leu/Leu had a synergistic effect on HCC risk, with an OR of 3.84 (p = 0.029).	Alanine	15-18	superoxide dismutase 2	Homo sapiens	9-14
19929244-7	2010	Combined MnSOD Ala/Ala and GPx1 Leu/Leu had a synergistic effect on HCC risk, with an OR of 3.84 (p = 0.029).	Alanine	19-22	superoxide dismutase 2	Homo sapiens	9-14
19929244-8	2010	Furthermore an even more pronounced risk was observed when we combined MnSOD Ala/Ala and CAT TT (OR = 13.60, p = 0.023).	Alanine	77-80	superoxide dismutase 2	Homo sapiens	71-76
19756960-1	2010	The manganese superoxide dismutase (MnSOD) ala16val polymorphism has been associated with various diseases including breast cancer.	ala16val	43-51	superoxide dismutase 2	Homo sapiens	4-34
19756960-1	2010	The manganese superoxide dismutase (MnSOD) ala16val polymorphism has been associated with various diseases including breast cancer.	ala16val	43-51	superoxide dismutase 2	Homo sapiens	36-41
19796678-4	2009	These PCBs also caused 1.5- to 5.0-fold increases in MnSOD activity in MCF-10A cells and 2.5- to 5-fold increases in CuZnSOD activity in RWPE-1 cells.	Polychlorinated Biphenyls	6-10	superoxide dismutase 2	Homo sapiens	53-58
20110685-4	2010	When cells where exposed to sustained H(2)O(2) production, a clear dose-response effect was detected in the activity of the antioxidant enzymes catalase, glutathione peroxidase and Mn-SOD, with higher concentrations of H(2)O(2) inducing greater enzyme activities.	Hydrogen Peroxide	38-46	superoxide dismutase 2	Homo sapiens	181-187
20110685-4	2010	When cells where exposed to sustained H(2)O(2) production, a clear dose-response effect was detected in the activity of the antioxidant enzymes catalase, glutathione peroxidase and Mn-SOD, with higher concentrations of H(2)O(2) inducing greater enzyme activities.	Hydrogen Peroxide	219-227	superoxide dismutase 2	Homo sapiens	181-187
20072932-3	2010	Manganese superoxide dismutase (MnSOD), copper zinc superoxide dismutase (CuZnSOD) and catalase are all known antioxidants whose over-expression can result in amelioration of pathology brought about by an excess of reactive oxygen species within a cell.	Reactive Oxygen Species	215-238	superoxide dismutase 2	Homo sapiens	0-30
20441054-4	2010	The detoxifying enzymes inactivate dangerous chemical compounds and anions for the cell; that is, why it is important to know if the polymorphisms pro198leu in GPX-1 and ile58thr in MnSOD are associated with bladder cancer.	pro198leu	147-156	superoxide dismutase 2	Homo sapiens	182-187
19796678-7	2009	These results support the hypothesis that exposure of exponentially growing human breast and prostate epithelial cells to PCBs causes increased steady-state levels of intracellular O(2)(*-) and H(2)O(2), induction of MnSOD or CuZnSOD activity, and clonogenic cell killing that could be inhibited by a clinically relevant thiol antioxidant, NAC, as well as by catalase and superoxide dismutase after PCB exposure.	Polychlorinated Biphenyls	122-126	superoxide dismutase 2	Homo sapiens	217-222
20041472-9	2010	Furthermore, we find evidence for an association between Ala-9Val (MnSOD) and TDof, but not TDlt.	ala-9val	57-65	superoxide dismutase 2	Homo sapiens	67-72
20930427-8	2010	A defect of mitochondrial NDUFV1 may reduce complex I, which produces most of the superoxide, which is then scavenged by the mitochondrial enzyme Mn-superoxide dismutase to produce H(2)O(2).	Superoxides	82-92	superoxide dismutase 2	Homo sapiens	146-169
20930427-8	2010	A defect of mitochondrial NDUFV1 may reduce complex I, which produces most of the superoxide, which is then scavenged by the mitochondrial enzyme Mn-superoxide dismutase to produce H(2)O(2).	Water	181-186	superoxide dismutase 2	Homo sapiens	146-169
20625417-3	2010	Mitochondrial superoxide dismutase (SOD2) plays a crucial role in the defence against ROS, thus protecting against several apoptotic stimuli.	Reactive Oxygen Species	86-89	superoxide dismutase 2	Homo sapiens	36-40
20625417-4	2010	Diclofenac decreased the protein levels and the enzymatic activity of SOD2, without any significant impairment of the corresponding mRNA levels in the SH-SY5Y extracts.	Diclofenac	0-10	superoxide dismutase 2	Homo sapiens	70-74
20625417-7	2010	These data suggest that mitochondria are involved in the diclofenac-induced apoptosis of SH-SY5Y cells and point to a possible role of SOD2 in this process.	Diclofenac	57-67	superoxide dismutase 2	Homo sapiens	135-139
19623544-4	2010	In this study, we investigated the expression and localization of MnSOD in response to the exposure to bile salts in an esophageal epithelial cell line.	Bile Acids and Salts	103-113	superoxide dismutase 2	Homo sapiens	66-71
19623544-9	2010	The protein level of MnSOD in mitochondria was increased at 4 h, but with a decreased enzymatic activity after bile salts treatment.	Bile Acids and Salts	111-121	superoxide dismutase 2	Homo sapiens	21-26
19623544-10	2010	Cytoplasmic MnSOD was detected in the cells with bile salts treatment.	Bile Acids and Salts	49-59	superoxide dismutase 2	Homo sapiens	12-17
19623544-11	2010	Immunocytochemical staining demonstrated that esophageal epithelial cell underwent morphological alteration and MnSOD relocalization after bile salts treatment.	Bile Acids and Salts	139-149	superoxide dismutase 2	Homo sapiens	112-117
19623544-13	2010	This suggests that bile salts may contribute to the dysfunction of mitochondria, by enzymatically inhibiting of MnSOD localization and thus activation in the mitochondria.	Bile Acids and Salts	19-29	superoxide dismutase 2	Homo sapiens	112-117
19796678-7	2009	These results support the hypothesis that exposure of exponentially growing human breast and prostate epithelial cells to PCBs causes increased steady-state levels of intracellular O(2)(*-) and H(2)O(2), induction of MnSOD or CuZnSOD activity, and clonogenic cell killing that could be inhibited by a clinically relevant thiol antioxidant, NAC, as well as by catalase and superoxide dismutase after PCB exposure.	Sulfhydryl Compounds	321-326	superoxide dismutase 2	Homo sapiens	217-222
19796678-7	2009	These results support the hypothesis that exposure of exponentially growing human breast and prostate epithelial cells to PCBs causes increased steady-state levels of intracellular O(2)(*-) and H(2)O(2), induction of MnSOD or CuZnSOD activity, and clonogenic cell killing that could be inhibited by a clinically relevant thiol antioxidant, NAC, as well as by catalase and superoxide dismutase after PCB exposure.	Acetylcysteine	340-343	superoxide dismutase 2	Homo sapiens	217-222
19219857-7	2009	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH dependence, two (AKT1 and GABRG2) with METH abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.	Methamphetamine	58-62	superoxide dismutase 2	Homo sapiens	251-255
20082261-0	2009	Dietary carotenoid-rich pequi oil reduces plasma lipid peroxidation and DNA damage in runners and evidence for an association with MnSOD genetic variant -Val9Ala.	Carotenoids	8-18	superoxide dismutase 2	Homo sapiens	131-136
19905985-2	2009	Following induction of H/R, MnSOD expression and activity levels increased and remained high for over 24 h. Hepatocytes silenced for MnSOD (siMnSOD) demonstrated increased susceptibility to H/R-induced apoptotic cell death and a lower capacity to generate mitochondrial reactive oxygen species.	r	25-26	superoxide dismutase 2	Homo sapiens	133-138
19715479-9	2009	The NQO1 C609T polymorphism may influence steroid resistance of UC patients, while the SOD2 Ala-9Val polymorphism may influence age of onset of UC.	ala-9val	92-100	superoxide dismutase 2	Homo sapiens	87-91
19905985-2	2009	Following induction of H/R, MnSOD expression and activity levels increased and remained high for over 24 h. Hepatocytes silenced for MnSOD (siMnSOD) demonstrated increased susceptibility to H/R-induced apoptotic cell death and a lower capacity to generate mitochondrial reactive oxygen species.	Reactive Oxygen Species	270-293	superoxide dismutase 2	Homo sapiens	28-33
19905985-2	2009	Following induction of H/R, MnSOD expression and activity levels increased and remained high for over 24 h. Hepatocytes silenced for MnSOD (siMnSOD) demonstrated increased susceptibility to H/R-induced apoptotic cell death and a lower capacity to generate mitochondrial reactive oxygen species.	Reactive Oxygen Species	270-293	superoxide dismutase 2	Homo sapiens	133-138
19755112-0	2009	In vitro metal uptake by recombinant human manganese superoxide dismutase.	Metals	9-14	superoxide dismutase 2	Homo sapiens	43-73
19951573-18	2009	The ability of alpha-LA to suppress mitochondrial oxidative damage is concomitant with an enhancement of Mn-SOD activity and an increase in the GSH content of myocardial mitochondria.	Thioctic Acid	15-23	superoxide dismutase 2	Homo sapiens	105-111
19749157-7	2009	Resveratrol upregulated MnSOD expression and increased cellular GSH content in a concentration-dependent manner (measured by HPLC coulometric analysis).	Resveratrol	0-11	superoxide dismutase 2	Homo sapiens	24-29
19755112-1	2009	Metal uptake by the antioxidant defense metalloenzyme manganese superoxide dismutase (MnSOD) is an essential step in the functional maturation of the protein that is just beginning to be investigated in detail.	Metals	0-5	superoxide dismutase 2	Homo sapiens	54-84
19755112-1	2009	Metal uptake by the antioxidant defense metalloenzyme manganese superoxide dismutase (MnSOD) is an essential step in the functional maturation of the protein that is just beginning to be investigated in detail.	Metals	0-5	superoxide dismutase 2	Homo sapiens	86-91
19755112-2	2009	We have extended earlier in vitro studies on metal binding by the dimeric Escherichia coli apo-MnSOD to investigate the mechanism of metal uptake by tetrameric human and Thermus thermophilus apo-MnSODs.	Metals	45-50	superoxide dismutase 2	Homo sapiens	95-100
19755112-3	2009	Like the E. coli apo-MnSOD, these proteins also bind metal ions in vitro in a thermally activated, pH-sensitive process.	Metals	53-58	superoxide dismutase 2	Homo sapiens	21-26
19755112-6	2009	The high concentration of metal ion that is required to achieve physiologically relevant metallation rates for tetrameric human apo-MnSOD in vitro suggests the possibility that co-translational metal binding or chaperone interactions may be required in vivo.	Metals	26-31	superoxide dismutase 2	Homo sapiens	132-137
19755112-6	2009	The high concentration of metal ion that is required to achieve physiologically relevant metallation rates for tetrameric human apo-MnSOD in vitro suggests the possibility that co-translational metal binding or chaperone interactions may be required in vivo.	Metals	89-94	superoxide dismutase 2	Homo sapiens	132-137
19467856-2	2009	Manganese superoxide dismutase (MnSOD) is the major antioxidant in the mitochondria, catalysing the dismutation of superoxide radicals to form hydrogen peroxide.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
19467856-2	2009	Manganese superoxide dismutase (MnSOD) is the major antioxidant in the mitochondria, catalysing the dismutation of superoxide radicals to form hydrogen peroxide.	Hydrogen Peroxide	143-160	superoxide dismutase 2	Homo sapiens	0-30
19467856-2	2009	Manganese superoxide dismutase (MnSOD) is the major antioxidant in the mitochondria, catalysing the dismutation of superoxide radicals to form hydrogen peroxide.	Hydrogen Peroxide	143-160	superoxide dismutase 2	Homo sapiens	32-37
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Valine	100-103	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Alanine	34-37	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Valine	115-118	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Alanine	104-107	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Alanine	104-107	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Valine	115-118	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Valine	115-118	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Valine	115-118	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Alanine	104-107	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Alanine	104-107	superoxide dismutase 2	Homo sapiens	27-32
19467856-6	2009	However, we found that the MnSOD 9Ala allele was associated with an increased prostate cancer risk (Val/Ala versus Val/Val: odds ratio (OR)=1.1; 95% confidence intervals (CI): 1.0-1.3; Ala/Ala versus Val/Val: OR=1.3; 95% CI: 1.0-1.6; Val/Ala+Ala/Ala versus Val/Val: OR=1.2; 95% CI, 1.0-1.3).	Alanine	104-107	superoxide dismutase 2	Homo sapiens	27-32
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	ala-9ala	37-45	superoxide dismutase 2	Homo sapiens	31-36
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Alanine	37-40	superoxide dismutase 2	Homo sapiens	31-36
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Alanine	42-45	superoxide dismutase 2	Homo sapiens	31-36
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Valine	181-184	superoxide dismutase 2	Homo sapiens	31-36
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Alanine	42-45	superoxide dismutase 2	Homo sapiens	31-36
19706356-10	2009	Decreased CIN1 risk in association with the MnSOD rs4880 variant genotype was also observed particularly for subjects with higher beta-carotene and gamma-tocopherol levels.	beta Carotene	130-143	superoxide dismutase 2	Homo sapiens	44-49
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Valine	189-192	superoxide dismutase 2	Homo sapiens	31-36
19706356-10	2009	Decreased CIN1 risk in association with the MnSOD rs4880 variant genotype was also observed particularly for subjects with higher beta-carotene and gamma-tocopherol levels.	gamma-Tocopherol	148-164	superoxide dismutase 2	Homo sapiens	44-49
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Valine	189-192	superoxide dismutase 2	Homo sapiens	31-36
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Ascorbic Acid	231-240	superoxide dismutase 2	Homo sapiens	31-36
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Vitamin E	286-295	superoxide dismutase 2	Homo sapiens	31-36
19467856-7	2009	In addition, we found that the MnSOD Ala-9Ala genotype contributed to an increased breast cancer risk in premenopausal women who had low consumption of antioxidants (Ala/Ala versus Val/Ala+Val/Val: OR=2.6, 95% CI: 1.0-6.4 with low vitamin C consumption; OR=2.1, 95%CI: 1.3-3.4 with low vitamin E consumption and OR=2.9, 95%CI: 1.5-5.7 with low carotenoid consumption).	Carotenoids	344-354	superoxide dismutase 2	Homo sapiens	31-36
19787204-1	2009	The present study is the first to evaluate the expression and activity of MnSOD, Cu/ZnSOD and catalase in human gastric samples, since ROS play a significant role in the pathogenesis of different forms of malignancy inducing mutations and various diseases such as gastric cancer.	ros	135-138	superoxide dismutase 2	Homo sapiens	74-79
19598258-7	2009	By contrast, the expression of Cu-Zn superoxide dismutase (SOD) and Mn-SOD proteins increased during heat-shock pretreatment before sorbitol exposure.	Sorbitol	132-140	superoxide dismutase 2	Homo sapiens	68-74
19731237-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide anion into hydrogen peroxide, which, unless detoxified by glutathione peroxidase or catalase (CAT), can form the hydroxyl radical with iron.	Superoxides	48-64	superoxide dismutase 2	Homo sapiens	0-30
19731237-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide anion into hydrogen peroxide, which, unless detoxified by glutathione peroxidase or catalase (CAT), can form the hydroxyl radical with iron.	Superoxides	48-64	superoxide dismutase 2	Homo sapiens	32-37
19731237-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide anion into hydrogen peroxide, which, unless detoxified by glutathione peroxidase or catalase (CAT), can form the hydroxyl radical with iron.	Hydrogen Peroxide	70-87	superoxide dismutase 2	Homo sapiens	0-30
19731237-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide anion into hydrogen peroxide, which, unless detoxified by glutathione peroxidase or catalase (CAT), can form the hydroxyl radical with iron.	Hydrogen Peroxide	70-87	superoxide dismutase 2	Homo sapiens	32-37
19731237-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide anion into hydrogen peroxide, which, unless detoxified by glutathione peroxidase or catalase (CAT), can form the hydroxyl radical with iron.	Hydroxyl Radical	172-188	superoxide dismutase 2	Homo sapiens	0-30
19731237-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide anion into hydrogen peroxide, which, unless detoxified by glutathione peroxidase or catalase (CAT), can form the hydroxyl radical with iron.	Hydroxyl Radical	172-188	superoxide dismutase 2	Homo sapiens	32-37
19731237-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide anion into hydrogen peroxide, which, unless detoxified by glutathione peroxidase or catalase (CAT), can form the hydroxyl radical with iron.	Iron	194-198	superoxide dismutase 2	Homo sapiens	0-30
19731237-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide anion into hydrogen peroxide, which, unless detoxified by glutathione peroxidase or catalase (CAT), can form the hydroxyl radical with iron.	Iron	194-198	superoxide dismutase 2	Homo sapiens	32-37
19731237-9	2009	Carriage of one or two Ala-SOD2 allele(s) was associated with higher liver iron scores and higher risks of HCC and death.	Iron	75-79	superoxide dismutase 2	Homo sapiens	27-31
19731237-12	2009	CONCLUSION: The combination of the GG-MPO genotype (leading to high MPO expression) and at least one Ala-SOD2 allele (associated with high liver iron score) markedly increased the risks of HCC occurrence and death in patients with alcoholic cirrhosis.	Iron	145-149	superoxide dismutase 2	Homo sapiens	105-109
19712751-1	2009	Manganese superoxide dismutase (MnSOD) acts as an antioxidant and protects cells from the harmful effects of reactive oxygen species.	Reactive Oxygen Species	109-132	superoxide dismutase 2	Homo sapiens	0-30
19900038-2	2009	Manganese superoxide dismutase (Mn SOD) is a mitochondrial enzyme that scavenges reactive oxygen species (ROS).	Reactive Oxygen Species	81-104	superoxide dismutase 2	Homo sapiens	0-30
19900038-2	2009	Manganese superoxide dismutase (Mn SOD) is a mitochondrial enzyme that scavenges reactive oxygen species (ROS).	Reactive Oxygen Species	81-104	superoxide dismutase 2	Homo sapiens	32-38
19900038-2	2009	Manganese superoxide dismutase (Mn SOD) is a mitochondrial enzyme that scavenges reactive oxygen species (ROS).	Reactive Oxygen Species	106-109	superoxide dismutase 2	Homo sapiens	0-30
19900038-2	2009	Manganese superoxide dismutase (Mn SOD) is a mitochondrial enzyme that scavenges reactive oxygen species (ROS).	Reactive Oxygen Species	106-109	superoxide dismutase 2	Homo sapiens	32-38
19712751-1	2009	Manganese superoxide dismutase (MnSOD) acts as an antioxidant and protects cells from the harmful effects of reactive oxygen species.	Reactive Oxygen Species	109-132	superoxide dismutase 2	Homo sapiens	32-37
19712751-2	2009	We investigated the relationship between the MnSOD Ala-9Val polymorphism and breast cancer.	ala-9val	51-59	superoxide dismutase 2	Homo sapiens	45-50
19712751-6	2009	In conclusion, the MnSOD Ala-9Val polymorphism may contribute to an increased risk for breast cancer development, particularly in the presence of a higher level of education, high BMI, late age at first pregnancy, and premenopausal status.	ala-9val	25-33	superoxide dismutase 2	Homo sapiens	19-24
19679656-4	2009	Elevations in mRNA and protein levels of HIF-dependent genes heme oxygenase-1 (Ho-1) and manganese superoxide dismutase (Mnsod) following DHB pretreatment alone are also maintained in the presence of MPTP.	3,4-dihydroxybenzoate	138-141	superoxide dismutase 2	Homo sapiens	89-119
19917352-9	2009	RESULTS: Serum creatinine and K(+), blood urea nitrogen, and aspartate aminotransferase activity decreased significantly, whereas serum Na(+) and renal function improved in the MnSOD group compared with the control and sham groups.	Urea	42-46	superoxide dismutase 2	Homo sapiens	177-182
19917352-9	2009	RESULTS: Serum creatinine and K(+), blood urea nitrogen, and aspartate aminotransferase activity decreased significantly, whereas serum Na(+) and renal function improved in the MnSOD group compared with the control and sham groups.	Nitrogen	47-55	superoxide dismutase 2	Homo sapiens	177-182
19917352-10	2009	On hematoxylin and eosin staining, the histological score indicated that acute tubular necrosis was significantly reduced by MnSOD administration.	Hematoxylin	3-14	superoxide dismutase 2	Homo sapiens	125-130
19917352-10	2009	On hematoxylin and eosin staining, the histological score indicated that acute tubular necrosis was significantly reduced by MnSOD administration.	Eosine Yellowish-(YS)	19-24	superoxide dismutase 2	Homo sapiens	125-130
19917352-11	2009	Periodic acid-Schiff staining was absent in the nonadministration group, whereas it persisted in the MnSOD group.	Periodic Acid	0-13	superoxide dismutase 2	Homo sapiens	101-106
19666009-8	2009	Silencing Mn-SOD attenuated PSS-mediated DeltaPsi(m) increase while adding Mn-SOD mimetic, MnTMPyP, increased DeltaPsi(m) to the similar extent as induced by PSS.	pss	28-31	superoxide dismutase 2	Homo sapiens	10-16
19666009-8	2009	Silencing Mn-SOD attenuated PSS-mediated DeltaPsi(m) increase while adding Mn-SOD mimetic, MnTMPyP, increased DeltaPsi(m) to the similar extent as induced by PSS.	pss	158-161	superoxide dismutase 2	Homo sapiens	10-16
19666009-8	2009	Silencing Mn-SOD attenuated PSS-mediated DeltaPsi(m) increase while adding Mn-SOD mimetic, MnTMPyP, increased DeltaPsi(m) to the similar extent as induced by PSS.	pss	158-161	superoxide dismutase 2	Homo sapiens	75-81
19666009-9	2009	Our findings suggest that PSS-increased mitochondrial DeltaPsi(m), in part, via Mn-SOD up-regulation.	pss	26-29	superoxide dismutase 2	Homo sapiens	80-86
19679656-4	2009	Elevations in mRNA and protein levels of HIF-dependent genes heme oxygenase-1 (Ho-1) and manganese superoxide dismutase (Mnsod) following DHB pretreatment alone are also maintained in the presence of MPTP.	3,4-dihydroxybenzoate	138-141	superoxide dismutase 2	Homo sapiens	121-126
19679656-4	2009	Elevations in mRNA and protein levels of HIF-dependent genes heme oxygenase-1 (Ho-1) and manganese superoxide dismutase (Mnsod) following DHB pretreatment alone are also maintained in the presence of MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	200-204	superoxide dismutase 2	Homo sapiens	89-119
19679656-4	2009	Elevations in mRNA and protein levels of HIF-dependent genes heme oxygenase-1 (Ho-1) and manganese superoxide dismutase (Mnsod) following DHB pretreatment alone are also maintained in the presence of MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	200-204	superoxide dismutase 2	Homo sapiens	121-126
19540247-9	2009	In MnSOD cells, ROS levels were reduced (p=0.02) and mitochondrial membrane potential increased (p=0.04).	Reactive Oxygen Species	16-19	superoxide dismutase 2	Homo sapiens	3-8
19696738-6	2009	Elevated FoxM1, in turn, downregulates ROS levels by stimulating expression of ROS scavenger genes, such as MnSOD, catalase and PRDX3.	Reactive Oxygen Species	79-82	superoxide dismutase 2	Homo sapiens	108-113
19696738-6	2009	Elevated FoxM1, in turn, downregulates ROS levels by stimulating expression of ROS scavenger genes, such as MnSOD, catalase and PRDX3.	Reactive Oxygen Species	39-42	superoxide dismutase 2	Homo sapiens	108-113
19616630-6	2009	Mn-SOD expression in the liver and kidney were significantly modulated by injection of LPS (1, 5, or 10 microg g(-1) body weight), Edwardsiella tarda challenge (5 x 10(3) or 5 x 10(5) cells/fish), and heavy metal exposure (Cd, Cu, or Zn at 5 microM).	Metals	207-212	superoxide dismutase 2	Homo sapiens	0-6
19616630-6	2009	Mn-SOD expression in the liver and kidney were significantly modulated by injection of LPS (1, 5, or 10 microg g(-1) body weight), Edwardsiella tarda challenge (5 x 10(3) or 5 x 10(5) cells/fish), and heavy metal exposure (Cd, Cu, or Zn at 5 microM).	Cadmium	223-225	superoxide dismutase 2	Homo sapiens	0-6
19616630-6	2009	Mn-SOD expression in the liver and kidney were significantly modulated by injection of LPS (1, 5, or 10 microg g(-1) body weight), Edwardsiella tarda challenge (5 x 10(3) or 5 x 10(5) cells/fish), and heavy metal exposure (Cd, Cu, or Zn at 5 microM).	Copper	227-229	superoxide dismutase 2	Homo sapiens	0-6
19616630-6	2009	Mn-SOD expression in the liver and kidney were significantly modulated by injection of LPS (1, 5, or 10 microg g(-1) body weight), Edwardsiella tarda challenge (5 x 10(3) or 5 x 10(5) cells/fish), and heavy metal exposure (Cd, Cu, or Zn at 5 microM).	Zinc	234-236	superoxide dismutase 2	Homo sapiens	0-6
19647751-3	2009	KEY FINDINGS: We showed that gAd induces the expression of a number of genes using PCR arrays, including MCP-1, VCAM-1, E-selectin, IL-6, and IL-8, all of which have been previously shown to be associated with adiponectin, as well as SOD2, PAI-1, and CSF2, which is a new finding.	ganoderic acid D	29-32	superoxide dismutase 2	Homo sapiens	234-238
19647296-1	2009	OBJECTIVES: To examine the association between 2 mitochondrial manganese superoxide dismutase (MnSOD) genetic polymorphisms (Ala-9Val and Ala-16Val) and prostate cancer susceptibility.	ala-9val	125-133	superoxide dismutase 2	Homo sapiens	63-93
19647296-1	2009	OBJECTIVES: To examine the association between 2 mitochondrial manganese superoxide dismutase (MnSOD) genetic polymorphisms (Ala-9Val and Ala-16Val) and prostate cancer susceptibility.	ala-9val	125-133	superoxide dismutase 2	Homo sapiens	95-100
19563893-3	2009	We have found that progestins stimulate MnSOD in T47D human breast cancer cells in a time and physiological concentration-dependent manner, exhibiting specificity for progestins and inhibition by the antiprogestin RU486.	Mifepristone	214-219	superoxide dismutase 2	Homo sapiens	40-45
19563893-5	2009	Cycloheximide inhibits stimulation at the mRNA level, suggesting that progestin induction of MnSOD mRNA depends on synthesis of protein.	Cycloheximide	0-13	superoxide dismutase 2	Homo sapiens	93-98
20090883-3	2009	MCF-10A, human breast epithelial cells were incubated with 0.1 microM 4-OHE(2), either with or without 30 microM tocopherols for 96 h. 4-OHE(2) caused the accumulation of intracellular ROS, while cellular GSH/GSSG ratio and MnSOD protein levels were decreased, indicating that there was an oxidative burden.	4-ohe	135-140	superoxide dismutase 2	Homo sapiens	224-229
20090883-5	2009	gamma-Tocopherol suppressed the 4-OHE(2)-induced increases in ROS, GSH/GSSG ratio, and MnSOD protein expression, while alpha-tocopherol up-regulated BRCA1 and PARP-1 protein expression.	gamma-Tocopherol	0-16	superoxide dismutase 2	Homo sapiens	87-92
20090883-5	2009	gamma-Tocopherol suppressed the 4-OHE(2)-induced increases in ROS, GSH/GSSG ratio, and MnSOD protein expression, while alpha-tocopherol up-regulated BRCA1 and PARP-1 protein expression.	4-ohe	32-37	superoxide dismutase 2	Homo sapiens	87-92
19666610-5	2009	We found that overexpression of SOD-2 decreased hippocampal superoxide, prevented AD-related learning and memory deficits, and reduced Abeta plaques.	Superoxides	60-70	superoxide dismutase 2	Homo sapiens	32-37
19546321-2	2009	O(2)(-) serves as the raw material for many reactive oxygen species (ROS) members like H(2)O(2) and OH(.-) radicals following its catalysis by superoxide dismutase (SOD) enzymes and also by autocatalysis (autodismutation) reactions.	o(2)(-)	0-7	superoxide dismutase 2	Homo sapiens	165-168
19546321-2	2009	O(2)(-) serves as the raw material for many reactive oxygen species (ROS) members like H(2)O(2) and OH(.-) radicals following its catalysis by superoxide dismutase (SOD) enzymes and also by autocatalysis (autodismutation) reactions.	Reactive Oxygen Species	44-67	superoxide dismutase 2	Homo sapiens	165-168
19546321-2	2009	O(2)(-) serves as the raw material for many reactive oxygen species (ROS) members like H(2)O(2) and OH(.-) radicals following its catalysis by superoxide dismutase (SOD) enzymes and also by autocatalysis (autodismutation) reactions.	Reactive Oxygen Species	69-72	superoxide dismutase 2	Homo sapiens	165-168
19546321-2	2009	O(2)(-) serves as the raw material for many reactive oxygen species (ROS) members like H(2)O(2) and OH(.-) radicals following its catalysis by superoxide dismutase (SOD) enzymes and also by autocatalysis (autodismutation) reactions.	Hydrogen Peroxide	87-95	superoxide dismutase 2	Homo sapiens	165-168
19546321-2	2009	O(2)(-) serves as the raw material for many reactive oxygen species (ROS) members like H(2)O(2) and OH(.-) radicals following its catalysis by superoxide dismutase (SOD) enzymes and also by autocatalysis (autodismutation) reactions.	oh(.-) radicals	100-115	superoxide dismutase 2	Homo sapiens	165-168
19546321-5	2009	With the help of a mitochondrial SOD2 loss-of-function mutant, Sod2(n283), we measured the sensitivity of muscles and neurons to ROS attack.	Reactive Oxygen Species	129-132	superoxide dismutase 2	Homo sapiens	63-67
19546321-8	2009	On the other hand, ultrastructural analysis of Sod2(n283) muscles revealed fewer mitochondria and reduced muscle ATP production.	Adenosine Triphosphate	113-116	superoxide dismutase 2	Homo sapiens	47-51
19373868-8	2009	Treatment of Hs578T and Her-2/neu-driven NF639 cells with 1,25-dihydroxyvitamin D3 decreased RelB/RELB gene expression and levels of pro-survival targets Survivin, MnSOD and Bcl-2, while increasing their sensitivity to gamma-irradiation.	Calcitriol	58-82	superoxide dismutase 2	Homo sapiens	164-169
19450565-5	2009	Protection by superoxide dismutase (Cu,Zn-SOD or Mn-SOD) or catalase indicates mediation of the toxicity by superoxide and hydrogen peroxide.	Hydrogen Peroxide	123-140	superoxide dismutase 2	Homo sapiens	49-55
19262996-2	2009	Since the dismutation of superoxide is catalyzed by superoxide dismutase enzymes, we tested the association between obesity and Ala16Val manganese-dependent superoxide dismutase gene (MnSOD) polymorphism.	Superoxides	25-35	superoxide dismutase 2	Homo sapiens	184-189
19848199-6	2009	CONCLUSIONS: The acting mechanism of BHQD for AP-CHD treatment might partially due to its effects in inducing gene expression of MnSOD in mononuclear cells, enhancing SOD activity, decreasing LPO content, maintaining oxidation/antioxidation equilibrium in myocardial cells, blocking the chain reaction of lipid peroxidation, intervening the production and enhancing the scavenging of oxygen free radicals.	Benzo[h]quinoline-5,6-dione	37-41	superoxide dismutase 2	Homo sapiens	129-134
19528373-2	2009	Our group previously demonstrated a strong interaction between plasma selenium and the manganese superoxide dismutase (SOD2) gene and incident prostate cancer risk.	Selenium	70-78	superoxide dismutase 2	Homo sapiens	87-117
19528373-2	2009	Our group previously demonstrated a strong interaction between plasma selenium and the manganese superoxide dismutase (SOD2) gene and incident prostate cancer risk.	Selenium	70-78	superoxide dismutase 2	Homo sapiens	119-123
19528373-3	2009	We now hypothesized that SOD2 modifies the association between selenium level and risk of aggressive prostate cancer at diagnosis.	Selenium	63-71	superoxide dismutase 2	Homo sapiens	25-29
19528373-7	2009	There was evidence of an interaction between SOD2 and selenium levels such that among men with the AA genotype, higher selenium levels were associated with a reduced risk of presenting with aggressive disease (RR = 0.60; 95% CI, 0.32 to 1.12), whereas among men with a V allele, higher selenium levels were associated with an increased risk of aggressive disease (for VV or VA men, RR = 1.82; 95% CI, 1.27 to 2.61; P for interaction = .007).	Selenium	119-127	superoxide dismutase 2	Homo sapiens	45-49
19528373-7	2009	There was evidence of an interaction between SOD2 and selenium levels such that among men with the AA genotype, higher selenium levels were associated with a reduced risk of presenting with aggressive disease (RR = 0.60; 95% CI, 0.32 to 1.12), whereas among men with a V allele, higher selenium levels were associated with an increased risk of aggressive disease (for VV or VA men, RR = 1.82; 95% CI, 1.27 to 2.61; P for interaction = .007).	Selenium	119-127	superoxide dismutase 2	Homo sapiens	45-49
19450565-5	2009	Protection by superoxide dismutase (Cu,Zn-SOD or Mn-SOD) or catalase indicates mediation of the toxicity by superoxide and hydrogen peroxide.	Superoxides	14-24	superoxide dismutase 2	Homo sapiens	49-55
19451660-3	2009	Manganese superoxide dismutase (MnSOD) is one important repair enzyme for reactive oxidative stress (ROS)-induced damage.	ros	101-104	superoxide dismutase 2	Homo sapiens	0-30
19451660-3	2009	Manganese superoxide dismutase (MnSOD) is one important repair enzyme for reactive oxidative stress (ROS)-induced damage.	ros	101-104	superoxide dismutase 2	Homo sapiens	32-37
19451660-11	2009	However, our data suggest a complex gene-to-phenotype interaction between the MnSOD genotype and alcohol misuse.	Alcohols	97-104	superoxide dismutase 2	Homo sapiens	78-83
19558795-0	2009	The subcellular distribution of MnSOD alters during sodium selenite-induced apoptosis.	Sodium Selenite	52-67	superoxide dismutase 2	Homo sapiens	32-37
19407826-8	2009	Mitochondrial electron transport chain (mETC) inhibitors in combination with the SOD inhibitor 2-methoxyestradiol (2-ME) increased O(2)(*-) levels, lowered H(2)O(2) levels, and increased autophagy.	2-Methoxyestradiol	115-119	superoxide dismutase 2	Homo sapiens	81-84
19228881-6	2009	Manganese superoxide dismutase (SOD2) was detected by Western blot in the nucleoid fractions.	nucleoid	74-82	superoxide dismutase 2	Homo sapiens	32-36
19228881-7	2009	DNA, mitochondrial glutathione peroxidase (GPx1), and Pol gamma were coimmunoprecipitated with SOD2 from nucleoid fractions, which suggests that an antioxidant system composed of SOD2 and GPx1 are integral constituents of nucleoids.	nucleoids	222-231	superoxide dismutase 2	Homo sapiens	95-99
19228881-9	2009	Using a sandwich filter-binding assay, direct association of SOD2 by salt-sensitive ionic forces with a chemically synthesized mtDNA fragment was demonstrated.	Salts	69-73	superoxide dismutase 2	Homo sapiens	61-65
19228881-10	2009	Increasing salt concentrations during nucleoid isolation on sucrose density gradients disrupted the association of SOD2 with mitochondrial nucleoids.	Salts	11-15	superoxide dismutase 2	Homo sapiens	115-119
19228881-10	2009	Increasing salt concentrations during nucleoid isolation on sucrose density gradients disrupted the association of SOD2 with mitochondrial nucleoids.	nucleoid	38-46	superoxide dismutase 2	Homo sapiens	115-119
19228881-10	2009	Increasing salt concentrations during nucleoid isolation on sucrose density gradients disrupted the association of SOD2 with mitochondrial nucleoids.	Sucrose	60-67	superoxide dismutase 2	Homo sapiens	115-119
19228881-10	2009	Increasing salt concentrations during nucleoid isolation on sucrose density gradients disrupted the association of SOD2 with mitochondrial nucleoids.	nucleoids	139-148	superoxide dismutase 2	Homo sapiens	115-119
19229592-0	2009	Gene expressions of Mn-SOD and GPx-1 in streptozotocin-induced diabetes: effect of antioxidants.	Streptozocin	40-54	superoxide dismutase 2	Homo sapiens	20-26
19229592-2	2009	In this study, we have reported the effects of the streptozotocin-induced diabetes on the gene expression and the activities of two antioxidant enzymes, manganese superoxide dismutase (MnSOD) and glutathione peroxidase (GPx).	Streptozocin	51-65	superoxide dismutase 2	Homo sapiens	153-183
19229592-2	2009	In this study, we have reported the effects of the streptozotocin-induced diabetes on the gene expression and the activities of two antioxidant enzymes, manganese superoxide dismutase (MnSOD) and glutathione peroxidase (GPx).	Streptozocin	51-65	superoxide dismutase 2	Homo sapiens	185-190
19229592-7	2009	LA, which is a water- and lipid-soluble antioxidant, decreased the protein expression of MnSOD, though mRNA levels and activities remained unchanged.	Water	15-20	superoxide dismutase 2	Homo sapiens	89-94
19229592-9	2009	Supplementing the animals with vitamin C, a powerful water-soluble antioxidant, increased the mRNA expression of MnSOD, though the protein expression and the activity did not change statistically.	Ascorbic Acid	31-40	superoxide dismutase 2	Homo sapiens	113-118
19558795-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide radical to hydrogen peroxide within the mitochondrial matrix and is one of the most important antioxidant enzymes.	Hydrogen Peroxide	70-87	superoxide dismutase 2	Homo sapiens	0-30
19558795-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide radical to hydrogen peroxide within the mitochondrial matrix and is one of the most important antioxidant enzymes.	Hydrogen Peroxide	70-87	superoxide dismutase 2	Homo sapiens	32-37
19558795-3	2009	In this study, we showed that 20 microM sodium selenite could alter subcellular distribution of MnSOD, namely a decrease in mitochondria and an increase in cytosol.	Sodium Selenite	40-55	superoxide dismutase 2	Homo sapiens	96-101
19558795-4	2009	The alteration of subcellular distribution of MnSOD is dependent on the production of superoxide induced by sodium selenite.	Superoxides	86-96	superoxide dismutase 2	Homo sapiens	46-51
19558795-4	2009	The alteration of subcellular distribution of MnSOD is dependent on the production of superoxide induced by sodium selenite.	Sodium Selenite	108-123	superoxide dismutase 2	Homo sapiens	46-51
19407826-8	2009	Mitochondrial electron transport chain (mETC) inhibitors in combination with the SOD inhibitor 2-methoxyestradiol (2-ME) increased O(2)(*-) levels, lowered H(2)O(2) levels, and increased autophagy.	2-Methoxyestradiol	95-113	superoxide dismutase 2	Homo sapiens	81-84
19376215-1	2009	Manganese superoxide dismutase 2 (SOD2) is a key metabolic anti-oxidant enzyme for detoxifying free radicals inside mitochondria.	free	95-99	superoxide dismutase 2	Homo sapiens	34-38
19558795-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide radical to hydrogen peroxide within the mitochondrial matrix and is one of the most important antioxidant enzymes.	Superoxides	48-66	superoxide dismutase 2	Homo sapiens	0-30
19558795-2	2009	Manganese superoxide dismutase (MnSOD) converts superoxide radical to hydrogen peroxide within the mitochondrial matrix and is one of the most important antioxidant enzymes.	Superoxides	48-66	superoxide dismutase 2	Homo sapiens	32-37
19509150-2	2009	A functional single-nucleotide polymorphism in codon 16 of SOD2 (rs4880), which encodes manganese superoxide dismutase, results in a substitution of valine by alanine (Val16Ala).	Valine	149-155	superoxide dismutase 2	Homo sapiens	59-63
19303434-6	2009	DOX induced a rapid increase in reactive oxygen species (ROS) production in cardiac cell mitochondria, which was inhibited by pretreatment with RV, most likely owing to an increase in MnSOD activity.	Doxorubicin	0-3	superoxide dismutase 2	Homo sapiens	184-189
19303434-6	2009	DOX induced a rapid increase in reactive oxygen species (ROS) production in cardiac cell mitochondria, which was inhibited by pretreatment with RV, most likely owing to an increase in MnSOD activity.	Reactive Oxygen Species	57-60	superoxide dismutase 2	Homo sapiens	184-189
19509150-2	2009	A functional single-nucleotide polymorphism in codon 16 of SOD2 (rs4880), which encodes manganese superoxide dismutase, results in a substitution of valine by alanine (Val16Ala).	Alanine	159-166	superoxide dismutase 2	Homo sapiens	59-63
19428325-6	2009	The activity of MnSOD was decreased by MG treatment.	Pyruvaldehyde	39-41	superoxide dismutase 2	Homo sapiens	16-21
19344704-4	2009	Whereas the expression of glutathione peroxidase (GPx), catalase, Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and heme oxygenase-1 (HO-1) increased with curcumin concentration and also with increase in time of incubation, the expression of Mn- superoxide dismutase (Mn-SOD) showed concentration dependant repression upon treatment with curcumin.	Curcumin	148-156	superoxide dismutase 2	Homo sapiens	235-259
19344704-4	2009	Whereas the expression of glutathione peroxidase (GPx), catalase, Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and heme oxygenase-1 (HO-1) increased with curcumin concentration and also with increase in time of incubation, the expression of Mn- superoxide dismutase (Mn-SOD) showed concentration dependant repression upon treatment with curcumin.	Curcumin	148-156	superoxide dismutase 2	Homo sapiens	261-267
19725468-9	2009	Increased FOXO3a, SOD-1 and SOD-2 expression and transient phosphorylation of ERK were detected after exposure of human hepatoma BEL-7402 cells to 0.5 nmol/L lidamycin.	C 1027	158-167	superoxide dismutase 2	Homo sapiens	28-33
19725468-15	2009	CONCLUSIONS: Cellular prosurvival molecules, such as SIRT1, Akt, SOD-1, SOD-2 and other unknown factors can influence the action of lidamycin on human tumor cells.	C 1027	132-141	superoxide dismutase 2	Homo sapiens	72-77
19424927-6	2009	Also they, as well as glutathione itself, slightly increased MnSOD activity in human brain mitochondria and inhibited oxidative burst caused by neutrophil NAD(P)H oxidase.	Glutathione	22-33	superoxide dismutase 2	Homo sapiens	61-66
19401447-1	2009	Overexpression of manganese superoxide dismutase (MnSOD), when combined with certain chemicals that inhibit peroxide removal, increases cancer cell cytotoxicity.	Peroxides	30-38	superoxide dismutase 2	Homo sapiens	50-55
19401447-2	2009	Elevating MnSOD levels in cells enhances the conversion of superoxide (O(2)(*-)) to hydrogen peroxide (H(2)O(2)), combined with inhibiting the removal of H(2)O(2), further increases H(2)O(2) levels, leading to increased cytotoxicity.	Superoxides	59-69	superoxide dismutase 2	Homo sapiens	10-15
19401447-2	2009	Elevating MnSOD levels in cells enhances the conversion of superoxide (O(2)(*-)) to hydrogen peroxide (H(2)O(2)), combined with inhibiting the removal of H(2)O(2), further increases H(2)O(2) levels, leading to increased cytotoxicity.	Superoxides	71-75	superoxide dismutase 2	Homo sapiens	10-15
19401447-2	2009	Elevating MnSOD levels in cells enhances the conversion of superoxide (O(2)(*-)) to hydrogen peroxide (H(2)O(2)), combined with inhibiting the removal of H(2)O(2), further increases H(2)O(2) levels, leading to increased cytotoxicity.	Hydrogen Peroxide	84-101	superoxide dismutase 2	Homo sapiens	10-15
19401447-2	2009	Elevating MnSOD levels in cells enhances the conversion of superoxide (O(2)(*-)) to hydrogen peroxide (H(2)O(2)), combined with inhibiting the removal of H(2)O(2), further increases H(2)O(2) levels, leading to increased cytotoxicity.	Hydrogen Peroxide	103-111	superoxide dismutase 2	Homo sapiens	10-15
19401447-2	2009	Elevating MnSOD levels in cells enhances the conversion of superoxide (O(2)(*-)) to hydrogen peroxide (H(2)O(2)), combined with inhibiting the removal of H(2)O(2), further increases H(2)O(2) levels, leading to increased cytotoxicity.	Hydrogen Peroxide	154-162	superoxide dismutase 2	Homo sapiens	10-15
19401447-2	2009	Elevating MnSOD levels in cells enhances the conversion of superoxide (O(2)(*-)) to hydrogen peroxide (H(2)O(2)), combined with inhibiting the removal of H(2)O(2), further increases H(2)O(2) levels, leading to increased cytotoxicity.	Hydrogen Peroxide	154-162	superoxide dismutase 2	Homo sapiens	10-15
19401447-3	2009	We hypothesized that increasing endogenous O(2)(*-) production in cells that were pretreated with adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) would lead to an increased level of intracellular H(2)O(2) accumulation and increased cell killing.	Superoxides	43-47	superoxide dismutase 2	Homo sapiens	109-114
19401447-3	2009	We hypothesized that increasing endogenous O(2)(*-) production in cells that were pretreated with adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) would lead to an increased level of intracellular H(2)O(2) accumulation and increased cell killing.	Carmustine	168-172	superoxide dismutase 2	Homo sapiens	109-114
19401447-3	2009	We hypothesized that increasing endogenous O(2)(*-) production in cells that were pretreated with adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) would lead to an increased level of intracellular H(2)O(2) accumulation and increased cell killing.	Hydrogen Peroxide	224-232	superoxide dismutase 2	Homo sapiens	109-114
19348625-4	2009	Further investigation revealed that SOD2 expression was suppressed by BetA-induced cAMP-response element-binding protein dephosphorylation at Ser133, which subsequently prevented SOD2 transcription through the cAMP-response element-binding protein-binding motif on the SOD2 promoter.	Cyclic AMP	83-87	superoxide dismutase 2	Homo sapiens	36-40
19348625-4	2009	Further investigation revealed that SOD2 expression was suppressed by BetA-induced cAMP-response element-binding protein dephosphorylation at Ser133, which subsequently prevented SOD2 transcription through the cAMP-response element-binding protein-binding motif on the SOD2 promoter.	Cyclic AMP	83-87	superoxide dismutase 2	Homo sapiens	179-183
19348625-4	2009	Further investigation revealed that SOD2 expression was suppressed by BetA-induced cAMP-response element-binding protein dephosphorylation at Ser133, which subsequently prevented SOD2 transcription through the cAMP-response element-binding protein-binding motif on the SOD2 promoter.	Cyclic AMP	83-87	superoxide dismutase 2	Homo sapiens	179-183
19348625-4	2009	Further investigation revealed that SOD2 expression was suppressed by BetA-induced cAMP-response element-binding protein dephosphorylation at Ser133, which subsequently prevented SOD2 transcription through the cAMP-response element-binding protein-binding motif on the SOD2 promoter.	Cyclic AMP	210-214	superoxide dismutase 2	Homo sapiens	36-40
19348625-4	2009	Further investigation revealed that SOD2 expression was suppressed by BetA-induced cAMP-response element-binding protein dephosphorylation at Ser133, which subsequently prevented SOD2 transcription through the cAMP-response element-binding protein-binding motif on the SOD2 promoter.	Cyclic AMP	210-214	superoxide dismutase 2	Homo sapiens	179-183
19348625-4	2009	Further investigation revealed that SOD2 expression was suppressed by BetA-induced cAMP-response element-binding protein dephosphorylation at Ser133, which subsequently prevented SOD2 transcription through the cAMP-response element-binding protein-binding motif on the SOD2 promoter.	Cyclic AMP	210-214	superoxide dismutase 2	Homo sapiens	179-183
19265433-0	2009	Contribution of human manganese superoxide dismutase tyrosine 34 to structure and catalysis.	Tyrosine	53-61	superoxide dismutase 2	Homo sapiens	22-52
18992840-0	2009	The p53-p66shc-Manganese Superoxide Dismutase (MnSOD) network: a mitochondrial intrigue to generate reactive oxygen species.	Reactive Oxygen Species	100-123	superoxide dismutase 2	Homo sapiens	15-45
18992840-0	2009	The p53-p66shc-Manganese Superoxide Dismutase (MnSOD) network: a mitochondrial intrigue to generate reactive oxygen species.	Reactive Oxygen Species	100-123	superoxide dismutase 2	Homo sapiens	47-52
19265433-1	2009	Superoxide dismutase (SOD) enzymes are critical in controlling levels of reactive oxygen species (ROS) that are linked to aging, cancer, and neurodegenerative disease.	Reactive Oxygen Species	73-96	superoxide dismutase 2	Homo sapiens	22-25
19265433-1	2009	Superoxide dismutase (SOD) enzymes are critical in controlling levels of reactive oxygen species (ROS) that are linked to aging, cancer, and neurodegenerative disease.	Reactive Oxygen Species	98-101	superoxide dismutase 2	Homo sapiens	22-25
19265433-2	2009	Superoxide (O(2)(*-)) produced during respiration is removed by the product of the SOD2 gene, the homotetrameric manganese superoxide dismutase (MnSOD).	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	83-87
19265433-2	2009	Superoxide (O(2)(*-)) produced during respiration is removed by the product of the SOD2 gene, the homotetrameric manganese superoxide dismutase (MnSOD).	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	113-143
19265433-2	2009	Superoxide (O(2)(*-)) produced during respiration is removed by the product of the SOD2 gene, the homotetrameric manganese superoxide dismutase (MnSOD).	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	145-150
19265433-2	2009	Superoxide (O(2)(*-)) produced during respiration is removed by the product of the SOD2 gene, the homotetrameric manganese superoxide dismutase (MnSOD).	Superoxides	12-16	superoxide dismutase 2	Homo sapiens	83-87
19265433-2	2009	Superoxide (O(2)(*-)) produced during respiration is removed by the product of the SOD2 gene, the homotetrameric manganese superoxide dismutase (MnSOD).	Superoxides	12-16	superoxide dismutase 2	Homo sapiens	113-143
19265433-2	2009	Superoxide (O(2)(*-)) produced during respiration is removed by the product of the SOD2 gene, the homotetrameric manganese superoxide dismutase (MnSOD).	Superoxides	12-16	superoxide dismutase 2	Homo sapiens	145-150
19306099-2	2009	We have studied fibroblasts stably overexpressing manganese superoxide dismutase (MnSOD) with a defined capacity for the removal of superoxide anions and concomitant accumulation of hydrogen peroxide to evaluate the role of enhanced MnSOD activity on the dynamics of cell-matrix interactions in the three-dimensional collagen lattice contraction assay.	Superoxides	132-149	superoxide dismutase 2	Homo sapiens	50-80
19351855-5	2009	These genes were functional antioxidant genes in pancreatic cancer cells because ectopic expression of SOD2 and ferroxidase in Mirk-depleted cells lowered ROS levels.	Reactive Oxygen Species	155-158	superoxide dismutase 2	Homo sapiens	103-107
19439213-8	2009	Transfection with siRNA of Mn-SOD abolished both up-regulation of Mn-SOD expression and protection from H(2)O(2) toxicity by IFN-gamma pretreatment.	Hydrogen Peroxide	104-112	superoxide dismutase 2	Homo sapiens	27-33
19306099-4	2009	The enhanced collagen lattice contraction was in part due to an increase in active TGF-beta1 and the accumulation of H2O2 in MnSOD overexpressing fibroblasts populated collagen lattices.	Hydrogen Peroxide	117-121	superoxide dismutase 2	Homo sapiens	125-130
19168439-5	2009	p66Shc links alpha(1)-ARs to an AKT signaling pathway that selectively phosphorylates/inactivates FOXO transcription factors and downregulates the ROS-scavenging protein manganese superoxide dismutase (MnSOD); the alpha(1)-AR-p66Shc-dependent pathway involving AKT does not regulate GSK3.	Reactive Oxygen Species	147-150	superoxide dismutase 2	Homo sapiens	170-200
19306099-5	2009	Inhibition of TGF-beta1 signalling by the ALK4,5,7 kinases" inhibitor SB431542 at least partly inhibited the enhanced collagen lattice contraction of MnSOD overexpressing fibroblasts populated lattices.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	70-78	superoxide dismutase 2	Homo sapiens	150-155
19306099-7	2009	In the presence of the antioxidant Ebselen, a mimic of H2O2 and other hydroperoxides/peroxynitrite-detoxifying glutathione peroxidase, collagen lattice contraction and the activation of TGF-beta1 were significantly reduced in collagen lattices populated with MnSOD overexpressing fibroblasts.	ebselen	35-42	superoxide dismutase 2	Homo sapiens	259-264
19306099-7	2009	In the presence of the antioxidant Ebselen, a mimic of H2O2 and other hydroperoxides/peroxynitrite-detoxifying glutathione peroxidase, collagen lattice contraction and the activation of TGF-beta1 were significantly reduced in collagen lattices populated with MnSOD overexpressing fibroblasts.	Peroxynitrous Acid	85-98	superoxide dismutase 2	Homo sapiens	259-264
19161988-9	2009	Finally, our data point superoxide dismutase (SOD)2 as a potential antioxidant factor involved in NFkappaB protective effects against ROH-induced oxidative stress.	roh	134-137	superoxide dismutase 2	Homo sapiens	46-51
19212855-2	2009	This study evaluated the concentration and time-dependent effects of H2O2-induced oxidative stress on MnSOD, Se:GPx and catalase and on aconitase.	Hydrogen Peroxide	69-73	superoxide dismutase 2	Homo sapiens	102-107
19136606-5	2009	In the cells cultured under a low-glucose condition when no increased HBP flux occurred, azaserine enhanced the manganese-superoxide dismutase (MnSOD) protein level and also inhibited the oxidative stress and the expression of VCAM-1 and ICAM-1 in response to TNF-alpha.	Azaserine	89-98	superoxide dismutase 2	Homo sapiens	112-142
19136606-5	2009	In the cells cultured under a low-glucose condition when no increased HBP flux occurred, azaserine enhanced the manganese-superoxide dismutase (MnSOD) protein level and also inhibited the oxidative stress and the expression of VCAM-1 and ICAM-1 in response to TNF-alpha.	Azaserine	89-98	superoxide dismutase 2	Homo sapiens	144-149
19084501-2	2009	We previously demonstrated that hyperglycemia-induced production of reactive oxygen species from mitochondria (mtROS) contributed to the development of diabetic complications, and metformin normalized mt ROS production by induction of MnSOD and promotion of mitochondrial biogenesis by activating the PGC-1alpha pathway.	Metformin	180-189	superoxide dismutase 2	Homo sapiens	235-240
18996949-6	2009	Manganese superoxide dismutase (MnSOD), a mitochondrial antioxidant enzyme, is an integral part of the nucleoids and may protect mitochondrial DNA from ROS.	nucleoids	103-112	superoxide dismutase 2	Homo sapiens	0-30
18996949-6	2009	Manganese superoxide dismutase (MnSOD), a mitochondrial antioxidant enzyme, is an integral part of the nucleoids and may protect mitochondrial DNA from ROS.	nucleoids	103-112	superoxide dismutase 2	Homo sapiens	32-37
18996949-6	2009	Manganese superoxide dismutase (MnSOD), a mitochondrial antioxidant enzyme, is an integral part of the nucleoids and may protect mitochondrial DNA from ROS.	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	0-30
18996949-6	2009	Manganese superoxide dismutase (MnSOD), a mitochondrial antioxidant enzyme, is an integral part of the nucleoids and may protect mitochondrial DNA from ROS.	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	32-37
18996949-7	2009	A model linking .NO, mitochondria, MnSOD and its acetylation/deacetylation by sirtuins (NAD+-dependent class III histone deacetylases) may be the basis for a potentially new powerful therapeutic intervention in the ageing process.	NAD	88-92	superoxide dismutase 2	Homo sapiens	35-40
19100713-2	2009	To investigate the events occurring soon after depletion of SOD2, we generated SOD2 gene knockout chicken DT40 cells complemented with a human SOD2 (hSOD2) cDNA, whose expression can be switched off by doxycycline (Dox).	Doxycycline	202-213	superoxide dismutase 2	Homo sapiens	79-83
19100713-2	2009	To investigate the events occurring soon after depletion of SOD2, we generated SOD2 gene knockout chicken DT40 cells complemented with a human SOD2 (hSOD2) cDNA, whose expression can be switched off by doxycycline (Dox).	Doxycycline	202-213	superoxide dismutase 2	Homo sapiens	149-154
19100713-2	2009	To investigate the events occurring soon after depletion of SOD2, we generated SOD2 gene knockout chicken DT40 cells complemented with a human SOD2 (hSOD2) cDNA, whose expression can be switched off by doxycycline (Dox).	Doxycycline	215-218	superoxide dismutase 2	Homo sapiens	149-154
19167605-1	2009	Manganese superoxide dismutase (MnSOD) is one of the major enzymes responsible for the defense against oxidative damage due to reactive oxygen species (ROS) in the mitochondria.	Reactive Oxygen Species	127-150	superoxide dismutase 2	Homo sapiens	0-30
19167605-1	2009	Manganese superoxide dismutase (MnSOD) is one of the major enzymes responsible for the defense against oxidative damage due to reactive oxygen species (ROS) in the mitochondria.	Reactive Oxygen Species	127-150	superoxide dismutase 2	Homo sapiens	32-37
19167605-1	2009	Manganese superoxide dismutase (MnSOD) is one of the major enzymes responsible for the defense against oxidative damage due to reactive oxygen species (ROS) in the mitochondria.	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	0-30
19167605-1	2009	Manganese superoxide dismutase (MnSOD) is one of the major enzymes responsible for the defense against oxidative damage due to reactive oxygen species (ROS) in the mitochondria.	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	32-37
19091570-7	2009	There was stable down-regulation of MDM2 and UGB as well as overexpression of SOD2, CSTB, and G3BP when RA-treated SHG-44 was compared with normal SHG-44.	Tretinoin	104-106	superoxide dismutase 2	Homo sapiens	78-82
18553161-0	2009	MnSOD gene polymorphism association with steroid-dependent cancer.	Steroids	41-48	superoxide dismutase 2	Homo sapiens	0-5
18553161-5	2009	Human genetic polymorphism Val16Ala of MnSOD was obtained from blood and paraffin-embedded tumor samples.	Paraffin	73-81	superoxide dismutase 2	Homo sapiens	39-44
18553161-10	2009	Even though the frequency of the Ala allele was low (9.6%) in the studied population, these data support the hypothesis that MnSOD and oxidative stress play a significant role in breast cancer risk both in males and females and also brings new information on the role of this polymorphism in prostate cancer.	Alanine	33-36	superoxide dismutase 2	Homo sapiens	125-130
19302750-11	2009	The cell lines containing lower expression level of MnSOD was found to have generally higher frequent DeltamtDNA(4977) and more ROS.	Reactive Oxygen Species	128-131	superoxide dismutase 2	Homo sapiens	52-57
19103181-8	2009	In this study, the association of 10 mg/kg memantine with 10 mg/kg galantamine increased the number of living pyramidal neurons, reduced TUNEL, active caspase-3 and SOD-2 immunoreactivity, and preserved spatial memory after ischemia-reperfusion injury; however, the effects of the combination were not statistically different from those observed in animals treated with galantamine alone.	Memantine	43-52	superoxide dismutase 2	Homo sapiens	165-170
19103181-8	2009	In this study, the association of 10 mg/kg memantine with 10 mg/kg galantamine increased the number of living pyramidal neurons, reduced TUNEL, active caspase-3 and SOD-2 immunoreactivity, and preserved spatial memory after ischemia-reperfusion injury; however, the effects of the combination were not statistically different from those observed in animals treated with galantamine alone.	Galantamine	67-78	superoxide dismutase 2	Homo sapiens	165-170
19084501-5	2009	Both TZDs increased the expression of NRF-1, TFAM and MnSOD mRNA.	Thiazolidinediones	5-9	superoxide dismutase 2	Homo sapiens	54-59
19013212-10	2009	To elucidate the mechanism of action, we identified a CXCL12 transfectant-specific increase in the pro-survival factor Mn-SOD, which is considered important for the inactivation of reactive oxygen species, thereby prolonging cell survival.	Reactive Oxygen Species	181-204	superoxide dismutase 2	Homo sapiens	119-125
19066606-6	2009	Double immunofluorescence using 8-oxo-dG and manganese superoxide dismutase (MnSOD) antibodies localised cytoplasmic 8-oxo-dG.	8-ohdg	117-125	superoxide dismutase 2	Homo sapiens	45-75
19066606-6	2009	Double immunofluorescence using 8-oxo-dG and manganese superoxide dismutase (MnSOD) antibodies localised cytoplasmic 8-oxo-dG.	8-ohdg	117-125	superoxide dismutase 2	Homo sapiens	77-82
19084501-7	2009	These results suggest that TZDs normalize hyperglycemia-induced mtROS production by induction of MnSOD and promotion of mitochondrial biogenesis by activating PGC-1alpha.	Thiazolidinediones	27-31	superoxide dismutase 2	Homo sapiens	97-102
19368118-2	2009	These carcinogens also produce reactive oxygen species that are metabolized by manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	31-54	superoxide dismutase 2	Homo sapiens	79-109
18930813-3	2009	A search of publicly available microarray data reveals that expression of mitochondrial manganese superoxide dismutase (Sod2), responsible for the conversion of superoxide (O(2)(-)) to hydrogen peroxide (H(2)O(2)), is consistently increased in high-grade and advanced-stage bladder tumors.	Superoxides	98-108	superoxide dismutase 2	Homo sapiens	120-124
18930813-3	2009	A search of publicly available microarray data reveals that expression of mitochondrial manganese superoxide dismutase (Sod2), responsible for the conversion of superoxide (O(2)(-)) to hydrogen peroxide (H(2)O(2)), is consistently increased in high-grade and advanced-stage bladder tumors.	Superoxides	173-177	superoxide dismutase 2	Homo sapiens	120-124
18930813-3	2009	A search of publicly available microarray data reveals that expression of mitochondrial manganese superoxide dismutase (Sod2), responsible for the conversion of superoxide (O(2)(-)) to hydrogen peroxide (H(2)O(2)), is consistently increased in high-grade and advanced-stage bladder tumors.	Hydrogen Peroxide	185-202	superoxide dismutase 2	Homo sapiens	120-124
18930813-3	2009	A search of publicly available microarray data reveals that expression of mitochondrial manganese superoxide dismutase (Sod2), responsible for the conversion of superoxide (O(2)(-)) to hydrogen peroxide (H(2)O(2)), is consistently increased in high-grade and advanced-stage bladder tumors.	h(2)	204-208	superoxide dismutase 2	Homo sapiens	120-124
18930813-7	2009	The increase in Sod2 expression was accompanied by a significant decrease in catalase activity, resulting in a net increase in H(2)O(2) production in the 253J B-V cell line.	Hydrogen Peroxide	127-135	superoxide dismutase 2	Homo sapiens	16-20
18379781-7	2009	CONCLUSIONS: This study demonstrates that selenite induces cell death and apoptosis by production of superoxide in mitochondria and activation of the mitochondrial apoptotic pathway and MnSOD plays an important role in protection against prooxidant effects of superoxide from selenite.	Selenious Acid	42-50	superoxide dismutase 2	Homo sapiens	186-191
18379781-7	2009	CONCLUSIONS: This study demonstrates that selenite induces cell death and apoptosis by production of superoxide in mitochondria and activation of the mitochondrial apoptotic pathway and MnSOD plays an important role in protection against prooxidant effects of superoxide from selenite.	Superoxides	260-270	superoxide dismutase 2	Homo sapiens	186-191
18379781-7	2009	CONCLUSIONS: This study demonstrates that selenite induces cell death and apoptosis by production of superoxide in mitochondria and activation of the mitochondrial apoptotic pathway and MnSOD plays an important role in protection against prooxidant effects of superoxide from selenite.	Selenious Acid	276-284	superoxide dismutase 2	Homo sapiens	186-191
19368118-2	2009	These carcinogens also produce reactive oxygen species that are metabolized by manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	31-54	superoxide dismutase 2	Homo sapiens	111-116
18977034-2	2008	The combined genotypes of T/T in NQO1 Pro187Ser and Val/Val in MnSOD Ala-9Val polymorphisms were found to be independently associated with a significantly higher risk of TD.	Valine	52-55	superoxide dismutase 2	Homo sapiens	63-68
18987137-8	2009	The induction of MnSOD expression was dependent on vFLIP/K13-mediated activation of NF-kappaB, occurred in a cell-intrinsic manner, and was correlated with decreased intracellular superoxide accumulation and increased resistance of endothelial cells to superoxide-induced death.	Superoxides	180-190	superoxide dismutase 2	Homo sapiens	17-22
18987137-8	2009	The induction of MnSOD expression was dependent on vFLIP/K13-mediated activation of NF-kappaB, occurred in a cell-intrinsic manner, and was correlated with decreased intracellular superoxide accumulation and increased resistance of endothelial cells to superoxide-induced death.	Superoxides	253-263	superoxide dismutase 2	Homo sapiens	17-22
19838948-5	2009	Moreover, quercetin combined with 2-methoxyestradiol increased superoxide levels, mitochondrial superoxide dismutase (MnSOD) in mRNA, protein levels, and SOD activity.	Quercetin	10-19	superoxide dismutase 2	Homo sapiens	118-123
19838948-5	2009	Moreover, quercetin combined with 2-methoxyestradiol increased superoxide levels, mitochondrial superoxide dismutase (MnSOD) in mRNA, protein levels, and SOD activity.	Quercetin	10-19	superoxide dismutase 2	Homo sapiens	120-123
19838948-5	2009	Moreover, quercetin combined with 2-methoxyestradiol increased superoxide levels, mitochondrial superoxide dismutase (MnSOD) in mRNA, protein levels, and SOD activity.	2-Methoxyestradiol	34-52	superoxide dismutase 2	Homo sapiens	118-123
19838948-5	2009	Moreover, quercetin combined with 2-methoxyestradiol increased superoxide levels, mitochondrial superoxide dismutase (MnSOD) in mRNA, protein levels, and SOD activity.	2-Methoxyestradiol	34-52	superoxide dismutase 2	Homo sapiens	120-123
18852031-5	2008	Our present data demonstrate that METH enhances lipid peroxidation and mitochondrial manganese superoxide dismutase (MnSOD) enzyme levels, and decreases the antioxidant-reduced glutathione (GSH) together with an inhibition of mitochondrial complex-I activity.	Methamphetamine	34-38	superoxide dismutase 2	Homo sapiens	85-115
18852031-5	2008	Our present data demonstrate that METH enhances lipid peroxidation and mitochondrial manganese superoxide dismutase (MnSOD) enzyme levels, and decreases the antioxidant-reduced glutathione (GSH) together with an inhibition of mitochondrial complex-I activity.	Methamphetamine	34-38	superoxide dismutase 2	Homo sapiens	117-122
19636420-1	2009	Manganese and extracellular superoxide dismutases (SOD2 and SOD3) are part of the enzymatic defence against reactive oxygen species, which are involved in the pathogenesis of asbestosis.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	51-55
19636420-1	2009	Manganese and extracellular superoxide dismutases (SOD2 and SOD3) are part of the enzymatic defence against reactive oxygen species, which are involved in the pathogenesis of asbestosis.	Reactive Oxygen Species	108-131	superoxide dismutase 2	Homo sapiens	51-55
19636420-7	2009	Asbestosis was associated with the homozygous SOD2 - 9Ala/Ala genotype (OR = 1.50, 95% CI 1.01-2.24), whereas the association for the SOD3 Arg/Gly genotype was not significant (OR = 1.63, 95% CI 0.62-4.27).	Alanine	54-57	superoxide dismutase 2	Homo sapiens	46-50
19636420-8	2009	The finding that the SOD2 - 9Ala/Ala genotype increases the risk for asbestosis indicates that, in addition to asbestos exposure, genetic factors may also have a significant influence on the development of asbestosis.	Asbestos	69-77	superoxide dismutase 2	Homo sapiens	21-25
19074884-3	2008	Selenium status also modifies the effect of the mitochondrial superoxide dismutase (SOD2) SNP Ala16Val on prostate cancer risk.	Selenium	0-8	superoxide dismutase 2	Homo sapiens	84-88
19074884-13	2008	In a low-selenium population, SOD2-Ala16+ men homozygous for SEPP1-Ala234 are at an increased risk of prostate cancer/aggressive prostate cancer especially if ever-smokers, because they are likely to produce more mitochondrial H(2)O(2) that they cannot remove, thereby promoting prostate tumor cell proliferation and migration.	Selenium	9-17	superoxide dismutase 2	Homo sapiens	30-34
19074884-13	2008	In a low-selenium population, SOD2-Ala16+ men homozygous for SEPP1-Ala234 are at an increased risk of prostate cancer/aggressive prostate cancer especially if ever-smokers, because they are likely to produce more mitochondrial H(2)O(2) that they cannot remove, thereby promoting prostate tumor cell proliferation and migration.	Water	227-232	superoxide dismutase 2	Homo sapiens	30-34
18790709-0	2008	Manganese superoxide dismutase gene Ala-9Val polymorphism might be related to the severity of abnormal involuntary movements in Korean schizophrenic patients.	ala-9val	36-44	superoxide dismutase 2	Homo sapiens	0-30
18790709-1	2008	OBJECTIVE: This study examined whether the manganese superoxide dismutase (MnSOD) gene Ala-9Val single-nucleotide polymorphism (SNP) is associated with neuroleptic-induced tardive dyskinesia (TD) and the severity of the abnormal involuntary movements in Korean schizophrenic patients.	ala-9val	87-95	superoxide dismutase 2	Homo sapiens	43-73
18790709-1	2008	OBJECTIVE: This study examined whether the manganese superoxide dismutase (MnSOD) gene Ala-9Val single-nucleotide polymorphism (SNP) is associated with neuroleptic-induced tardive dyskinesia (TD) and the severity of the abnormal involuntary movements in Korean schizophrenic patients.	ala-9val	87-95	superoxide dismutase 2	Homo sapiens	75-80
18977034-2	2008	The combined genotypes of T/T in NQO1 Pro187Ser and Val/Val in MnSOD Ala-9Val polymorphisms were found to be independently associated with a significantly higher risk of TD.	Valine	56-59	superoxide dismutase 2	Homo sapiens	63-68
18977034-2	2008	The combined genotypes of T/T in NQO1 Pro187Ser and Val/Val in MnSOD Ala-9Val polymorphisms were found to be independently associated with a significantly higher risk of TD.	ala-9val	69-77	superoxide dismutase 2	Homo sapiens	63-68
19016244-6	2008	Analyses of associations between SOD genotypes and levels of plasma SOD activity demonstrated that SOD2 Ala16Val, a dimorphism leading to substitution in the mitochondrial targeting sequence of SOD2, significantly influences plasma SOD2 activity, and that SOD3 Arg231Gly, leading to substitution in the heparin-binding domain of SOD3, significantly influences plasma total SOD activity.	Heparin	303-310	superoxide dismutase 2	Homo sapiens	99-103
18784358-2	2008	The MnSOD allele with Val as amino acid 16 encodes a protein that has 30-40% lower activity compared with the MnSOD Ala variant, hence possibly increasing susceptibility to oxidative stress.	Valine	22-25	superoxide dismutase 2	Homo sapiens	4-9
18784358-2	2008	The MnSOD allele with Val as amino acid 16 encodes a protein that has 30-40% lower activity compared with the MnSOD Ala variant, hence possibly increasing susceptibility to oxidative stress.	Valine	22-25	superoxide dismutase 2	Homo sapiens	110-115
18784358-2	2008	The MnSOD allele with Val as amino acid 16 encodes a protein that has 30-40% lower activity compared with the MnSOD Ala variant, hence possibly increasing susceptibility to oxidative stress.	Alanine	116-119	superoxide dismutase 2	Homo sapiens	4-9
18784358-2	2008	The MnSOD allele with Val as amino acid 16 encodes a protein that has 30-40% lower activity compared with the MnSOD Ala variant, hence possibly increasing susceptibility to oxidative stress.	Alanine	116-119	superoxide dismutase 2	Homo sapiens	110-115
18784358-10	2008	However, men with the MnSOD Ala/Ala genotype who had low long-term lycopene status had a higher risk of aggressive prostate cancer compared with individuals with the other genotypes.	Alanine	28-31	superoxide dismutase 2	Homo sapiens	22-27
18784358-10	2008	However, men with the MnSOD Ala/Ala genotype who had low long-term lycopene status had a higher risk of aggressive prostate cancer compared with individuals with the other genotypes.	Alanine	32-35	superoxide dismutase 2	Homo sapiens	22-27
18784358-10	2008	However, men with the MnSOD Ala/Ala genotype who had low long-term lycopene status had a higher risk of aggressive prostate cancer compared with individuals with the other genotypes.	Lycopene	67-75	superoxide dismutase 2	Homo sapiens	22-27
18784358-11	2008	These results are consistent with findings from earlier studies that reported when antioxidant status is low, the MnSOD Ala/Ala genotype may be associated with an increased risk of aggressive prostate cancer.	Alanine	120-123	superoxide dismutase 2	Homo sapiens	114-119
18784358-11	2008	These results are consistent with findings from earlier studies that reported when antioxidant status is low, the MnSOD Ala/Ala genotype may be associated with an increased risk of aggressive prostate cancer.	Alanine	124-127	superoxide dismutase 2	Homo sapiens	114-119
19064542-2	2008	Mitochondrial superoxide dismutase [SOD; manganese SOD (MnSOD) or SOD2] neutralizes highly reactive superoxide radical (O(*-)(2)), the first member in the plethora of mitochondrial reactive oxygen species.	Superoxides	100-118	superoxide dismutase 2	Homo sapiens	41-54
19064542-2	2008	Mitochondrial superoxide dismutase [SOD; manganese SOD (MnSOD) or SOD2] neutralizes highly reactive superoxide radical (O(*-)(2)), the first member in the plethora of mitochondrial reactive oxygen species.	Superoxides	100-118	superoxide dismutase 2	Homo sapiens	56-61
19016244-6	2008	Analyses of associations between SOD genotypes and levels of plasma SOD activity demonstrated that SOD2 Ala16Val, a dimorphism leading to substitution in the mitochondrial targeting sequence of SOD2, significantly influences plasma SOD2 activity, and that SOD3 Arg231Gly, leading to substitution in the heparin-binding domain of SOD3, significantly influences plasma total SOD activity.	Heparin	303-310	superoxide dismutase 2	Homo sapiens	194-198
19016244-6	2008	Analyses of associations between SOD genotypes and levels of plasma SOD activity demonstrated that SOD2 Ala16Val, a dimorphism leading to substitution in the mitochondrial targeting sequence of SOD2, significantly influences plasma SOD2 activity, and that SOD3 Arg231Gly, leading to substitution in the heparin-binding domain of SOD3, significantly influences plasma total SOD activity.	Heparin	303-310	superoxide dismutase 2	Homo sapiens	194-198
18845242-7	2008	Lastly, we show that treatment with the histone deacetylase inhibitors trichostatin A and sodium butyrate can reactivate SOD2 expression in breast cancer cell lines.	trichostatin A	71-85	superoxide dismutase 2	Homo sapiens	121-125
18845242-7	2008	Lastly, we show that treatment with the histone deacetylase inhibitors trichostatin A and sodium butyrate can reactivate SOD2 expression in breast cancer cell lines.	Butyric Acid	90-105	superoxide dismutase 2	Homo sapiens	121-125
18840609-9	2008	These results therefore suggest that BTG2/TIS21/PC3 works as an enhancer of DOXO-induced cell death via accumulation of H2O2 by up-regulating manganese-superoxide dismutase without any other antioxidant enzymes.	Doxorubicin	76-80	superoxide dismutase 2	Homo sapiens	142-172
19064542-2	2008	Mitochondrial superoxide dismutase [SOD; manganese SOD (MnSOD) or SOD2] neutralizes highly reactive superoxide radical (O(*-)(2)), the first member in the plethora of mitochondrial reactive oxygen species.	Superoxides	100-118	superoxide dismutase 2	Homo sapiens	66-70
19064542-2	2008	Mitochondrial superoxide dismutase [SOD; manganese SOD (MnSOD) or SOD2] neutralizes highly reactive superoxide radical (O(*-)(2)), the first member in the plethora of mitochondrial reactive oxygen species.	Reactive Oxygen Species	181-204	superoxide dismutase 2	Homo sapiens	41-54
19064542-2	2008	Mitochondrial superoxide dismutase [SOD; manganese SOD (MnSOD) or SOD2] neutralizes highly reactive superoxide radical (O(*-)(2)), the first member in the plethora of mitochondrial reactive oxygen species.	Reactive Oxygen Species	181-204	superoxide dismutase 2	Homo sapiens	56-61
19064542-2	2008	Mitochondrial superoxide dismutase [SOD; manganese SOD (MnSOD) or SOD2] neutralizes highly reactive superoxide radical (O(*-)(2)), the first member in the plethora of mitochondrial reactive oxygen species.	Reactive Oxygen Species	181-204	superoxide dismutase 2	Homo sapiens	66-70
19064542-3	2008	A polymorphism in the target sequence of MnSOD enzyme, Val(16)Ala, is known to disrupt proper targeting of the enzyme from cytosol to mitochondrial matrix where it acts on O(*-)(2) to dismutate it to hydrogen peroxide (H(2)O(2)).	Hydrogen Peroxide	200-217	superoxide dismutase 2	Homo sapiens	41-46
18840609-9	2008	These results therefore suggest that BTG2/TIS21/PC3 works as an enhancer of DOXO-induced cell death via accumulation of H2O2 by up-regulating manganese-superoxide dismutase without any other antioxidant enzymes.	Hydrogen Peroxide	120-124	superoxide dismutase 2	Homo sapiens	142-172
18646267-3	2008	Manganese superoxide dismutase (MnSOD) is the only known superoxide scavenger in mitochondria.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
18760346-0	2008	The manganese superoxide dismutase Ala16Val dimorphism modulates iron accumulation in human hepatoma cells.	Iron	65-69	superoxide dismutase 2	Homo sapiens	4-34
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Alanine	38-45	superoxide dismutase 2	Homo sapiens	111-141
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Alanine	38-45	superoxide dismutase 2	Homo sapiens	143-148
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Alanine	38-45	superoxide dismutase 2	Homo sapiens	161-166
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Alanine	4-7	superoxide dismutase 2	Homo sapiens	111-141
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Alanine	4-7	superoxide dismutase 2	Homo sapiens	143-148
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Alanine	4-7	superoxide dismutase 2	Homo sapiens	161-166
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Valine	55-61	superoxide dismutase 2	Homo sapiens	111-141
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Valine	55-61	superoxide dismutase 2	Homo sapiens	143-148
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Valine	55-61	superoxide dismutase 2	Homo sapiens	161-166
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Valine	10-13	superoxide dismutase 2	Homo sapiens	111-141
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Valine	10-13	superoxide dismutase 2	Homo sapiens	143-148
18760346-1	2008	The Ala/16Val dimorphism incorporates alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), modifying MnSOD mitochondrial import and activity.	Valine	10-13	superoxide dismutase 2	Homo sapiens	161-166
18760346-2	2008	In alcoholic cirrhotic patients, the Ala-MnSOD allele is associated with hepatic iron accumulation and an increased risk of hepatocellular carcinoma.	Iron	81-85	superoxide dismutase 2	Homo sapiens	41-46
18760346-3	2008	The Ala-MnSOD variant could modulate the expression of proteins involved in iron storage (cytosolic ferritin), uptake (transferrin receptors, TfR-1 and-2), extrusion (hepcidin), and intracellular distribution (frataxin) to trigger hepatic iron accumulation.	Iron	76-80	superoxide dismutase 2	Homo sapiens	8-13
18760346-3	2008	The Ala-MnSOD variant could modulate the expression of proteins involved in iron storage (cytosolic ferritin), uptake (transferrin receptors, TfR-1 and-2), extrusion (hepcidin), and intracellular distribution (frataxin) to trigger hepatic iron accumulation.	Iron	239-243	superoxide dismutase 2	Homo sapiens	8-13
18760346-5	2008	In our cohort, this hepatic iron score increased with the number of Ala-MnSOD alleles.	Iron	28-32	superoxide dismutase 2	Homo sapiens	72-77
18760346-8	2008	Additionally, iron supplementation decreased transfected MnSOD proteins and activities.	Iron	14-18	superoxide dismutase 2	Homo sapiens	57-62
18760346-9	2008	Ala-MnSOD transfection increased the mRNAs and proteins of ferritin, hepcidin, and TfR2, decreased the expression of frataxin, and caused cellular iron accumulation.	Iron	147-151	superoxide dismutase 2	Homo sapiens	4-9
18646267-5	2008	A T-->C single nucleotide substitution, resulting in a Val-->Ala change at position 9 (Ala-9Val), which alters the secondary structure of the protein, has been noted to affect transport of MnSOD into the mitochondria.	Valine	58-61	superoxide dismutase 2	Homo sapiens	195-200
18646267-5	2008	A T-->C single nucleotide substitution, resulting in a Val-->Ala change at position 9 (Ala-9Val), which alters the secondary structure of the protein, has been noted to affect transport of MnSOD into the mitochondria.	Alanine	67-70	superoxide dismutase 2	Homo sapiens	195-200
18646267-5	2008	A T-->C single nucleotide substitution, resulting in a Val-->Ala change at position 9 (Ala-9Val), which alters the secondary structure of the protein, has been noted to affect transport of MnSOD into the mitochondria.	Alanine	93-96	superoxide dismutase 2	Homo sapiens	195-200
18760346-11	2008	In conclusion, the Ala-MnSOD variant favors hepatic iron accumulation by modulating the expression of proteins involved in iron homeostasis.	Iron	52-56	superoxide dismutase 2	Homo sapiens	23-28
18760346-11	2008	In conclusion, the Ala-MnSOD variant favors hepatic iron accumulation by modulating the expression of proteins involved in iron homeostasis.	Iron	123-127	superoxide dismutase 2	Homo sapiens	23-28
18991268-4	2008	The distinct effect of capsaicin-induced apoptosis on the expression pattern of HepG2 proteins includes the downregulation of some antioxidant enzymes including aldose reductase (AR), catalase, enolase 1, peroxiredoxin 1, but upregulation of peroxiredoxin 6, cytochrome c oxidase, and SOD2.	Capsaicin	23-32	superoxide dismutase 2	Homo sapiens	285-289
18692129-5	2008	Hyperoxia resulted in significant increases in ROS generation, AP-1 activation, and IL-8 production, which were significantly attenuated by overexpression of either MnSOD or CuZnSOD.	Reactive Oxygen Species	47-50	superoxide dismutase 2	Homo sapiens	165-170
18653258-1	2008	AIMS: Recent evidence indicates that oxidative stress may play an important role in the pathogenesis of insulin resistance and that gene polymorphism (Ala16Val) of manganese superoxide dismutase (MnSOD) may protect against reactive oxygen species (ROS) function.	Reactive Oxygen Species	223-246	superoxide dismutase 2	Homo sapiens	164-194
18829485-4	2008	Expression of manganese superoxide dismutase (SOD2), which regulates cellular ROS, is markedly down-regulated in CRPC when compared with hormone-responsive tumors.	ros	78-81	superoxide dismutase 2	Homo sapiens	46-50
18829485-6	2008	RESULTS: SOD2 knockdown results in an increase in ROS.	ros	50-53	superoxide dismutase 2	Homo sapiens	9-13
18829485-8	2008	The induction of many of these genes with SOD2 knockdown, such as VEGFA and FKBP5, is reversible with the antioxidant N-acetylcysteine, suggesting that this mechanism is directly linked to ROS.	Acetylcysteine	118-134	superoxide dismutase 2	Homo sapiens	42-46
18829485-8	2008	The induction of many of these genes with SOD2 knockdown, such as VEGFA and FKBP5, is reversible with the antioxidant N-acetylcysteine, suggesting that this mechanism is directly linked to ROS.	ros	189-192	superoxide dismutase 2	Homo sapiens	42-46
18829485-10	2008	SOD2 knockdown-induced AR activation was confirmed by electrophoretic mobility shift assay and luciferase activity, and both were readily reversible with N-acetylcysteine.	Acetylcysteine	154-170	superoxide dismutase 2	Homo sapiens	0-4
18829485-11	2008	CONCLUSIONS: These findings show that down-regulation of SOD2 induces AR activity in a ROS-dependent manner, and suggest that there may be a role for antioxidant therapy in CRPC.	ros	87-90	superoxide dismutase 2	Homo sapiens	57-61
18633101-12	2008	Palmitate also increased IL-6 and SOD2 gene expression, and this effect was prevented by inhibiting NFkappaB.	Palmitates	0-9	superoxide dismutase 2	Homo sapiens	34-38
18682580-5	2008	There was also indication of increased acoustic neuroma risk with the SOD2 rs4880 Ala variant (OR(CT/CC)=2.0; 95% CI, 1.0-4.2) and decreased acoustic neuroma risk with the CAT rs1001179 T allele variant (OR(CT/TT)=0.6; 95% CI, 0.3-1.0).	Alanine	82-85	superoxide dismutase 2	Homo sapiens	70-74
18653258-1	2008	AIMS: Recent evidence indicates that oxidative stress may play an important role in the pathogenesis of insulin resistance and that gene polymorphism (Ala16Val) of manganese superoxide dismutase (MnSOD) may protect against reactive oxygen species (ROS) function.	Reactive Oxygen Species	223-246	superoxide dismutase 2	Homo sapiens	196-201
18653258-1	2008	AIMS: Recent evidence indicates that oxidative stress may play an important role in the pathogenesis of insulin resistance and that gene polymorphism (Ala16Val) of manganese superoxide dismutase (MnSOD) may protect against reactive oxygen species (ROS) function.	Reactive Oxygen Species	248-251	superoxide dismutase 2	Homo sapiens	164-194
18653258-1	2008	AIMS: Recent evidence indicates that oxidative stress may play an important role in the pathogenesis of insulin resistance and that gene polymorphism (Ala16Val) of manganese superoxide dismutase (MnSOD) may protect against reactive oxygen species (ROS) function.	Reactive Oxygen Species	248-251	superoxide dismutase 2	Homo sapiens	196-201
18417547-8	2008	Importantly, prevention of the exercise-induced increase in MnSOD activity via antisense oligonucleotides greatly attenuated the cardioprotection conferred by exercise.	Oligonucleotides	89-105	superoxide dismutase 2	Homo sapiens	60-65
18424257-2	2008	Here, we report that treatment of human breast epithelial (MCF10A) cells with EGCG induces the expression of glutamate-cysteine ligase, manganese superoxide dismutase (MnSOD), and heme oxygenase-1 (HO-1).	epigallocatechin gallate	78-82	superoxide dismutase 2	Homo sapiens	136-166
18424257-2	2008	Here, we report that treatment of human breast epithelial (MCF10A) cells with EGCG induces the expression of glutamate-cysteine ligase, manganese superoxide dismutase (MnSOD), and heme oxygenase-1 (HO-1).	epigallocatechin gallate	78-82	superoxide dismutase 2	Homo sapiens	168-173
18424257-5	2008	Silencing of Nrf2 by siRNA gene knockdown rendered the MCF10A cells less sensitive to the EGCG-induced expression of HO-1 and MnSOD.	epigallocatechin gallate	90-94	superoxide dismutase 2	Homo sapiens	126-131
18751342-2	2008	The antioxidant enzymes--superoxide dismutase (SOD): manganese SOD (MnSOD) and copper-zinc SOD (CuZnSOD), as well as glutathione (GSH), are the most important intracellular antioxidants in the metabolism of ROS.	Reactive Oxygen Species	207-210	superoxide dismutase 2	Homo sapiens	47-50
18434081-0	2008	Cytotoxic activity of 3,3",4,4",5,5"-hexahydroxystilbene against breast cancer cells is mediated by induction of p53 and downregulation of mitochondrial superoxide dismutase.	3,3',4,4',5,5'-hexahydroxystilbene	22-56	superoxide dismutase 2	Homo sapiens	139-173
18434081-8	2008	MnSOD is a key enzyme providing antioxidative defense in mitochondria - the cellular center of reactive oxygen species" generation.	Reactive Oxygen Species	95-118	superoxide dismutase 2	Homo sapiens	0-5
18751342-2	2008	The antioxidant enzymes--superoxide dismutase (SOD): manganese SOD (MnSOD) and copper-zinc SOD (CuZnSOD), as well as glutathione (GSH), are the most important intracellular antioxidants in the metabolism of ROS.	Reactive Oxygen Species	207-210	superoxide dismutase 2	Homo sapiens	53-66
18751342-2	2008	The antioxidant enzymes--superoxide dismutase (SOD): manganese SOD (MnSOD) and copper-zinc SOD (CuZnSOD), as well as glutathione (GSH), are the most important intracellular antioxidants in the metabolism of ROS.	Reactive Oxygen Species	207-210	superoxide dismutase 2	Homo sapiens	68-73
18594523-2	2008	Manganese superoxide disumutase (MnSOD) is an important antioxidant enzyme responsible for the elimination of superoxide radicals.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	33-38
18683149-2	2008	METHODS: The Ala(-9)Val polymorphism of the Mn-SOD gene was determined by polymerase chain reaction and direct sequencing in 198 normal control subjects and 264 patients with type 2 diabetes mellitus, among them there were 139 non-diabetic retinopathy (NDR) subjects and 125 subjects with diabetic retinopathy (DR).	Valine	20-23	superoxide dismutase 2	Homo sapiens	44-50
18683149-7	2008	CONCLUSION: The Ala(-9)Val polymorphism in the Mn-SOD gene may not be related to the etiology of type 2 diabetes, but it seems to contribute to the development of diabetic retinopathy in Chinese type 2 diabetic patients.	Alanine	16-19	superoxide dismutase 2	Homo sapiens	47-53
18683149-7	2008	CONCLUSION: The Ala(-9)Val polymorphism in the Mn-SOD gene may not be related to the etiology of type 2 diabetes, but it seems to contribute to the development of diabetic retinopathy in Chinese type 2 diabetic patients.	Valine	23-26	superoxide dismutase 2	Homo sapiens	47-53
18594523-4	2008	Knockdown of MnSOD by small-interfering RNA (siRNA) led to an increase in superoxide generation and sensitisation of ovarian cancer cells to the two front-line anti-cancer agents doxorubicin and paclitaxel whose action involved free-radical generation.	Superoxides	74-84	superoxide dismutase 2	Homo sapiens	13-18
18594523-4	2008	Knockdown of MnSOD by small-interfering RNA (siRNA) led to an increase in superoxide generation and sensitisation of ovarian cancer cells to the two front-line anti-cancer agents doxorubicin and paclitaxel whose action involved free-radical generation.	Doxorubicin	179-190	superoxide dismutase 2	Homo sapiens	13-18
18594523-4	2008	Knockdown of MnSOD by small-interfering RNA (siRNA) led to an increase in superoxide generation and sensitisation of ovarian cancer cells to the two front-line anti-cancer agents doxorubicin and paclitaxel whose action involved free-radical generation.	Paclitaxel	195-205	superoxide dismutase 2	Homo sapiens	13-18
18594523-4	2008	Knockdown of MnSOD by small-interfering RNA (siRNA) led to an increase in superoxide generation and sensitisation of ovarian cancer cells to the two front-line anti-cancer agents doxorubicin and paclitaxel whose action involved free-radical generation.	Free Radicals	228-240	superoxide dismutase 2	Homo sapiens	13-18
18594523-7	2008	Evaluation of signalling pathways showed that MnSOD siRNA enhanced doxorubicin- and paclitaxel-induced phosphorylation of extracellular signal-regulated kinase 1/2.	Doxorubicin	67-78	superoxide dismutase 2	Homo sapiens	46-51
18594523-7	2008	Evaluation of signalling pathways showed that MnSOD siRNA enhanced doxorubicin- and paclitaxel-induced phosphorylation of extracellular signal-regulated kinase 1/2.	Paclitaxel	84-94	superoxide dismutase 2	Homo sapiens	46-51
18270969-7	2008	MnSOD is a key member of the mitochondrial defense system against mitochondrial-derived superoxide.	Superoxides	88-98	superoxide dismutase 2	Homo sapiens	0-5
18779124-1	2008	MnSOD, which is an important oxygen free radical scavenger in organisms, has an effect to resist oxidative stress and tumor.	Oxygen	29-35	superoxide dismutase 2	Homo sapiens	0-5
18490896-7	2008	In fact, MnSOD upregulation by exposure to ethanol in vitro was much more pronounced in p66KO versus wild-type isolated liver cells, and blunted in HepG2 cells overexpressing p66shc.	Ethanol	43-50	superoxide dismutase 2	Homo sapiens	9-14
18420387-0	2008	Combined NMR and computational study for azide binding to human manganese superoxide dismutase.	Azides	41-46	superoxide dismutase 2	Homo sapiens	64-94
18420387-1	2008	Human manganese superoxide dismutase (MnSOD) labeled with 3-fluorotyrosine (Tyf) was complexed with the (15)N-labeled inhibitor azide ([(15)N(3)(-)]).	3-fluorotyrosine	58-74	superoxide dismutase 2	Homo sapiens	6-36
18420387-1	2008	Human manganese superoxide dismutase (MnSOD) labeled with 3-fluorotyrosine (Tyf) was complexed with the (15)N-labeled inhibitor azide ([(15)N(3)(-)]).	3-fluorotyrosine	58-74	superoxide dismutase 2	Homo sapiens	38-43
18420387-1	2008	Human manganese superoxide dismutase (MnSOD) labeled with 3-fluorotyrosine (Tyf) was complexed with the (15)N-labeled inhibitor azide ([(15)N(3)(-)]).	(S)-2-hydroxy-3-(4-hydroxyphenyl)propanoic acid	76-79	superoxide dismutase 2	Homo sapiens	6-36
18420387-1	2008	Human manganese superoxide dismutase (MnSOD) labeled with 3-fluorotyrosine (Tyf) was complexed with the (15)N-labeled inhibitor azide ([(15)N(3)(-)]).	(S)-2-hydroxy-3-(4-hydroxyphenyl)propanoic acid	76-79	superoxide dismutase 2	Homo sapiens	38-43
18420387-1	2008	Human manganese superoxide dismutase (MnSOD) labeled with 3-fluorotyrosine (Tyf) was complexed with the (15)N-labeled inhibitor azide ([(15)N(3)(-)]).	Azides	128-133	superoxide dismutase 2	Homo sapiens	6-36
18420387-1	2008	Human manganese superoxide dismutase (MnSOD) labeled with 3-fluorotyrosine (Tyf) was complexed with the (15)N-labeled inhibitor azide ([(15)N(3)(-)]).	Azides	128-133	superoxide dismutase 2	Homo sapiens	38-43
18420387-9	2008	As a consequence the azide forms an H bond with Gln143 instead with Tyf34, in contrast to non-(19)F-labeled MnSOD, where the azide is hydrogen bonded to the hydroxy group of Tyr34.	Azides	125-130	superoxide dismutase 2	Homo sapiens	108-113
18420387-9	2008	As a consequence the azide forms an H bond with Gln143 instead with Tyf34, in contrast to non-(19)F-labeled MnSOD, where the azide is hydrogen bonded to the hydroxy group of Tyr34.	Hydrogen	134-142	superoxide dismutase 2	Homo sapiens	108-113
18518943-2	2008	We focus here on the SOD family that uses Fe or Mn as cofactor.	Iron	42-44	superoxide dismutase 2	Homo sapiens	21-24
18413139-1	2008	Manganese superoxide dismutase (MnSOD) is the only primary antioxidant enzyme in mitochondria that scavenges superoxide radicals.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
18384434-0	2008	Nuclear factor-kappaB dependency of doxorubicin sensitivity in gastric cancer cells is determined by manganese superoxide dismutase expression.	Doxorubicin	36-47	superoxide dismutase 2	Homo sapiens	101-131
18434620-8	2008	In the presence of LDL, treatment with Mn-SOD small interfering RNA increased intracellular nitrotyrosine level (P < 0.5, n = 4), a fingerprint for nitrotyrosine formation.	3-nitrotyrosine	92-105	superoxide dismutase 2	Homo sapiens	39-45
18434620-8	2008	In the presence of LDL, treatment with Mn-SOD small interfering RNA increased intracellular nitrotyrosine level (P < 0.5, n = 4), a fingerprint for nitrotyrosine formation.	3-nitrotyrosine	151-164	superoxide dismutase 2	Homo sapiens	39-45
18384434-4	2008	In addition, the association between NF-kappaB and manganese superoxide dismutase (MnSOD) in relation to DOX sensitivity was analyzed after the modulation of MnSOD expression.	Doxorubicin	105-108	superoxide dismutase 2	Homo sapiens	51-81
18384434-4	2008	In addition, the association between NF-kappaB and manganese superoxide dismutase (MnSOD) in relation to DOX sensitivity was analyzed after the modulation of MnSOD expression.	Doxorubicin	105-108	superoxide dismutase 2	Homo sapiens	83-88
18384434-6	2008	Overexpression of mIkappaBalpha or pyrrolidine dithiocarbamate pretreatment decreased the DOX resistance in SNU-601 cells with low MnSOD expression, but not in SNU-216 cells with high MnSOD expression.	mikappabalpha	18-31	superoxide dismutase 2	Homo sapiens	131-136
18384434-6	2008	Overexpression of mIkappaBalpha or pyrrolidine dithiocarbamate pretreatment decreased the DOX resistance in SNU-601 cells with low MnSOD expression, but not in SNU-216 cells with high MnSOD expression.	mikappabalpha	18-31	superoxide dismutase 2	Homo sapiens	184-189
18384434-6	2008	Overexpression of mIkappaBalpha or pyrrolidine dithiocarbamate pretreatment decreased the DOX resistance in SNU-601 cells with low MnSOD expression, but not in SNU-216 cells with high MnSOD expression.	pyrrolidine dithiocarbamic acid	35-62	superoxide dismutase 2	Homo sapiens	131-136
18384434-6	2008	Overexpression of mIkappaBalpha or pyrrolidine dithiocarbamate pretreatment decreased the DOX resistance in SNU-601 cells with low MnSOD expression, but not in SNU-216 cells with high MnSOD expression.	Doxorubicin	90-93	superoxide dismutase 2	Homo sapiens	131-136
18384434-6	2008	Overexpression of mIkappaBalpha or pyrrolidine dithiocarbamate pretreatment decreased the DOX resistance in SNU-601 cells with low MnSOD expression, but not in SNU-216 cells with high MnSOD expression.	Doxorubicin	90-93	superoxide dismutase 2	Homo sapiens	184-189
18384434-7	2008	In comparison, the overexpression of MnSOD, which also suppressed NF-kappaB activation in both cell lines, increased DOX resistance in SNU-601 cells.	Doxorubicin	117-120	superoxide dismutase 2	Homo sapiens	37-42
18384434-8	2008	Blocking of MnSOD expression using RNA interference techniques increased DOX sensitivity in SNU-216 cells, which was further augmented by the additional inhibition of NF-kappaB activity.	Doxorubicin	73-76	superoxide dismutase 2	Homo sapiens	12-17
18384434-9	2008	Our results showed that whether NF-kappaB contributes to DOX sensitivity in gastric cancer cells is determined by the level of MnSOD expression.	Doxorubicin	57-60	superoxide dismutase 2	Homo sapiens	127-132
18384434-10	2008	Thus, targeting both MnSOD and NF-kappaB may be helpful for increasing the efficacy of DOX treatment of DOX-resistant SNU gastric cancer cells.	Doxorubicin	87-90	superoxide dismutase 2	Homo sapiens	21-26
18384434-10	2008	Thus, targeting both MnSOD and NF-kappaB may be helpful for increasing the efficacy of DOX treatment of DOX-resistant SNU gastric cancer cells.	Doxorubicin	104-107	superoxide dismutase 2	Homo sapiens	21-26
18433119-4	2008	Intriguingly, the LMCT transition energies correlate almost linearly with the Fe(3+/2+) reduction potentials of the corresponding Fe(3+)-bound SOD species in the absence of azide, which span a range of approximately 1 V (see the preceding paper).	Azides	173-178	superoxide dismutase 2	Homo sapiens	143-146
18400355-6	2008	Moreover, ghrelin increased mitochondrial anti-apoptosis related gene protein expression such as bcl-2 and MnSOD, reduced cytoplasmic cytochrome C (Cyt C) release and strengthened the activation of NF-kappaB.	Ghrelin	10-17	superoxide dismutase 2	Homo sapiens	107-112
18466086-3	2008	The MnSOD 60C > T polymorphism within exon 3 changes leucine to phenylalanine, rendering the protein sensitive to redox regulation by intracellular thiols.	Sulfhydryl Compounds	151-157	superoxide dismutase 2	Homo sapiens	4-9
18296681-1	2008	Iron overload may increase prostate cancer risk through stimulation of oxidative stress, and endogenous pro- and antioxidant capabilities, i.e. manganese superoxide dismutase (MnSOD) and myeloperoxidase (MPO), may modify these associations.	Iron	0-4	superoxide dismutase 2	Homo sapiens	144-174
18433119-4	2008	Intriguingly, the LMCT transition energies correlate almost linearly with the Fe(3+/2+) reduction potentials of the corresponding Fe(3+)-bound SOD species in the absence of azide, which span a range of approximately 1 V (see the preceding paper).	lmct	18-22	superoxide dismutase 2	Homo sapiens	143-146
18433119-4	2008	Intriguingly, the LMCT transition energies correlate almost linearly with the Fe(3+/2+) reduction potentials of the corresponding Fe(3+)-bound SOD species in the absence of azide, which span a range of approximately 1 V (see the preceding paper).	ferric sulfate	130-136	superoxide dismutase 2	Homo sapiens	143-146
18264764-4	2008	A system biology model was developed to shed more light on how MnSOD affects the biological state of cells depending upon the production of H(2)O(2).	Hydrogen Peroxide	140-148	superoxide dismutase 2	Homo sapiens	63-68
18490963-8	2008	The results suggest that (estrogen-activated) MnSOD plays an important role against mitochondrial oxidative stress by diminishing reactive oxygen species, thus promoting cell survival.	Reactive Oxygen Species	130-153	superoxide dismutase 2	Homo sapiens	46-51
18281048-3	2008	Overexpression of the superoxide scavenger MnSOD and the hydrogen peroxide scavenger catalase inhibited tube formation in estrogen treated endothelial cells.	Superoxides	22-32	superoxide dismutase 2	Homo sapiens	43-48
18296681-1	2008	Iron overload may increase prostate cancer risk through stimulation of oxidative stress, and endogenous pro- and antioxidant capabilities, i.e. manganese superoxide dismutase (MnSOD) and myeloperoxidase (MPO), may modify these associations.	Iron	0-4	superoxide dismutase 2	Homo sapiens	176-181
17967822-3	2008	We investigated the associations of the MnSOD polymorphism (valine-to-alanine in the mitochondrial-targeting domain) with its activity in leukocytes, with macrophage apoptosis by oxidized low-density lipoprotein (oxLDL), and with coronary artery disease (CAD).	Valine	60-66	superoxide dismutase 2	Homo sapiens	40-45
17967822-3	2008	We investigated the associations of the MnSOD polymorphism (valine-to-alanine in the mitochondrial-targeting domain) with its activity in leukocytes, with macrophage apoptosis by oxidized low-density lipoprotein (oxLDL), and with coronary artery disease (CAD).	Alanine	70-77	superoxide dismutase 2	Homo sapiens	40-45
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Valine	195-201	superoxide dismutase 2	Homo sapiens	18-23
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Alanine	83-90	superoxide dismutase 2	Homo sapiens	18-23
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Valine	195-201	superoxide dismutase 2	Homo sapiens	18-23
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Alanine	91-98	superoxide dismutase 2	Homo sapiens	18-23
17967822-8	2008	The association of the MnSOD polymorphism with CAD was investigated using blood samples collected from 498 CAD patients and 627 healthy subjects; the alanine allele was found to reduce the risk of CAD and acute myocardial infarction (AMI).	Alanine	150-157	superoxide dismutase 2	Homo sapiens	23-28
17967822-9	2008	CONCLUSION: Our data indicate that the alanine variant of signal peptide increases the mitochondrial MnSOD activity, protects macrophages against the oxLDL-induced apoptosis, and reduces the risk of CAD and AMI.	Alanine	39-46	superoxide dismutase 2	Homo sapiens	101-106
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Alanine	91-98	superoxide dismutase 2	Homo sapiens	18-23
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Valine	145-151	superoxide dismutase 2	Homo sapiens	18-23
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Valine	195-201	superoxide dismutase 2	Homo sapiens	18-23
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Valine	195-201	superoxide dismutase 2	Homo sapiens	18-23
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Valine	195-201	superoxide dismutase 2	Homo sapiens	18-23
17967822-5	2008	The mitochondrial MnSOD activities in leukocytes were 542.4 +/- 71.6 U/mg protein (alanine/alanine, n = 2), 302.0 +/- 94.9 U/mg protein (alanine/valine, n = 12), and 134.0 +/- 67.1 U/mg protein (valine/valine, n = 36; P < 0.0001 for non-valine/valine vs. valine/valine).	Valine	195-201	superoxide dismutase 2	Homo sapiens	18-23
18280257-0	2008	All-trans-retinoic acid induces manganese superoxide dismutase in human neuroblastoma through NF-kappaB.	Tretinoin	0-23	superoxide dismutase 2	Homo sapiens	32-62
18234413-9	2008	Protein concentration of the different antioxidant enzymes was generally reduced by kaempferol and quercetin in comparison to CM, although quercetin 25 and 50 microM increased Mn SOD protein concentration.	Quercetin	139-148	superoxide dismutase 2	Homo sapiens	176-182
18439041-0	2008	Maintenance of manganese superoxide dismutase (SOD2)-mediated delayed radioprotection induced by repeated administration of the free thiol form of amifostine.	Amifostine	147-157	superoxide dismutase 2	Homo sapiens	47-51
18373354-0	2008	Role of a glutamate bridge spanning the dimeric interface of human manganese superoxide dismutase.	Glutamic Acid	10-19	superoxide dismutase 2	Homo sapiens	67-97
18373354-2	2008	Glu162 in homotetrameric human MnSOD spans a dimeric interface and forms a hydrogen bond with His163 of an adjacent subunit which is a direct ligand of the manganese.	Hydrogen	75-83	superoxide dismutase 2	Homo sapiens	31-36
18373354-2	2008	Glu162 in homotetrameric human MnSOD spans a dimeric interface and forms a hydrogen bond with His163 of an adjacent subunit which is a direct ligand of the manganese.	Manganese	156-165	superoxide dismutase 2	Homo sapiens	31-36
18373354-4	2008	The X-ray crystal structures of E162D and E162A MnSOD reveal no significant structural changes compared with the wild type other than the removal of the hydrogen bond interaction with His163 in E162A MnSOD.	Hydrogen	153-161	superoxide dismutase 2	Homo sapiens	200-205
18373354-5	2008	In the case of E162D MnSOD, an intervening solvent molecule fills the void created by the mutation to conserve the hydrogen bond interaction between His163 and residue 162.	Hydrogen	115-123	superoxide dismutase 2	Homo sapiens	21-26
18373354-8	2008	Differential scanning calorimetry indicates that the hydrogen bond between Glu162 and His163 contributes to the stability of MnSOD, with the major unfolding transition occurring at 81 degrees C for E162A compared to 90 degrees C for wild-type MnSOD.	Hydrogen	53-61	superoxide dismutase 2	Homo sapiens	125-130
18373354-8	2008	Differential scanning calorimetry indicates that the hydrogen bond between Glu162 and His163 contributes to the stability of MnSOD, with the major unfolding transition occurring at 81 degrees C for E162A compared to 90 degrees C for wild-type MnSOD.	Hydrogen	53-61	superoxide dismutase 2	Homo sapiens	243-248
18439041-0	2008	Maintenance of manganese superoxide dismutase (SOD2)-mediated delayed radioprotection induced by repeated administration of the free thiol form of amifostine.	Sulfhydryl Compounds	133-138	superoxide dismutase 2	Homo sapiens	15-45
18439041-0	2008	Maintenance of manganese superoxide dismutase (SOD2)-mediated delayed radioprotection induced by repeated administration of the free thiol form of amifostine.	Sulfhydryl Compounds	133-138	superoxide dismutase 2	Homo sapiens	47-51
18439041-0	2008	Maintenance of manganese superoxide dismutase (SOD2)-mediated delayed radioprotection induced by repeated administration of the free thiol form of amifostine.	Amifostine	147-157	superoxide dismutase 2	Homo sapiens	15-45
18280257-4	2008	Using the SK-N-SH human neuroblastoma cell line we investigated the effects of the differentiation agent all-trans-retinoic acid (ATRA) on the expression of manganese superoxide dismutase (MnSOD), an enzyme previously shown to enhance differentiation in vitro.	Tretinoin	105-128	superoxide dismutase 2	Homo sapiens	157-187
18280257-4	2008	Using the SK-N-SH human neuroblastoma cell line we investigated the effects of the differentiation agent all-trans-retinoic acid (ATRA) on the expression of manganese superoxide dismutase (MnSOD), an enzyme previously shown to enhance differentiation in vitro.	Tretinoin	105-128	superoxide dismutase 2	Homo sapiens	189-194
18280257-4	2008	Using the SK-N-SH human neuroblastoma cell line we investigated the effects of the differentiation agent all-trans-retinoic acid (ATRA) on the expression of manganese superoxide dismutase (MnSOD), an enzyme previously shown to enhance differentiation in vitro.	Tretinoin	130-134	superoxide dismutase 2	Homo sapiens	157-187
18280257-4	2008	Using the SK-N-SH human neuroblastoma cell line we investigated the effects of the differentiation agent all-trans-retinoic acid (ATRA) on the expression of manganese superoxide dismutase (MnSOD), an enzyme previously shown to enhance differentiation in vitro.	Tretinoin	130-134	superoxide dismutase 2	Homo sapiens	189-194
18404530-10	2008	Hydrogen peroxide is mainly produced in males and this subsequently leads to increases in MnSOD gene expression and activity.	Hydrogen Peroxide	0-17	superoxide dismutase 2	Homo sapiens	90-95
18280257-5	2008	Manganese superoxide dismutase mRNA, protein, and activity levels increased in a time-dependent manner upon treatment with ATRA.	Tretinoin	123-127	superoxide dismutase 2	Homo sapiens	0-30
18280257-8	2008	Furthermore an increase in DNA binding to a NF-kappaB element occurred within a 342-bp enhancer (I2E) of the SOD2 gene with 10 microM ATRA treatment.	Tretinoin	134-138	superoxide dismutase 2	Homo sapiens	109-113
18280257-9	2008	Reporter analysis showed that ATRA-mediated I2E-dependent luciferase expression was attenuated upon mutation of the NF-kappaB element, suggesting a contribution of this transcription factor to retinoid-mediated upregulation of MnSOD.	Retinoids	193-201	superoxide dismutase 2	Homo sapiens	227-232
18280257-10	2008	This study identifies SOD2 as a retinoid-responsive gene and demonstrates activation of the NF-kappaB pathway in response to ATRA treatment of SK-N-SH cells.	Retinoids	32-40	superoxide dismutase 2	Homo sapiens	22-26
18280257-10	2008	This study identifies SOD2 as a retinoid-responsive gene and demonstrates activation of the NF-kappaB pathway in response to ATRA treatment of SK-N-SH cells.	Tretinoin	125-129	superoxide dismutase 2	Homo sapiens	22-26
18280257-11	2008	These results suggest that signaling events involving NF-kappaB and SOD2 may contribute to the effects of retinoids used in cancer therapy.	Retinoids	106-115	superoxide dismutase 2	Homo sapiens	68-72
18284447-2	2008	Fungal tolerance to 2,3-dihydroxybenzaldehyde or 2,3-dihydroxybenzoic acid was found to rely upon mitochondrial superoxide dismutase (SOD2) or glutathione reductase (GLR1), genes regulated by the HOG1 signaling pathway, respectively.	2,3-dihydroxybenzaldehyde	20-45	superoxide dismutase 2	Homo sapiens	134-138
18284447-2	2008	Fungal tolerance to 2,3-dihydroxybenzaldehyde or 2,3-dihydroxybenzoic acid was found to rely upon mitochondrial superoxide dismutase (SOD2) or glutathione reductase (GLR1), genes regulated by the HOG1 signaling pathway, respectively.	2,3-dihydroxybenzoic acid	49-74	superoxide dismutase 2	Homo sapiens	134-138
18413745-3	2008	The antioxidant enzyme manganese superoxide dismutase (MnSOD) modulates the cellular redox environment by converting superoxide (O(2)(*-)) to hydrogen peroxide and dioxygen.	Superoxides	33-43	superoxide dismutase 2	Homo sapiens	55-60
18413745-3	2008	The antioxidant enzyme manganese superoxide dismutase (MnSOD) modulates the cellular redox environment by converting superoxide (O(2)(*-)) to hydrogen peroxide and dioxygen.	o(2)	129-133	superoxide dismutase 2	Homo sapiens	23-53
18413745-3	2008	The antioxidant enzyme manganese superoxide dismutase (MnSOD) modulates the cellular redox environment by converting superoxide (O(2)(*-)) to hydrogen peroxide and dioxygen.	o(2)	129-133	superoxide dismutase 2	Homo sapiens	55-60
18413745-3	2008	The antioxidant enzyme manganese superoxide dismutase (MnSOD) modulates the cellular redox environment by converting superoxide (O(2)(*-)) to hydrogen peroxide and dioxygen.	Hydrogen Peroxide	142-159	superoxide dismutase 2	Homo sapiens	23-53
18413745-3	2008	The antioxidant enzyme manganese superoxide dismutase (MnSOD) modulates the cellular redox environment by converting superoxide (O(2)(*-)) to hydrogen peroxide and dioxygen.	Hydrogen Peroxide	142-159	superoxide dismutase 2	Homo sapiens	55-60
18413745-3	2008	The antioxidant enzyme manganese superoxide dismutase (MnSOD) modulates the cellular redox environment by converting superoxide (O(2)(*-)) to hydrogen peroxide and dioxygen.	Oxygen	164-172	superoxide dismutase 2	Homo sapiens	23-53
18413745-3	2008	The antioxidant enzyme manganese superoxide dismutase (MnSOD) modulates the cellular redox environment by converting superoxide (O(2)(*-)) to hydrogen peroxide and dioxygen.	Oxygen	164-172	superoxide dismutase 2	Homo sapiens	55-60
18413745-5	2008	Here, we tested the hypothesis that MnSOD regulates the expression of HIF-1 alpha by modulating the steady-state level of O(2)(*-).	o(2)	122-126	superoxide dismutase 2	Homo sapiens	36-41
18413745-6	2008	We found that decreasing MnSOD with small interfering RNA in MCF-7 cells resulted in (a) an associated increase in the hypoxic accumulation of HIF-1 alpha immunoreactive protein, (b) a significant increase in the levels of O(2)(*-) (P < 0.01), but (c) no significant change in the steady-state level of H(2)O(2).	o(2)	223-227	superoxide dismutase 2	Homo sapiens	25-30
18413745-6	2008	We found that decreasing MnSOD with small interfering RNA in MCF-7 cells resulted in (a) an associated increase in the hypoxic accumulation of HIF-1 alpha immunoreactive protein, (b) a significant increase in the levels of O(2)(*-) (P < 0.01), but (c) no significant change in the steady-state level of H(2)O(2).	Water	306-311	superoxide dismutase 2	Homo sapiens	25-30
17593366-8	2008	Together, at both the mRNA and protein levels, SAHA suppressed the expression of reticulocalbin 1 precursor (RCN1), annexin A3 (ANXA3) and heat shock 27 kDa protein 1 (HSP27), while increasing the expression of aldose reductase (AR), triosephosphate isomerase 1 (TPI) and manganese superoxide dismutase (SOD2).	Vorinostat	47-51	superoxide dismutase 2	Homo sapiens	304-308
17473980-5	2008	For MDA-MB231 cells, the high-MnSOD level was accompanied by an overproduction of intracellular hydrogen peroxide (H2O2) and by a low expression of the major H2O2-detoxifying enzymes, catalase, and peroxiredoxin 3, compared to MCF-7 cells.	Hydrogen Peroxide	96-113	superoxide dismutase 2	Homo sapiens	30-35
18327084-0	2008	Nifedipine improves the migratory ability of circulating endothelial progenitor cells depending on manganese superoxide dismutase upregulation.	Nifedipine	0-10	superoxide dismutase 2	Homo sapiens	99-129
18327084-4	2008	As nifedipine is a dihydropyridine calcium antagonist known to enhance MnSOD expression in mature endothelial cells, we investigated the effects of nifedipine on MnSOD expression and motility in EPCs.	Nifedipine	3-13	superoxide dismutase 2	Homo sapiens	71-76
18327084-8	2008	The study of SOD showed a nifedipine-dependent upregulation of MnSOD in a time-dependent and dose-dependent manner.	Nifedipine	26-36	superoxide dismutase 2	Homo sapiens	13-16
18327084-8	2008	The study of SOD showed a nifedipine-dependent upregulation of MnSOD in a time-dependent and dose-dependent manner.	Nifedipine	26-36	superoxide dismutase 2	Homo sapiens	63-68
18327084-9	2008	MnSOD expression blockade by RNA interference abolished nifedipine effect on EPC motility.	Nifedipine	56-66	superoxide dismutase 2	Homo sapiens	0-5
18327084-11	2008	CONCLUSION: Nifedipine improves EPC motility due to MnSOD upregulation.	Nifedipine	12-22	superoxide dismutase 2	Homo sapiens	52-57
18167310-0	2008	Molecular mechanisms of oxidative stress resistance induced by resveratrol: Specific and progressive induction of MnSOD.	Resveratrol	63-74	superoxide dismutase 2	Homo sapiens	114-119
17941088-6	2008	RA inhibited stretch- and Ang II-induced intracellular reactive oxygen species (ROS) generation and upregulated the SOD2 level.	Tretinoin	0-2	superoxide dismutase 2	Homo sapiens	116-120
18206666-4	2008	HDF treated with EGCG at 25 and 50 microM for 24 h considerably increased catalase, superoxide dismutase (SOD)1, SOD2, and glutathione peroxidase gene expressions and their enzyme activities, thus protecting HDF against H2O2-induced oxidative damage, accompanied with decreased intracellular ROS accumulation and well-maintained mitochondrial potential.	epigallocatechin gallate	17-21	superoxide dismutase 2	Homo sapiens	113-117
17473980-5	2008	For MDA-MB231 cells, the high-MnSOD level was accompanied by an overproduction of intracellular hydrogen peroxide (H2O2) and by a low expression of the major H2O2-detoxifying enzymes, catalase, and peroxiredoxin 3, compared to MCF-7 cells.	Hydrogen Peroxide	115-119	superoxide dismutase 2	Homo sapiens	30-35
17473980-5	2008	For MDA-MB231 cells, the high-MnSOD level was accompanied by an overproduction of intracellular hydrogen peroxide (H2O2) and by a low expression of the major H2O2-detoxifying enzymes, catalase, and peroxiredoxin 3, compared to MCF-7 cells.	Hydrogen Peroxide	158-162	superoxide dismutase 2	Homo sapiens	30-35
17473980-6	2008	Suppression of MnSOD expression by antisense RNA was associated with a decrease of H2O2 content and caused a stimulation of growth with a reduced cell doubling time but induced a decrease of colony formation.	Hydrogen Peroxide	83-87	superoxide dismutase 2	Homo sapiens	15-20
17473980-10	2008	These action are mediated by MnSOD-dependent H2O2 production.	Hydrogen Peroxide	45-49	superoxide dismutase 2	Homo sapiens	29-34
18205184-2	2008	Myeloperoxidase (MPO) and superoxide dismutase (SOD2) are enzymes that regulate reactive oxygen species and contain recognized single nucleotide polymorphisms (SNPs) that confer altered enzyme activity.	Reactive Oxygen Species	80-103	superoxide dismutase 2	Homo sapiens	48-52
18023606-5	2008	A valine (Val) to alanine (Ala) substitution at amino acid 9, mapping within the mitochondrion-targeting sequence of the MnSOD gene, has been associated with an increased cancer risk.	Valine	2-8	superoxide dismutase 2	Homo sapiens	121-126
18247479-2	2008	As MnSOD has been shown to remove superoxide radical with varying efficiency depending upon its cellular origin, a comparison of the Drad MnSOD efficiency with that of both human and Escherichia coli MnSODs was undertaken.	Superoxides	34-52	superoxide dismutase 2	Homo sapiens	3-8
18247479-3	2008	Pulse radiolysis studies demonstrate that, under identical ratios of enzyme to superoxide radical, the dismutation efficiencies scaled as Drad MnSOD > E. coli MnSOD > human MnSOD.	Superoxides	79-97	superoxide dismutase 2	Homo sapiens	143-148
18247479-3	2008	Pulse radiolysis studies demonstrate that, under identical ratios of enzyme to superoxide radical, the dismutation efficiencies scaled as Drad MnSOD > E. coli MnSOD > human MnSOD.	Superoxides	79-97	superoxide dismutase 2	Homo sapiens	162-167
18247479-3	2008	Pulse radiolysis studies demonstrate that, under identical ratios of enzyme to superoxide radical, the dismutation efficiencies scaled as Drad MnSOD > E. coli MnSOD > human MnSOD.	Superoxides	79-97	superoxide dismutase 2	Homo sapiens	162-167
18247479-4	2008	Further, Drad MnSOD is most effective at high superoxide fluxes found under conditions of high radioactivity.	Superoxides	46-56	superoxide dismutase 2	Homo sapiens	14-19
18083891-6	2008	Superoxide dismutase 2 (SOD2) converts intramitochondrial superoxide to diffusible H(2)O(2), which serves as a redox-signaling molecule, regulating pulmonary vascular tone and structure through effects on Kv1.5 and transcription factors.	Superoxides	58-68	superoxide dismutase 2	Homo sapiens	0-22
18083891-6	2008	Superoxide dismutase 2 (SOD2) converts intramitochondrial superoxide to diffusible H(2)O(2), which serves as a redox-signaling molecule, regulating pulmonary vascular tone and structure through effects on Kv1.5 and transcription factors.	Superoxides	58-68	superoxide dismutase 2	Homo sapiens	24-28
17632733-6	2008	In vitro experiments with SW620 colorectal carcinoma cell line demonstrated that it was sensitive to ZD55-MnSOD, especially most sensitive to ZD55-MnSOD plus 5-FU treatment.	Fluorouracil	158-162	superoxide dismutase 2	Homo sapiens	106-111
17632733-7	2008	Treatment with both ZD55-MnSOD and 5-FU could induce more significant apoptosis in cancer cells compared with ZD55-MnSOD or 5-FU alone, respectively.	Fluorouracil	35-39	superoxide dismutase 2	Homo sapiens	115-120
17632733-7	2008	Treatment with both ZD55-MnSOD and 5-FU could induce more significant apoptosis in cancer cells compared with ZD55-MnSOD or 5-FU alone, respectively.	Fluorouracil	124-128	superoxide dismutase 2	Homo sapiens	25-30
17949999-7	2008	Animals were sacrificed for H&E staining, and immunohistochemical staining for glutamine synthetase (GS) and Mn-superoxide dismutase (Mn-SOD), which are two Mn-binding enzymes against glutamate toxicity and oxidative stress respectively in neurodegeneration.	Glutamic Acid	188-197	superoxide dismutase 2	Homo sapiens	138-144
18155673-5	2008	Our data indicate that BCNU when combined with SOD overexpression increased oxidative stress as suggested by elevated glutathione disulfide (GSSG) production in one of three breast cancer cell lines tested, at least in part due to glutathione reductase (GR) inactivation.	Glutathione Disulfide	118-139	superoxide dismutase 2	Homo sapiens	47-50
18155673-5	2008	Our data indicate that BCNU when combined with SOD overexpression increased oxidative stress as suggested by elevated glutathione disulfide (GSSG) production in one of three breast cancer cell lines tested, at least in part due to glutathione reductase (GR) inactivation.	Glutathione Disulfide	141-145	superoxide dismutase 2	Homo sapiens	47-50
17653087-9	2008	Hence, high levels of MnSOD, which decompose and neutralize these reactive oxygen species, might contribute to metastasis formation by allowing disseminated tumor cells to escape from TRAIL-mediated tumor surveillance.	Reactive Oxygen Species	66-89	superoxide dismutase 2	Homo sapiens	22-27
18023606-5	2008	A valine (Val) to alanine (Ala) substitution at amino acid 9, mapping within the mitochondrion-targeting sequence of the MnSOD gene, has been associated with an increased cancer risk.	Valine	10-13	superoxide dismutase 2	Homo sapiens	121-126
18023606-5	2008	A valine (Val) to alanine (Ala) substitution at amino acid 9, mapping within the mitochondrion-targeting sequence of the MnSOD gene, has been associated with an increased cancer risk.	Alanine	18-25	superoxide dismutase 2	Homo sapiens	121-126
18023606-5	2008	A valine (Val) to alanine (Ala) substitution at amino acid 9, mapping within the mitochondrion-targeting sequence of the MnSOD gene, has been associated with an increased cancer risk.	Alanine	27-30	superoxide dismutase 2	Homo sapiens	121-126
18023606-10	2008	Our findings provide further evidence of an association between the Ala-9Val MnSOD polymorphism and HCC occurrence in hepatitis C virus-infected Moroccan patients.	ala-9val	68-76	superoxide dismutase 2	Homo sapiens	77-82
18032526-8	2008	AGE-induced phosphorylation of FKHRL1 led to a 70% downregulation of MnSOD, an effect partially blocked by a phosphatidylinositol 3-kinase inhibitor (LY-294002) and strongly inhibited by an antioxidant (N-acetylcysteine).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	150-159	superoxide dismutase 2	Homo sapiens	69-74
18032526-8	2008	AGE-induced phosphorylation of FKHRL1 led to a 70% downregulation of MnSOD, an effect partially blocked by a phosphatidylinositol 3-kinase inhibitor (LY-294002) and strongly inhibited by an antioxidant (N-acetylcysteine).	Acetylcysteine	203-219	superoxide dismutase 2	Homo sapiens	69-74
18032526-10	2008	These studies point to a new pathway for the induction of OS by AGEs involving FKHRL1 inactivation and MnSOD suppression via Ser-36 phosphorylation of p66(shc) in human kidney cells.	Serine	125-128	superoxide dismutase 2	Homo sapiens	103-108
18755401-3	2008	We also aimed to investigate whether the alterations were related to the intracellular status of metal-containing superoxide dismutase (SOD).	Metals	97-102	superoxide dismutase 2	Homo sapiens	136-139
17652337-0	2007	Chronic exposure to 12-O-tetradecanoylphorbol-13-acetate represses sod2 induction in vivo: the negative role of p50.	Tetradecanoylphorbol Acetate	20-56	superoxide dismutase 2	Homo sapiens	67-71
18094428-5	2007	Increased SOD activity decreased superoxide levels and increased hydrogen peroxide levels.	Superoxides	33-43	superoxide dismutase 2	Homo sapiens	10-13
18094428-5	2007	Increased SOD activity decreased superoxide levels and increased hydrogen peroxide levels.	Hydrogen Peroxide	65-82	superoxide dismutase 2	Homo sapiens	10-13
18094428-8	2007	In contrast, inhibiting endogenous SOD with small interfering RNA increased superoxide levels and promoted tumor growth.	Superoxides	76-86	superoxide dismutase 2	Homo sapiens	35-38
18044968-6	2007	Moreover, the mechanism of this weakened product inhibition was similar to that in E. coli MnSOD, specifically a decrease in the rate constant for the oxidative addition of superoxide to Mn2+MnSOD leading to the formation of the peroxide-inhibited enzyme.	Superoxides	173-183	superoxide dismutase 2	Homo sapiens	91-96
18044968-6	2007	Moreover, the mechanism of this weakened product inhibition was similar to that in E. coli MnSOD, specifically a decrease in the rate constant for the oxidative addition of superoxide to Mn2+MnSOD leading to the formation of the peroxide-inhibited enzyme.	Superoxides	173-183	superoxide dismutase 2	Homo sapiens	191-196
18044968-6	2007	Moreover, the mechanism of this weakened product inhibition was similar to that in E. coli MnSOD, specifically a decrease in the rate constant for the oxidative addition of superoxide to Mn2+MnSOD leading to the formation of the peroxide-inhibited enzyme.	Peroxides	175-183	superoxide dismutase 2	Homo sapiens	91-96
18044968-6	2007	Moreover, the mechanism of this weakened product inhibition was similar to that in E. coli MnSOD, specifically a decrease in the rate constant for the oxidative addition of superoxide to Mn2+MnSOD leading to the formation of the peroxide-inhibited enzyme.	Peroxides	175-183	superoxide dismutase 2	Homo sapiens	191-196
18167182-10	2007	siRNA-mediated silencing of MnSOD in KYSE450 and KYSE150 cell lines revealed that MnSOD protected ESCC cells from apoptosis induced by ultraviolet (UV) and doxorubicin (DOX).	Doxorubicin	156-167	superoxide dismutase 2	Homo sapiens	82-87
18167182-10	2007	siRNA-mediated silencing of MnSOD in KYSE450 and KYSE150 cell lines revealed that MnSOD protected ESCC cells from apoptosis induced by ultraviolet (UV) and doxorubicin (DOX).	Doxorubicin	169-172	superoxide dismutase 2	Homo sapiens	82-87
17652337-1	2007	It is well documented that the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) can activate manganese superoxide dismutase (MnSOD) expression.	Tetradecanoylphorbol Acetate	46-82	superoxide dismutase 2	Homo sapiens	102-132
17652337-1	2007	It is well documented that the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) can activate manganese superoxide dismutase (MnSOD) expression.	Tetradecanoylphorbol Acetate	46-82	superoxide dismutase 2	Homo sapiens	134-139
17652337-1	2007	It is well documented that the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) can activate manganese superoxide dismutase (MnSOD) expression.	Tetradecanoylphorbol Acetate	84-87	superoxide dismutase 2	Homo sapiens	102-132
17652337-1	2007	It is well documented that the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) can activate manganese superoxide dismutase (MnSOD) expression.	Tetradecanoylphorbol Acetate	84-87	superoxide dismutase 2	Homo sapiens	134-139
17652337-3	2007	We generated transgenic mice expressing human MnSOD promoter- and enhancer-driven luciferase reporter gene and used a non-invasive imaging system to investigate the effects of TPA on MnSOD expression in vivo.	Tetradecanoylphorbol Acetate	176-179	superoxide dismutase 2	Homo sapiens	183-188
17652337-4	2007	Our data indicate that TPA initially activates MnSOD expression, but this positive effect declines after repeated applications.	Tetradecanoylphorbol Acetate	23-26	superoxide dismutase 2	Homo sapiens	47-52
17652337-6	2007	Using chromatin immunoprecipitation coupled to Western analysis of the transcription factors known to be essential for the constitutive and TPA-induced transcription of MnSOD, we found that TPA treatment leads to both activation and inactivation of MnSOD gene transcription.	Tetradecanoylphorbol Acetate	140-143	superoxide dismutase 2	Homo sapiens	169-174
17652337-6	2007	Using chromatin immunoprecipitation coupled to Western analysis of the transcription factors known to be essential for the constitutive and TPA-induced transcription of MnSOD, we found that TPA treatment leads to both activation and inactivation of MnSOD gene transcription.	Tetradecanoylphorbol Acetate	140-143	superoxide dismutase 2	Homo sapiens	249-254
17652337-6	2007	Using chromatin immunoprecipitation coupled to Western analysis of the transcription factors known to be essential for the constitutive and TPA-induced transcription of MnSOD, we found that TPA treatment leads to both activation and inactivation of MnSOD gene transcription.	Tetradecanoylphorbol Acetate	190-193	superoxide dismutase 2	Homo sapiens	169-174
17652337-6	2007	Using chromatin immunoprecipitation coupled to Western analysis of the transcription factors known to be essential for the constitutive and TPA-induced transcription of MnSOD, we found that TPA treatment leads to both activation and inactivation of MnSOD gene transcription.	Tetradecanoylphorbol Acetate	190-193	superoxide dismutase 2	Homo sapiens	249-254
17652337-8	2007	Sustained treatments with TPA lead to further increase of p50 but not p65, Sp1 or NPM, suggesting that excess p50 may have inhibitory effects leading to the suppression of MnSOD.	Tetradecanoylphorbol Acetate	26-29	superoxide dismutase 2	Homo sapiens	172-177
17652337-10	2007	These findings identify p50 as having a negative effect on MnSOD induction upon repeated applications of TPA and provide an insight into a cause for the reduction of MnSOD expression during early stages of skin carcinogenesis.	Tetradecanoylphorbol Acetate	105-108	superoxide dismutase 2	Homo sapiens	59-64
18032788-9	2007	Overexpression of manganese-superoxide dismutase (SOD2) in HeLa cells decreased autophagy and cell death induced by rotenone and TTFA.	Rotenone	116-124	superoxide dismutase 2	Homo sapiens	18-48
18032788-9	2007	Overexpression of manganese-superoxide dismutase (SOD2) in HeLa cells decreased autophagy and cell death induced by rotenone and TTFA.	Rotenone	116-124	superoxide dismutase 2	Homo sapiens	50-54
18032788-9	2007	Overexpression of manganese-superoxide dismutase (SOD2) in HeLa cells decreased autophagy and cell death induced by rotenone and TTFA.	Thenoyltrifluoroacetone	129-133	superoxide dismutase 2	Homo sapiens	18-48
18032788-9	2007	Overexpression of manganese-superoxide dismutase (SOD2) in HeLa cells decreased autophagy and cell death induced by rotenone and TTFA.	Thenoyltrifluoroacetone	129-133	superoxide dismutase 2	Homo sapiens	50-54
18032788-10	2007	Furthermore, blocking SOD2 expression by siRNA in HeLa cells increased ROS generation, autophagy and cell death induced by rotenone and TTFA.	Reactive Oxygen Species	71-74	superoxide dismutase 2	Homo sapiens	22-26
18032788-10	2007	Furthermore, blocking SOD2 expression by siRNA in HeLa cells increased ROS generation, autophagy and cell death induced by rotenone and TTFA.	Rotenone	123-131	superoxide dismutase 2	Homo sapiens	22-26
18032788-10	2007	Furthermore, blocking SOD2 expression by siRNA in HeLa cells increased ROS generation, autophagy and cell death induced by rotenone and TTFA.	Thenoyltrifluoroacetone	136-140	superoxide dismutase 2	Homo sapiens	22-26
17948227-5	2007	Fibroblasts from several MMA patients showed a significant increase in intracellular reactive oxygen species (ROS) content and in MnSOD expression level with respect to controls, suggesting a cellular response to intrinsic ROS stress.	Reactive Oxygen Species	223-226	superoxide dismutase 2	Homo sapiens	130-135
17895890-1	2007	Manganese superoxide dismutase (SOD2) is an enzyme that catalyses the dismutation of superoxide in the mitochondria, leading to reduced levels of reactive oxygen species.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-36
18349501-3	2007	It is of particular importance to photosynthetic organisms in the chloroplast of which a cluster of Mn atoms at the catalytic centre function in the light-induced water oxidation by photosystem II, and also function as a cofactor for a variety of enzymes, such as Mn-SOD.	Water	163-168	superoxide dismutase 2	Homo sapiens	264-270
17680990-8	2007	When the neurons were treated with L-NAME, a well known NOS inhibitor, the increase in Mn-SOD expression occurring during IPC was reduced and, as a result, IPC-induced neuroprotection was prevented.	NG-Nitroarginine Methyl Ester	35-41	superoxide dismutase 2	Homo sapiens	87-93
17680990-9	2007	Similarly, when ERK1/2 was inhibited by its selective inhibitor PD98059, the increase in Mn-SOD expression observed during IPC was almost completely abolished.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	64-71	superoxide dismutase 2	Homo sapiens	89-95
17895890-1	2007	Manganese superoxide dismutase (SOD2) is an enzyme that catalyses the dismutation of superoxide in the mitochondria, leading to reduced levels of reactive oxygen species.	Reactive Oxygen Species	146-169	superoxide dismutase 2	Homo sapiens	0-30
17895890-1	2007	Manganese superoxide dismutase (SOD2) is an enzyme that catalyses the dismutation of superoxide in the mitochondria, leading to reduced levels of reactive oxygen species.	Reactive Oxygen Species	146-169	superoxide dismutase 2	Homo sapiens	32-36
17895890-5	2007	We demonstrate, through sodium bisulphite sequencing, that the sod2 locus is methylated in some pancreatic cell lines leading to a corresponding decrease in SOD2 expression.	sodium bisulfite	24-41	superoxide dismutase 2	Homo sapiens	63-67
17895890-5	2007	We demonstrate, through sodium bisulphite sequencing, that the sod2 locus is methylated in some pancreatic cell lines leading to a corresponding decrease in SOD2 expression.	sodium bisulfite	24-41	superoxide dismutase 2	Homo sapiens	157-161
17895890-6	2007	Methylation can be reversed by treatment with zebularine, a methyltransferase inhibitor, resulting in restored SOD2 expression.	pyrimidin-2-one beta-ribofuranoside	46-56	superoxide dismutase 2	Homo sapiens	111-115
17895890-7	2007	Furthermore, we demonstrate that sensitivity of pancreatic carcinoma cell lines to 2-methoxyestradiol correlates with SOD2 expression and SOD2 modulation can alter the sensitivity of these cells.	2-Methoxyestradiol	83-101	superoxide dismutase 2	Homo sapiens	118-122
17825902-14	2007	An interesting role of polyphenols in modulating the expression levels of PGHS-2 in endometrial tissue and on the activation of TIS11b and SOD2 through c-AMP-dependent signalling was suggested.	Polyphenols	23-34	superoxide dismutase 2	Homo sapiens	139-143
17854710-7	2007	Cells with mutant K-ras had significantly lower amounts of manganese superoxide dismutase (MnSOD) vs those with wild-type K-ras, but MnSOD protein correlated positively with superoxide levels.	Superoxides	69-79	superoxide dismutase 2	Homo sapiens	91-96
17628794-4	2007	A valine (Val) to alanine (Ala) substitution at amino acid 16, occurring in the mitochondrial targeting sequence of the MnSOD gene, has been associated with an increase in urolithiasis risk.	Valine	2-8	superoxide dismutase 2	Homo sapiens	120-125
17851796-9	2007	Our findings also suggest that while plasma Mn-SOD might play a significant role in detoxifying the superoxide anions produced in the placenta, the decomposition of hydrogen peroxide in erythrocytes is mainly due to CAT activity.	Superoxides	100-117	superoxide dismutase 2	Homo sapiens	44-50
18059618-2	2007	While an acute bout of exercise activates NF kappaB and MAPK signaling and upregulates MnSOD and iNOS, administration of chemical agents that suppress reactive oxygen species (ROS) production can cause attenuation of exercise-induced MnSOD and iNOS expression.	Reactive Oxygen Species	151-174	superoxide dismutase 2	Homo sapiens	234-239
18059618-2	2007	While an acute bout of exercise activates NF kappaB and MAPK signaling and upregulates MnSOD and iNOS, administration of chemical agents that suppress reactive oxygen species (ROS) production can cause attenuation of exercise-induced MnSOD and iNOS expression.	Reactive Oxygen Species	176-179	superoxide dismutase 2	Homo sapiens	234-239
17583406-8	2007	The overexpression of antioxidant enzyme Mn SOD protein levels, which was promoted to a new type tumor suppressor gene in several human cancer cells recently, may be an important role in kaempferol-induced H460 cell apoptosis.	kaempferol	187-197	superoxide dismutase 2	Homo sapiens	41-47
19093460-4	2007	The recombinant human MnSOD was expressed in E. coli strain BL21(DE3)pLysS and purified to homogeneity by Ni2+ -NTA.	nickel nitrilotriacetic acid	106-115	superoxide dismutase 2	Homo sapiens	22-27
19093460-5	2007	Supplementation of Mn2+ in the bacterial growth media was proven to be crucial for production of enzymatically active hMnSOD.	Manganese(2+)	19-23	superoxide dismutase 2	Homo sapiens	118-124
19093460-8	2007	More interestingly, E. coli expressing hMnSOD provides resistance against oxidative stress induced by the herbicide paraquat up to 1.2 mM.	Paraquat	116-124	superoxide dismutase 2	Homo sapiens	39-45
17628794-4	2007	A valine (Val) to alanine (Ala) substitution at amino acid 16, occurring in the mitochondrial targeting sequence of the MnSOD gene, has been associated with an increase in urolithiasis risk.	Valine	10-13	superoxide dismutase 2	Homo sapiens	120-125
17628794-4	2007	A valine (Val) to alanine (Ala) substitution at amino acid 16, occurring in the mitochondrial targeting sequence of the MnSOD gene, has been associated with an increase in urolithiasis risk.	Alanine	18-25	superoxide dismutase 2	Homo sapiens	120-125
17628794-4	2007	A valine (Val) to alanine (Ala) substitution at amino acid 16, occurring in the mitochondrial targeting sequence of the MnSOD gene, has been associated with an increase in urolithiasis risk.	Alanine	27-30	superoxide dismutase 2	Homo sapiens	120-125
17719580-5	2007	Furthermore, the MnSOD-overexpressing stable transfectants exhibited reduced soft-agarose colony-forming ability and metastatic properties, unlike control cell lines.	Sepharose	82-89	superoxide dismutase 2	Homo sapiens	17-22
17876045-4	2007	Parthenolide inhibits radiation-induced NF-kappaB DNA-binding activity and the expression of its downstream target sod2, the gene coding for an important antiapoptotic and antioxidant enzyme (manganese superoxide dismutase) in the three prostate cancer cells.	parthenolide	0-12	superoxide dismutase 2	Homo sapiens	115-119
17452060-4	2007	Here we demonstrate that hyperglycemia-induced production of ROS is abrogated by inhibitors of mitochondrial metabolism, or by overexpression of uncoupling protein-1 or manganese superoxide dismutase.	Reactive Oxygen Species	61-64	superoxide dismutase 2	Homo sapiens	169-199
17576015-3	2007	The manganese-containing enzyme, manganese superoxide dismutase (Mn-SOD), is the principal antioxidant enzyme which neutralizes the toxic effects of reactive oxygen species.	Manganese	4-13	superoxide dismutase 2	Homo sapiens	65-71
17576015-3	2007	The manganese-containing enzyme, manganese superoxide dismutase (Mn-SOD), is the principal antioxidant enzyme which neutralizes the toxic effects of reactive oxygen species.	Reactive Oxygen Species	149-172	superoxide dismutase 2	Homo sapiens	33-63
17576015-3	2007	The manganese-containing enzyme, manganese superoxide dismutase (Mn-SOD), is the principal antioxidant enzyme which neutralizes the toxic effects of reactive oxygen species.	Manganese	4-13	superoxide dismutase 2	Homo sapiens	33-63
17576015-3	2007	The manganese-containing enzyme, manganese superoxide dismutase (Mn-SOD), is the principal antioxidant enzyme which neutralizes the toxic effects of reactive oxygen species.	Reactive Oxygen Species	149-172	superoxide dismutase 2	Homo sapiens	65-71
17526807-9	2007	Galantamine significantly reduced TUNEL, active caspase-3, and SOD-2 immunoreactivity.	Galantamine	0-11	superoxide dismutase 2	Homo sapiens	63-68
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Alanine	20-23	superoxide dismutase 2	Homo sapiens	35-39
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Valine	195-198	superoxide dismutase 2	Homo sapiens	35-39
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Alanine	199-202	superoxide dismutase 2	Homo sapiens	35-39
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Valine	210-213	superoxide dismutase 2	Homo sapiens	35-39
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Valine	210-213	superoxide dismutase 2	Homo sapiens	35-39
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Alanine	199-202	superoxide dismutase 2	Homo sapiens	35-39
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Alanine	199-202	superoxide dismutase 2	Homo sapiens	35-39
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Valine	210-213	superoxide dismutase 2	Homo sapiens	35-39
17646272-5	2007	The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P(trend) = 0.03).	Valine	210-213	superoxide dismutase 2	Homo sapiens	35-39
17646272-6	2007	Stratification by quartiles of dietary and supplemental vitamin E intake (IU/d) showed risks of prostate cancer tended to be increased among SOD2 Ala allele carriers, except at the highest quartile of vitamin E intake (>222; P(interaction) = 0.06, Q1-Q3 versus Q4).	Vitamin E	56-65	superoxide dismutase 2	Homo sapiens	141-145
17646272-6	2007	Stratification by quartiles of dietary and supplemental vitamin E intake (IU/d) showed risks of prostate cancer tended to be increased among SOD2 Ala allele carriers, except at the highest quartile of vitamin E intake (>222; P(interaction) = 0.06, Q1-Q3 versus Q4).	Alanine	146-149	superoxide dismutase 2	Homo sapiens	141-145
17646272-9	2007	These results suggest that the Ala variant of SOD2 is associated with moderately increased risk of prostate cancer, particularly among men with lower intakes of dietary and supplemental vitamin E.	Alanine	31-34	superoxide dismutase 2	Homo sapiens	46-50
17646272-9	2007	These results suggest that the Ala variant of SOD2 is associated with moderately increased risk of prostate cancer, particularly among men with lower intakes of dietary and supplemental vitamin E.	Vitamin E	186-195	superoxide dismutase 2	Homo sapiens	46-50
17394531-5	2007	Additionally, we tested the hypothesis that mutant SOD1 increases mitochondrial-produced superoxide (O(2) (*)) levels and that SOD2 overexpression protects neurons from mutant SOD1-induced toxicity by reducing O(2) (*) levels in mitochondria.	Oxygen	210-214	superoxide dismutase 2	Homo sapiens	127-131
17394531-8	2007	These elevated O(2) (*) levels in mitochondria were significantly diminished by the overexpression of SOD2.	Oxygen	15-19	superoxide dismutase 2	Homo sapiens	102-106
17602958-0	2007	In vitro preparation of iron-substituted human manganese superoxide dismutase: possible toxic properties for mitochondria.	Iron	24-28	superoxide dismutase 2	Homo sapiens	47-77
17602958-1	2007	We prepared an iron-substituted form of recombinant human manganese superoxide dismutase (MnSOD) by using guanidine hydrochloride for the first time as a model of iron-misincorporated MnSOD, the formation of which has been reported by M. Yang et al.	Iron	15-19	superoxide dismutase 2	Homo sapiens	58-88
17602958-1	2007	We prepared an iron-substituted form of recombinant human manganese superoxide dismutase (MnSOD) by using guanidine hydrochloride for the first time as a model of iron-misincorporated MnSOD, the formation of which has been reported by M. Yang et al.	Iron	15-19	superoxide dismutase 2	Homo sapiens	90-95
17602958-1	2007	We prepared an iron-substituted form of recombinant human manganese superoxide dismutase (MnSOD) by using guanidine hydrochloride for the first time as a model of iron-misincorporated MnSOD, the formation of which has been reported by M. Yang et al.	Iron	15-19	superoxide dismutase 2	Homo sapiens	184-189
17602958-1	2007	We prepared an iron-substituted form of recombinant human manganese superoxide dismutase (MnSOD) by using guanidine hydrochloride for the first time as a model of iron-misincorporated MnSOD, the formation of which has been reported by M. Yang et al.	Guanidine	106-129	superoxide dismutase 2	Homo sapiens	58-88
17602958-1	2007	We prepared an iron-substituted form of recombinant human manganese superoxide dismutase (MnSOD) by using guanidine hydrochloride for the first time as a model of iron-misincorporated MnSOD, the formation of which has been reported by M. Yang et al.	Guanidine	106-129	superoxide dismutase 2	Homo sapiens	90-95
17602958-1	2007	We prepared an iron-substituted form of recombinant human manganese superoxide dismutase (MnSOD) by using guanidine hydrochloride for the first time as a model of iron-misincorporated MnSOD, the formation of which has been reported by M. Yang et al.	Iron	163-167	superoxide dismutase 2	Homo sapiens	58-88
17602958-1	2007	We prepared an iron-substituted form of recombinant human manganese superoxide dismutase (MnSOD) by using guanidine hydrochloride for the first time as a model of iron-misincorporated MnSOD, the formation of which has been reported by M. Yang et al.	Iron	163-167	superoxide dismutase 2	Homo sapiens	90-95
17602958-1	2007	We prepared an iron-substituted form of recombinant human manganese superoxide dismutase (MnSOD) by using guanidine hydrochloride for the first time as a model of iron-misincorporated MnSOD, the formation of which has been reported by M. Yang et al.	Iron	163-167	superoxide dismutase 2	Homo sapiens	184-189
17602958-5	2007	The iron-substituted enzyme contained 0.79 g atoms of Fe/mol of subunits and had a specific activity of 80 units/mg protein/g atom of Fe/mol of subunit, which was less than 3% of the activity of the purified MnSOD.	Iron	4-8	superoxide dismutase 2	Homo sapiens	208-213
17602958-8	2007	The Fe-substituted enzyme showed a hydrogen-peroxide-mediated radical-generating activity, which was monitored by a cation radical of 2,2"-azinobis-(3-ethylbenzthiazoline-6-sulfonate) formation similar to that of Cu,ZnSOD, but native human MnSOD and FeSOD showed no radical-generation ability.	Iron	4-6	superoxide dismutase 2	Homo sapiens	240-245
17602958-8	2007	The Fe-substituted enzyme showed a hydrogen-peroxide-mediated radical-generating activity, which was monitored by a cation radical of 2,2"-azinobis-(3-ethylbenzthiazoline-6-sulfonate) formation similar to that of Cu,ZnSOD, but native human MnSOD and FeSOD showed no radical-generation ability.	Hydrogen Peroxide	35-52	superoxide dismutase 2	Homo sapiens	240-245
17602958-8	2007	The Fe-substituted enzyme showed a hydrogen-peroxide-mediated radical-generating activity, which was monitored by a cation radical of 2,2"-azinobis-(3-ethylbenzthiazoline-6-sulfonate) formation similar to that of Cu,ZnSOD, but native human MnSOD and FeSOD showed no radical-generation ability.	2,2"-azinobis-(3-ethylbenzthiazoline-6-sulfonate	134-182	superoxide dismutase 2	Homo sapiens	240-245
17602958-8	2007	The Fe-substituted enzyme showed a hydrogen-peroxide-mediated radical-generating activity, which was monitored by a cation radical of 2,2"-azinobis-(3-ethylbenzthiazoline-6-sulfonate) formation similar to that of Cu,ZnSOD, but native human MnSOD and FeSOD showed no radical-generation ability.	Copper	213-215	superoxide dismutase 2	Homo sapiens	240-245
17602958-8	2007	The Fe-substituted enzyme showed a hydrogen-peroxide-mediated radical-generating activity, which was monitored by a cation radical of 2,2"-azinobis-(3-ethylbenzthiazoline-6-sulfonate) formation similar to that of Cu,ZnSOD, but native human MnSOD and FeSOD showed no radical-generation ability.	znsod	216-221	superoxide dismutase 2	Homo sapiens	240-245
17602958-9	2007	This evidence suggests that a substitution of Mn to Fe in human MnSOD in mitochondria may produce a disadvantage for oxidative stress in three ways: loss of the enzymatic activity, increase of stability, and gain of radical-generating ability.	Iron	52-54	superoxide dismutase 2	Homo sapiens	64-69
17537404-4	2007	However, tumor cells that adapt to oxidative stress by increasing manganese superoxide dismutase (MnSOD), Prx I, and Bcl-2 showed drug resistance to 5-FU.	Fluorouracil	149-153	superoxide dismutase 2	Homo sapiens	66-96
17537404-4	2007	However, tumor cells that adapt to oxidative stress by increasing manganese superoxide dismutase (MnSOD), Prx I, and Bcl-2 showed drug resistance to 5-FU.	Fluorouracil	149-153	superoxide dismutase 2	Homo sapiens	98-103
17616690-5	2007	At the early phase of selenite treatment, high levels of superoxide anion were generated and overexpression of copper/zinc superoxide dismutase or manganese superoxide dismutase, but not catalase, significantly blocked selenite-induced mitochondrial damage and subsequent autophagic cell death.	Selenious Acid	22-30	superoxide dismutase 2	Homo sapiens	147-177
17616690-5	2007	At the early phase of selenite treatment, high levels of superoxide anion were generated and overexpression of copper/zinc superoxide dismutase or manganese superoxide dismutase, but not catalase, significantly blocked selenite-induced mitochondrial damage and subsequent autophagic cell death.	Selenious Acid	219-227	superoxide dismutase 2	Homo sapiens	147-177
32689372-5	2007	Ten superoxide dismutase (SOD) isoenzymes were detected and the two major Mn-SOD isoenzymes (bands V and VI) responded more to 0.05 mm selenite.	Selenious Acid	135-143	superoxide dismutase 2	Homo sapiens	74-80
17548672-7	2007	When calculating the number of risk alleles of MnSOD, CAT, and GPX1 hypothetically related to reduced protection against ROS, there was a nonsignificant relationship between prostate cancer and carriage of five or more risk alleles, in comparison to men with less than five risk alleles (OR, 2.0; 95% CI, 0.90-4.42).	Reactive Oxygen Species	121-124	superoxide dismutase 2	Homo sapiens	47-52
17435022-0	2007	Gene expression of manganese-containing superoxide dismutase as a biomarker of manganese bioavailability for manganese sources in broilers.	Manganese	79-88	superoxide dismutase 2	Homo sapiens	19-60
17192397-2	2007	SOD2 is a key enzyme in the conversion of reactive oxygen species and has been implicated in a host of disease states, including cancer.	Reactive Oxygen Species	42-65	superoxide dismutase 2	Homo sapiens	0-4
17192397-6	2007	Overexpression of SOD2 results in decreased proliferation and altered sensitivity to 2-methoxyestradiol-induced DNA damage and apoptosis.	2-Methoxyestradiol	85-103	superoxide dismutase 2	Homo sapiens	18-22
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Adenosine Monophosphate	12-15	superoxide dismutase 2	Homo sapiens	136-166
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Adenosine Monophosphate	12-15	superoxide dismutase 2	Homo sapiens	168-173
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Alanine	63-70	superoxide dismutase 2	Homo sapiens	136-166
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Alanine	63-70	superoxide dismutase 2	Homo sapiens	168-173
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Alanine	72-75	superoxide dismutase 2	Homo sapiens	136-166
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Alanine	72-75	superoxide dismutase 2	Homo sapiens	168-173
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Valine	80-86	superoxide dismutase 2	Homo sapiens	136-166
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Valine	80-86	superoxide dismutase 2	Homo sapiens	168-173
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Valine	88-91	superoxide dismutase 2	Homo sapiens	136-166
17336594-1	2007	BACKGROUND & AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import and activity.	Valine	88-91	superoxide dismutase 2	Homo sapiens	168-173
17336594-3	2007	The aim of this study was to assess the influence of the Ala-9Val MnSOD dimorphism on the same parameters and events in hepatitis C virus (HCV)-infected patients.	ala-9val	57-65	superoxide dismutase 2	Homo sapiens	66-71
17336594-9	2007	CONCLUSIONS: Contrary to previous findings in French alcoholic patients, the Ala-encoding MnSOD allele is represented equally in controls and patients with HCV-related cirrhosis, and it does not significantly influence the risks of liver iron overload, HCC, or death in these patients.	Alanine	77-80	superoxide dismutase 2	Homo sapiens	90-95
17309078-9	2007	Thus, these results suggest that GD-induced cell death mode is determined by the protein kinase C/ERK1/2 signal pathway that regulates MnSOD and CuZnSOD and that these antioxidants may exert their known tumor suppressive activities by inducing necrosis-to-apoptosis switch.	Gadolinium	33-35	superoxide dismutase 2	Homo sapiens	135-140
17395009-1	2007	Human recombinant MnSOD and CuZnSOD were both inactivated when exposed to simultaneous fluxes of superoxide (JO(2)(*-)) and nitric oxide (J*NO).	Superoxides	97-107	superoxide dismutase 2	Homo sapiens	18-23
17395009-1	2007	Human recombinant MnSOD and CuZnSOD were both inactivated when exposed to simultaneous fluxes of superoxide (JO(2)(*-)) and nitric oxide (J*NO).	Nitric Oxide	124-136	superoxide dismutase 2	Homo sapiens	18-23
17395009-4	2007	The formation of protein radicals was followed by tyrosine nitration in the case of MnSOD.	Tyrosine	50-58	superoxide dismutase 2	Homo sapiens	84-89
17395009-5	2007	When MnSOD was exposed to J*NO and JO(2)(*-) in the presence of uric acid, a scavenger of peroxynitrite-derived free radicals, nitration was decreased but inactivation was not prevented.	Uric Acid	64-73	superoxide dismutase 2	Homo sapiens	5-10
17395009-5	2007	When MnSOD was exposed to J*NO and JO(2)(*-) in the presence of uric acid, a scavenger of peroxynitrite-derived free radicals, nitration was decreased but inactivation was not prevented.	Peroxynitrous Acid	90-103	superoxide dismutase 2	Homo sapiens	5-10
17395009-5	2007	When MnSOD was exposed to J*NO and JO(2)(*-) in the presence of uric acid, a scavenger of peroxynitrite-derived free radicals, nitration was decreased but inactivation was not prevented.	derived free radicals	104-125	superoxide dismutase 2	Homo sapiens	5-10
17395009-6	2007	On the other hand, glutathione, known to react with both peroxynitrite and nitrogen dioxide, totally protected MnSOD from inactivation and nitration on addition of authentic peroxynitrite but, notably, it was only partially inhibitory in the presence of the more biologically relevant J*NO and JO(2)(*-).	Glutathione	19-30	superoxide dismutase 2	Homo sapiens	111-116
17395009-6	2007	On the other hand, glutathione, known to react with both peroxynitrite and nitrogen dioxide, totally protected MnSOD from inactivation and nitration on addition of authentic peroxynitrite but, notably, it was only partially inhibitory in the presence of the more biologically relevant J*NO and JO(2)(*-).	Peroxynitrous Acid	57-70	superoxide dismutase 2	Homo sapiens	111-116
17395009-6	2007	On the other hand, glutathione, known to react with both peroxynitrite and nitrogen dioxide, totally protected MnSOD from inactivation and nitration on addition of authentic peroxynitrite but, notably, it was only partially inhibitory in the presence of the more biologically relevant J*NO and JO(2)(*-).	Nitrogen Dioxide	75-91	superoxide dismutase 2	Homo sapiens	111-116
17395009-6	2007	On the other hand, glutathione, known to react with both peroxynitrite and nitrogen dioxide, totally protected MnSOD from inactivation and nitration on addition of authentic peroxynitrite but, notably, it was only partially inhibitory in the presence of the more biologically relevant J*NO and JO(2)(*-).	Peroxynitrous Acid	174-187	superoxide dismutase 2	Homo sapiens	111-116
17395009-7	2007	The data are consistent with the direct reaction of peroxynitrite with the Mn center and a metal-catalyzed nitration of Tyr-34 in MnSOD.	Peroxynitrous Acid	52-65	superoxide dismutase 2	Homo sapiens	130-135
17395009-7	2007	The data are consistent with the direct reaction of peroxynitrite with the Mn center and a metal-catalyzed nitration of Tyr-34 in MnSOD.	Metals	91-96	superoxide dismutase 2	Homo sapiens	130-135
17395009-7	2007	The data are consistent with the direct reaction of peroxynitrite with the Mn center and a metal-catalyzed nitration of Tyr-34 in MnSOD.	Tyrosine	120-123	superoxide dismutase 2	Homo sapiens	130-135
17395009-9	2007	Our results help to rationalize MnSOD tyrosine nitration observed in inflammatory conditions in vivo in the presence of low molecular weight scavengers such as glutathione that otherwise would completely consume nitrogen dioxide and prevent nitration reactions.	Tyrosine	38-46	superoxide dismutase 2	Homo sapiens	32-37
17395009-9	2007	Our results help to rationalize MnSOD tyrosine nitration observed in inflammatory conditions in vivo in the presence of low molecular weight scavengers such as glutathione that otherwise would completely consume nitrogen dioxide and prevent nitration reactions.	Glutathione	160-171	superoxide dismutase 2	Homo sapiens	32-37
17395009-9	2007	Our results help to rationalize MnSOD tyrosine nitration observed in inflammatory conditions in vivo in the presence of low molecular weight scavengers such as glutathione that otherwise would completely consume nitrogen dioxide and prevent nitration reactions.	Nitrogen Dioxide	212-228	superoxide dismutase 2	Homo sapiens	32-37
17185981-0	2007	Human epidermal keratinocytes accumulate superoxide due to low activity of Mn-SOD, leading to mitochondrial functional impairment.	Superoxides	41-51	superoxide dismutase 2	Homo sapiens	75-81
17435022-4	2007	At 7 d, chicks fed the diet supplemented with Mn AA B had higher MnSOD mRNA levels than those fed the diet supplemented with Mn sulfate and Mn Met E, and the same tendency was observed at 14 or 21 d. The results suggest that MnSOD gene expression, which is regulated by dietary Mn at transcriptional level, could reflect differences among bio-availabilities of organic Mn sources as early as 7 d. Therefore, the estimation of relative bioavailabilities of Mn sources based on heart MnSOD mRNA level could require a shorter experimental period and a smaller number of animals, and thus less cost.	mn sulfate	125-135	superoxide dismutase 2	Homo sapiens	225-230
17435022-4	2007	At 7 d, chicks fed the diet supplemented with Mn AA B had higher MnSOD mRNA levels than those fed the diet supplemented with Mn sulfate and Mn Met E, and the same tendency was observed at 14 or 21 d. The results suggest that MnSOD gene expression, which is regulated by dietary Mn at transcriptional level, could reflect differences among bio-availabilities of organic Mn sources as early as 7 d. Therefore, the estimation of relative bioavailabilities of Mn sources based on heart MnSOD mRNA level could require a shorter experimental period and a smaller number of animals, and thus less cost.	mn sulfate	125-135	superoxide dismutase 2	Homo sapiens	225-230
17394464-1	2007	Manganese superoxide dismutase (MnSOD) provides the first line of defense against superoxide generated in mitochondria.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
17192393-4	2007	The cells showed an increase of protoporphyrin IX, a higher sensitivity to H(2)O(2) toxicity, and a reduced activity of mitochondrial superoxide dismutase 2 (SOD2), while the activity of mitochondrial enzymes, such as citrate synthase or succinate dehydrogenase, and ATP content were not decreased.	Adenosine Triphosphate	267-270	superoxide dismutase 2	Homo sapiens	158-162
17291655-0	2007	Association between the MnSOD Ala-9Val polymorphism and development of schizophrenia and abnormal involuntary movements in the Xhosa population.	ala-9val	30-38	superoxide dismutase 2	Homo sapiens	24-29
17291655-2	2007	Recently, the functional polymorphism (Ala-9Val) in the manganese superoxide dismutase (MnSOD) gene (part of the antioxidant defense mechanism) was found to be associated with schizophrenia in a Turkish population.	ala-9val	39-47	superoxide dismutase 2	Homo sapiens	56-86
17291655-2	2007	Recently, the functional polymorphism (Ala-9Val) in the manganese superoxide dismutase (MnSOD) gene (part of the antioxidant defense mechanism) was found to be associated with schizophrenia in a Turkish population.	ala-9val	39-47	superoxide dismutase 2	Homo sapiens	88-93
17453961-2	2007	METHODS: Ala (GTT) or Val (GCT) polymorphism in the signal peptide of Mn-SOD gene was evaluated using a primer pair to amplify a 107-bp fragment followed by digestion with restriction enzyme NgoM IV.	Alanine	9-12	superoxide dismutase 2	Homo sapiens	70-76
17453961-2	2007	METHODS: Ala (GTT) or Val (GCT) polymorphism in the signal peptide of Mn-SOD gene was evaluated using a primer pair to amplify a 107-bp fragment followed by digestion with restriction enzyme NgoM IV.	Valine	22-25	superoxide dismutase 2	Homo sapiens	70-76
17394464-2	2007	SOD competes with nitric oxide for reaction with superoxide and prevents generation of peroxynitrite, a potent oxidant that can modify proteins to form 3-nitrotyrosine.	Nitric Oxide	18-30	superoxide dismutase 2	Homo sapiens	0-3
17394464-2	2007	SOD competes with nitric oxide for reaction with superoxide and prevents generation of peroxynitrite, a potent oxidant that can modify proteins to form 3-nitrotyrosine.	Superoxides	49-59	superoxide dismutase 2	Homo sapiens	0-3
17394464-2	2007	SOD competes with nitric oxide for reaction with superoxide and prevents generation of peroxynitrite, a potent oxidant that can modify proteins to form 3-nitrotyrosine.	Peroxynitrous Acid	87-100	superoxide dismutase 2	Homo sapiens	0-3
17394464-2	2007	SOD competes with nitric oxide for reaction with superoxide and prevents generation of peroxynitrite, a potent oxidant that can modify proteins to form 3-nitrotyrosine.	3-nitrotyrosine	152-167	superoxide dismutase 2	Homo sapiens	0-3
17394464-11	2007	Nitration of MnSOD is a likely consequence of peroxynitrite within the intracellular milieu of neurons after TBI.	Peroxynitrous Acid	46-59	superoxide dismutase 2	Homo sapiens	13-18
17394464-12	2007	Nitration and inactivation of MnSOD could lead to self-amplification of oxidative stress in the brain progressively enhancing peroxynitrite production and secondary damage.	Peroxynitrous Acid	126-139	superoxide dismutase 2	Homo sapiens	30-35
17465268-1	2007	BACKGROUND: Manganese superoxide dismutase (MnSOD) is a major enzyme that is responsible for the detoxification of reactive oxygen species in the mitochondria.	Reactive Oxygen Species	115-138	superoxide dismutase 2	Homo sapiens	12-42
17291583-5	2007	Antioxidant enzymes include two types of superoxide dismutase (SOD), which specifically scavenges superoxide radicals: copper-zinc SOD, which is located in the cytosol and Mn-SOD, which is located in the mitochondria.	Superoxides	41-51	superoxide dismutase 2	Homo sapiens	172-178
17388698-0	2007	Manganese superoxide dismutase (SOD2)-mediated delayed radioprotection induced by the free thiol form of amifostine and tumor necrosis factor alpha.	Sulfhydryl Compounds	91-96	superoxide dismutase 2	Homo sapiens	0-30
17388698-0	2007	Manganese superoxide dismutase (SOD2)-mediated delayed radioprotection induced by the free thiol form of amifostine and tumor necrosis factor alpha.	Sulfhydryl Compounds	91-96	superoxide dismutase 2	Homo sapiens	32-36
17388698-0	2007	Manganese superoxide dismutase (SOD2)-mediated delayed radioprotection induced by the free thiol form of amifostine and tumor necrosis factor alpha.	Amifostine	105-115	superoxide dismutase 2	Homo sapiens	0-30
17388698-0	2007	Manganese superoxide dismutase (SOD2)-mediated delayed radioprotection induced by the free thiol form of amifostine and tumor necrosis factor alpha.	Amifostine	105-115	superoxide dismutase 2	Homo sapiens	32-36
17293063-6	2007	Genes up-regulated by selenium supplementation included TNF, IL1B, IL8, SOD2, CXCL2 and several other immunological and oxidative stress-related genes.	Selenium	22-30	superoxide dismutase 2	Homo sapiens	72-76
17184177-2	2007	In endothelial cells, high-glucose treatment increases mitochondrial ROS and normalization of the ROS production by inhibitors of mitochondrial metabolism, or by overexpression of UCP-1 or MnSOD, prevents glucose-induced activation of PKC, formation of AGE, and accumulation of sorbitol, all of which are believed to be the main molecular mechanisms of diabetic complications.	Glucose	27-34	superoxide dismutase 2	Homo sapiens	189-194
17184177-2	2007	In endothelial cells, high-glucose treatment increases mitochondrial ROS and normalization of the ROS production by inhibitors of mitochondrial metabolism, or by overexpression of UCP-1 or MnSOD, prevents glucose-induced activation of PKC, formation of AGE, and accumulation of sorbitol, all of which are believed to be the main molecular mechanisms of diabetic complications.	Glucose	205-212	superoxide dismutase 2	Homo sapiens	189-194
17465268-1	2007	BACKGROUND: Manganese superoxide dismutase (MnSOD) is a major enzyme that is responsible for the detoxification of reactive oxygen species in the mitochondria.	Reactive Oxygen Species	115-138	superoxide dismutase 2	Homo sapiens	44-49
17465268-3	2007	The aim of this study was to investigate the relationship between prostate cancer and MnSOD Ala-9Val polymorphism in Turkish men with prostate cancer.	ala-9val	92-100	superoxide dismutase 2	Homo sapiens	86-91
17465268-9	2007	It was concluded that MnSOD Ala allele might be the cause of prostate cancer risk among alcohol users.	Alanine	28-31	superoxide dismutase 2	Homo sapiens	22-27
17465268-9	2007	It was concluded that MnSOD Ala allele might be the cause of prostate cancer risk among alcohol users.	Alcohols	88-95	superoxide dismutase 2	Homo sapiens	22-27
16927372-7	2007	DFO treatment to TRAP1-overexpressing cells resulted in decreases in levels of ROS, Cav-1, glutathione peroxidase (GPX), and manganese superoxide dismutase (MnSOD) levels as well as senescence-associated beta-galactosidase (SA beta-gal) activity.	Deferoxamine	0-3	superoxide dismutase 2	Homo sapiens	125-155
17070997-4	2007	Compared to placebo, rofecoxib treatment increased the gene expression of ANXA3 (annexin 3), SOD2 (superoxide dismutase 2), SOCS3 (suppressor of cytokine signaling 3) and IL1RN (IL1 receptor antagonist) which are associated with inhibition of phospholipase A(2) and suppression of cytokine signaling cascades, respectively.	rofecoxib	21-30	superoxide dismutase 2	Homo sapiens	93-97
17070997-4	2007	Compared to placebo, rofecoxib treatment increased the gene expression of ANXA3 (annexin 3), SOD2 (superoxide dismutase 2), SOCS3 (suppressor of cytokine signaling 3) and IL1RN (IL1 receptor antagonist) which are associated with inhibition of phospholipase A(2) and suppression of cytokine signaling cascades, respectively.	rofecoxib	21-30	superoxide dismutase 2	Homo sapiens	99-121
17296905-7	2007	RESULTS: Comparisons of AAV-SOD2-infected LHON cells relative to control cells infected with AAV-green fluorescent protein showed increased expression of mitochondrial SOD that attenuated superoxide-induced fluorescence by 26% (P = .003) and suppressed TUNEL-induced fluorescence by 21% (P = .048) after 2 days of growth in galactose medium, when cell survival increased by 25% (P=.05).	Superoxides	188-198	superoxide dismutase 2	Homo sapiens	28-31
17296905-7	2007	RESULTS: Comparisons of AAV-SOD2-infected LHON cells relative to control cells infected with AAV-green fluorescent protein showed increased expression of mitochondrial SOD that attenuated superoxide-induced fluorescence by 26% (P = .003) and suppressed TUNEL-induced fluorescence by 21% (P = .048) after 2 days of growth in galactose medium, when cell survival increased by 25% (P=.05).	Galactose	324-333	superoxide dismutase 2	Homo sapiens	28-31
17296905-8	2007	After 3 days in galactose medium, SOD2 increased LHON survival by 89% (P = .006) relative to controls.	Galactose	16-25	superoxide dismutase 2	Homo sapiens	34-38
17186424-8	2007	We observed an interaction between total vitamin C intake and the MnSOD polymorphism on melanoma risk.	Ascorbic Acid	41-50	superoxide dismutase 2	Homo sapiens	66-71
17210452-7	2007	An increase in nitrated MnSOD was detected in BAEC treated with CsA and the peroxynitrite donor SIN-1 and recapitulated in recombinant MnSOD, exposed to the conditioned media from BAEC.	Cyclosporine	64-67	superoxide dismutase 2	Homo sapiens	24-29
17210452-7	2007	An increase in nitrated MnSOD was detected in BAEC treated with CsA and the peroxynitrite donor SIN-1 and recapitulated in recombinant MnSOD, exposed to the conditioned media from BAEC.	Peroxynitrous Acid	76-89	superoxide dismutase 2	Homo sapiens	24-29
17331249-2	2007	SOD2 polymorphisms are of interest because of their potential roles in the modulation of free radical-mediated macromolecular damage during aging.	Free Radicals	89-101	superoxide dismutase 2	Homo sapiens	0-4
17709902-4	2007	Both Klotho-CM and 6His-tagged Klotho protein enhanced Mn-SOD expression by approximately two-fold, partially via activation of the cAMP signaling pathway.	6his	19-23	superoxide dismutase 2	Homo sapiens	55-61
17709902-4	2007	Both Klotho-CM and 6His-tagged Klotho protein enhanced Mn-SOD expression by approximately two-fold, partially via activation of the cAMP signaling pathway.	Cyclic AMP	132-136	superoxide dismutase 2	Homo sapiens	55-61
17210452-8	2007	We propose that CsA promotes nitration of specific molecular targets, such as MnSOD, within vascular endothelial cells.	Cyclosporine	16-19	superoxide dismutase 2	Homo sapiens	78-83
16927372-7	2007	DFO treatment to TRAP1-overexpressing cells resulted in decreases in levels of ROS, Cav-1, glutathione peroxidase (GPX), and manganese superoxide dismutase (MnSOD) levels as well as senescence-associated beta-galactosidase (SA beta-gal) activity.	Deferoxamine	0-3	superoxide dismutase 2	Homo sapiens	157-162
17208654-9	2007	GP and Mn-SOD gene expression were induced by pilocarpine treatment.	Pilocarpine	46-57	superoxide dismutase 2	Homo sapiens	7-13
17307400-13	2007	Furthermore, manganese superoxide dismutase (MnSOD) cDNA-transfected cells had decreased ROS.	Reactive Oxygen Species	89-92	superoxide dismutase 2	Homo sapiens	13-43
17307400-13	2007	Furthermore, manganese superoxide dismutase (MnSOD) cDNA-transfected cells had decreased ROS.	Reactive Oxygen Species	89-92	superoxide dismutase 2	Homo sapiens	45-50
17211829-6	2007	Several proteins involved in defense against toxic superoxide (O2-) and other reactive oxygen species, such as manganese-containing superoxide dismutase (SOD2), glutathione peroxidase, and peroxiredoxins 1 and 6 were highly upregulated after TLR7/8 activation.	Superoxides	51-61	superoxide dismutase 2	Homo sapiens	154-158
17211829-6	2007	Several proteins involved in defense against toxic superoxide (O2-) and other reactive oxygen species, such as manganese-containing superoxide dismutase (SOD2), glutathione peroxidase, and peroxiredoxins 1 and 6 were highly upregulated after TLR7/8 activation.	Reactive Oxygen Species	78-101	superoxide dismutase 2	Homo sapiens	154-158
17095854-6	2007	From this functional perspective, we found differences between the CR and BP groups with regard to nucleotide metabolism (PBEF1, G6PD; p = 0.048), apoptosis (TNFAIP3, TNFAIP8, MPO, BCL2A1, BAX, SON, BNIP3L; p = 0.039) and reactive oxygen species metabolism (SOD2, KIAA0179; p = 0.048).	Chromium	67-69	superoxide dismutase 2	Homo sapiens	258-262
17916951-2	2007	Manganese (Mn), the key component of the Mitochondrial antioxidant (MnSOD), plays a key role in the superoxide uncoupling protein 2 (UCP-2) pathway in inhibiting of glucose-stimulated insulin secretion (GSIS).	Manganese	0-9	superoxide dismutase 2	Homo sapiens	68-73
17095854-6	2007	From this functional perspective, we found differences between the CR and BP groups with regard to nucleotide metabolism (PBEF1, G6PD; p = 0.048), apoptosis (TNFAIP3, TNFAIP8, MPO, BCL2A1, BAX, SON, BNIP3L; p = 0.039) and reactive oxygen species metabolism (SOD2, KIAA0179; p = 0.048).	Benzo(a)pyrene	74-76	superoxide dismutase 2	Homo sapiens	258-262
17916951-2	2007	Manganese (Mn), the key component of the Mitochondrial antioxidant (MnSOD), plays a key role in the superoxide uncoupling protein 2 (UCP-2) pathway in inhibiting of glucose-stimulated insulin secretion (GSIS).	Superoxides	100-110	superoxide dismutase 2	Homo sapiens	68-73
17916951-2	2007	Manganese (Mn), the key component of the Mitochondrial antioxidant (MnSOD), plays a key role in the superoxide uncoupling protein 2 (UCP-2) pathway in inhibiting of glucose-stimulated insulin secretion (GSIS).	Glucose	165-172	superoxide dismutase 2	Homo sapiens	68-73
17157182-1	2006	Manganese superoxide dismutase (MnSOD, SOD2) is an essential primary antioxidant enzyme which converts superoxide radical to hydrogen peroxide within the mitochondrial matrix.	Superoxides	103-121	superoxide dismutase 2	Homo sapiens	0-30
17192491-4	2007	The present study aimed to determine whether a valine/alanine polymorphism in MnSOD (V16A, rs4880), alone or in combination with smoking, can contribute to development of diabetic nephropathy in 1,510 Finnish and Swedish patients with type 1 diabetes.	Valine	47-53	superoxide dismutase 2	Homo sapiens	78-83
17192491-4	2007	The present study aimed to determine whether a valine/alanine polymorphism in MnSOD (V16A, rs4880), alone or in combination with smoking, can contribute to development of diabetic nephropathy in 1,510 Finnish and Swedish patients with type 1 diabetes.	Alanine	54-61	superoxide dismutase 2	Homo sapiens	78-83
17822322-1	2007	The aim of the study was to investigate relationship between activity of superoxide dismutase (SOD), malondialdehyde (MDA) and tumor necrosis factor alpha (TNFalpha) and between Ala-9Val polymorphism in the gene encoding MnSOD (SOD2) and the initial stage and prognosis of the head and neck squamous cell carcinoma (HNSCC).	ala-9val	178-186	superoxide dismutase 2	Homo sapiens	221-226
17822322-1	2007	The aim of the study was to investigate relationship between activity of superoxide dismutase (SOD), malondialdehyde (MDA) and tumor necrosis factor alpha (TNFalpha) and between Ala-9Val polymorphism in the gene encoding MnSOD (SOD2) and the initial stage and prognosis of the head and neck squamous cell carcinoma (HNSCC).	ala-9val	178-186	superoxide dismutase 2	Homo sapiens	228-232
17822322-11	2007	Progression of the disease might be further modified by the presence of Ala/Ala genotype of the SOD2.	Alanine	72-75	superoxide dismutase 2	Homo sapiens	96-100
17822322-11	2007	Progression of the disease might be further modified by the presence of Ala/Ala genotype of the SOD2.	Alanine	76-79	superoxide dismutase 2	Homo sapiens	96-100
17157182-1	2006	Manganese superoxide dismutase (MnSOD, SOD2) is an essential primary antioxidant enzyme which converts superoxide radical to hydrogen peroxide within the mitochondrial matrix.	Superoxides	103-121	superoxide dismutase 2	Homo sapiens	32-37
17157182-1	2006	Manganese superoxide dismutase (MnSOD, SOD2) is an essential primary antioxidant enzyme which converts superoxide radical to hydrogen peroxide within the mitochondrial matrix.	Superoxides	103-121	superoxide dismutase 2	Homo sapiens	39-43
17157182-1	2006	Manganese superoxide dismutase (MnSOD, SOD2) is an essential primary antioxidant enzyme which converts superoxide radical to hydrogen peroxide within the mitochondrial matrix.	Hydrogen Peroxide	125-142	superoxide dismutase 2	Homo sapiens	0-30
17157182-1	2006	Manganese superoxide dismutase (MnSOD, SOD2) is an essential primary antioxidant enzyme which converts superoxide radical to hydrogen peroxide within the mitochondrial matrix.	Hydrogen Peroxide	125-142	superoxide dismutase 2	Homo sapiens	32-37
17157182-1	2006	Manganese superoxide dismutase (MnSOD, SOD2) is an essential primary antioxidant enzyme which converts superoxide radical to hydrogen peroxide within the mitochondrial matrix.	Hydrogen Peroxide	125-142	superoxide dismutase 2	Homo sapiens	39-43
17157182-5	2006	In the presence of cycloheximide, an inhibitor of protein synthesis, the rates of cell death and MnSOD degradation were accelerated.	Cycloheximide	19-32	superoxide dismutase 2	Homo sapiens	97-102
17157182-6	2006	Fas-induced MnSOD cleavage was partially inhibited in the presence of the pan-caspase inhibitor, z-VAD-fmk.	ammonium ferrous sulfate	0-3	superoxide dismutase 2	Homo sapiens	12-17
17157182-6	2006	Fas-induced MnSOD cleavage was partially inhibited in the presence of the pan-caspase inhibitor, z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	97-106	superoxide dismutase 2	Homo sapiens	12-17
17157182-11	2006	Our data indicate that inactivation of MnSOD in receptor-mediated apoptosis by caspase-specific degradation would render the mitochondria sensitive to the steady-state production of superoxide, decrease the steady-state flux of H(2)O(2), expedite the loss of mitochondrial function, and potentiate apoptosis.	Superoxides	182-192	superoxide dismutase 2	Homo sapiens	39-44
17157182-11	2006	Our data indicate that inactivation of MnSOD in receptor-mediated apoptosis by caspase-specific degradation would render the mitochondria sensitive to the steady-state production of superoxide, decrease the steady-state flux of H(2)O(2), expedite the loss of mitochondrial function, and potentiate apoptosis.	Hydrogen Peroxide	228-236	superoxide dismutase 2	Homo sapiens	39-44
17142144-15	2006	In conclusion, our results suggest that V16A polymorphism of the Mn-SOD gene is not related to the development of diabetes and progression of DR, but is associated with DME in Korean type 2 diabetic patients.	dme	169-172	superoxide dismutase 2	Homo sapiens	65-71
17050167-2	2006	We altered the intracellular status of ROS by the overexpression of manganese superoxide dismutase (MnSOD) and/or catalase.	Reactive Oxygen Species	39-42	superoxide dismutase 2	Homo sapiens	68-98
16931792-10	2006	Transfection of EPCs with MnSOD-RNAi resulted in a reduction in CRP-induced ROS production, apoptosis, and telomerase inactivation.	Reactive Oxygen Species	76-79	superoxide dismutase 2	Homo sapiens	26-31
17140381-2	2006	Significant increase in mRNA level and activity of Mn-superoxide dismutase (Mn-SOD), catalase, and selenium-dependent glutathione peroxidase-1 (GPx-1) and reduced ROS level was found in resistant K562/DOX and SKVLB cells.	Reactive Oxygen Species	163-166	superoxide dismutase 2	Homo sapiens	51-74
17140381-2	2006	Significant increase in mRNA level and activity of Mn-superoxide dismutase (Mn-SOD), catalase, and selenium-dependent glutathione peroxidase-1 (GPx-1) and reduced ROS level was found in resistant K562/DOX and SKVLB cells.	Doxorubicin	201-204	superoxide dismutase 2	Homo sapiens	51-74
17140381-2	2006	Significant increase in mRNA level and activity of Mn-superoxide dismutase (Mn-SOD), catalase, and selenium-dependent glutathione peroxidase-1 (GPx-1) and reduced ROS level was found in resistant K562/DOX and SKVLB cells.	Doxorubicin	201-204	superoxide dismutase 2	Homo sapiens	76-82
17079457-9	2006	In addition, manganese superoxide dismutase, a major mitochondrial antioxidant enzyme, exhibits increased immunoreactivity but decreased enzyme activity in unstable clones, which along with decreased respiration rates may explain the increased levels of cellular ROS.	Reactive Oxygen Species	263-266	superoxide dismutase 2	Homo sapiens	13-43
17050167-2	2006	We altered the intracellular status of ROS by the overexpression of manganese superoxide dismutase (MnSOD) and/or catalase.	Reactive Oxygen Species	39-42	superoxide dismutase 2	Homo sapiens	100-105
17050167-5	2006	The overexpression of MnSOD enhanced the accumulation of 8-oxodGuo by UV.	8-ohdg	57-66	superoxide dismutase 2	Homo sapiens	22-27
17050167-6	2006	The co-overexpression of catalase inhibited the accumulation of 8-oxodGuo by UV in MnSOD-transfectants.	8-ohdg	64-73	superoxide dismutase 2	Homo sapiens	83-88
17050167-10	2006	Our results suggest that the accumulation of hydrogen peroxide plays a key role in the oxidative damage to mtDNA of UV-irradiated cells, and also that the overexpression of both MnSOD and catalase reduces the mtDNA damage and blocks the growth inhibition by UV.	Hydrogen Peroxide	45-62	superoxide dismutase 2	Homo sapiens	178-183
16956821-4	2006	Genetic variation in the genes coding for these enzymes (SOD2, GPX1, and CAT, respectively) alters ROS production and therefore may provide a mechanism for the relationship between inflammation and NHL.	Reactive Oxygen Species	99-102	superoxide dismutase 2	Homo sapiens	57-61
17015180-0	2006	A new paradigm: manganese superoxide dismutase influences the production of H2O2 in cells and thereby their biological state.	Hydrogen Peroxide	76-80	superoxide dismutase 2	Homo sapiens	16-46
17015180-1	2006	The principal source of hydrogen peroxide in mitochondria is thought to be from the dismutation of superoxide via the enzyme manganese superoxide dismutase (MnSOD).	Hydrogen Peroxide	24-41	superoxide dismutase 2	Homo sapiens	125-155
17015180-1	2006	The principal source of hydrogen peroxide in mitochondria is thought to be from the dismutation of superoxide via the enzyme manganese superoxide dismutase (MnSOD).	Hydrogen Peroxide	24-41	superoxide dismutase 2	Homo sapiens	157-162
17015180-1	2006	The principal source of hydrogen peroxide in mitochondria is thought to be from the dismutation of superoxide via the enzyme manganese superoxide dismutase (MnSOD).	Superoxides	99-109	superoxide dismutase 2	Homo sapiens	125-155
17015180-1	2006	The principal source of hydrogen peroxide in mitochondria is thought to be from the dismutation of superoxide via the enzyme manganese superoxide dismutase (MnSOD).	Superoxides	99-109	superoxide dismutase 2	Homo sapiens	157-162
17015180-8	2006	We measured the rate of release of H(2)O(2) into culture medium from cells with differing levels of MnSOD.	Hydrogen Peroxide	35-43	superoxide dismutase 2	Homo sapiens	100-105
17015180-13	2006	These observations indicate that MnSOD contributes to the flux of H(2)O(2) in cells and thereby is involved in establishing the cellular redox environment and thus the biological state of the cell.	Hydrogen Peroxide	66-74	superoxide dismutase 2	Homo sapiens	33-38
16713057-3	2006	The enzyme is inhibited by sodium azide and inactivated by hydrogen peroxide; it is also very sensitive to peroxynitrite, a physiological inactivator of the human mitochondrial Mn-SOD.	Sodium Azide	27-39	superoxide dismutase 2	Homo sapiens	177-183
16713057-3	2006	The enzyme is inhibited by sodium azide and inactivated by hydrogen peroxide; it is also very sensitive to peroxynitrite, a physiological inactivator of the human mitochondrial Mn-SOD.	Hydrogen Peroxide	59-76	superoxide dismutase 2	Homo sapiens	177-183
16713057-3	2006	The enzyme is inhibited by sodium azide and inactivated by hydrogen peroxide; it is also very sensitive to peroxynitrite, a physiological inactivator of the human mitochondrial Mn-SOD.	Peroxynitrous Acid	107-120	superoxide dismutase 2	Homo sapiens	177-183
17965603-4	2006	Analysis of a region in the SOD2 promoter by sodium bisulfite genomic sequencing demonstrated significantly higher levels of CpG methylation in both human breast carcinoma cell lines assessed than in MCF-10A cells.	sodium bisulfite	45-61	superoxide dismutase 2	Homo sapiens	28-32
17965603-6	2006	Increased cytosine methylation was also accompanied by a significant decrease in the level of acetylated histones in the same region of the SOD2 promoter.	Cytosine	10-18	superoxide dismutase 2	Homo sapiens	140-144
17965603-7	2006	Finally, a causal link between cytosine methylation and transcriptional repression was established by increasing MnSOD mRNA, protein and activity in breast carcinoma cells using the DNA methyltransferase inhibitor 5-aza-2"-deoxycytidine.	Cytosine	31-39	superoxide dismutase 2	Homo sapiens	113-118
17965603-7	2006	Finally, a causal link between cytosine methylation and transcriptional repression was established by increasing MnSOD mRNA, protein and activity in breast carcinoma cells using the DNA methyltransferase inhibitor 5-aza-2"-deoxycytidine.	Decitabine	214-236	superoxide dismutase 2	Homo sapiens	113-118
16626843-1	2006	This study examined the relationship between a MnSOD gene (MnSOD) polymorphism (Ala-9Val) and mood disorders such as major depressive disorder (MDD) and bipolar I disorder (BD).	Alanine	80-83	superoxide dismutase 2	Homo sapiens	47-52
16626843-1	2006	This study examined the relationship between a MnSOD gene (MnSOD) polymorphism (Ala-9Val) and mood disorders such as major depressive disorder (MDD) and bipolar I disorder (BD).	Alanine	80-83	superoxide dismutase 2	Homo sapiens	59-64
16626843-1	2006	This study examined the relationship between a MnSOD gene (MnSOD) polymorphism (Ala-9Val) and mood disorders such as major depressive disorder (MDD) and bipolar I disorder (BD).	9val	84-88	superoxide dismutase 2	Homo sapiens	47-52
16626843-1	2006	This study examined the relationship between a MnSOD gene (MnSOD) polymorphism (Ala-9Val) and mood disorders such as major depressive disorder (MDD) and bipolar I disorder (BD).	9val	84-88	superoxide dismutase 2	Homo sapiens	59-64
16626843-3	2006	The patients with MDD and BD, and the controls had a similar distribution of the genotypes and alleles in the Ala-9Val MnSOD polymorphism.	ala-9val	110-118	superoxide dismutase 2	Homo sapiens	119-124
16807759-0	2006	Association analysis of SOD2 variants with methamphetamine psychosis in Japanese and Taiwanese populations.	Methamphetamine	43-58	superoxide dismutase 2	Homo sapiens	24-28
17165602-4	2006	Manganese plays significant role in the free radical defense system as MnSOD, which protects the endothelial and red blood cells and mitochondria from the damage caused by superoxide radicals.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	71-76
17165602-4	2006	Manganese plays significant role in the free radical defense system as MnSOD, which protects the endothelial and red blood cells and mitochondria from the damage caused by superoxide radicals.	Superoxides	172-182	superoxide dismutase 2	Homo sapiens	71-76
16933053-0	2006	Manganese superoxide dismutase Ala-9Val polymorphism, environmental modifiers, and risk of breast cancer in a German population.	ala-9val	31-39	superoxide dismutase 2	Homo sapiens	0-30
16933053-1	2006	OBJECTIVE: A functional polymorphism at codon 16 (Alanine-to-Valine) of manganese superoxide dismutase (MnSOD) has been hypothesized to increase the risk of breast cancer and to modify the effects of oxidative stress.	Alanine	50-57	superoxide dismutase 2	Homo sapiens	72-102
16933053-1	2006	OBJECTIVE: A functional polymorphism at codon 16 (Alanine-to-Valine) of manganese superoxide dismutase (MnSOD) has been hypothesized to increase the risk of breast cancer and to modify the effects of oxidative stress.	Alanine	50-57	superoxide dismutase 2	Homo sapiens	104-109
16933053-1	2006	OBJECTIVE: A functional polymorphism at codon 16 (Alanine-to-Valine) of manganese superoxide dismutase (MnSOD) has been hypothesized to increase the risk of breast cancer and to modify the effects of oxidative stress.	Valine	61-67	superoxide dismutase 2	Homo sapiens	72-102
16933053-1	2006	OBJECTIVE: A functional polymorphism at codon 16 (Alanine-to-Valine) of manganese superoxide dismutase (MnSOD) has been hypothesized to increase the risk of breast cancer and to modify the effects of oxidative stress.	Valine	61-67	superoxide dismutase 2	Homo sapiens	104-109
16933053-8	2006	CONCLUSIONS: The MnSOD Ala-9Val polymorphism may contribute to an increase in breast cancer risk in the context of high alcohol consumption, however the polymorphism is not an overall risk factor for breast cancer in this primarily premenopausal population.	ala-9val	23-31	superoxide dismutase 2	Homo sapiens	17-22
16933053-8	2006	CONCLUSIONS: The MnSOD Ala-9Val polymorphism may contribute to an increase in breast cancer risk in the context of high alcohol consumption, however the polymorphism is not an overall risk factor for breast cancer in this primarily premenopausal population.	Alcohols	120-127	superoxide dismutase 2	Homo sapiens	17-22
16969494-0	2006	Breast cancer risk and polymorphisms in genes involved in metabolism of estrogens (CYP17, HSD17beta1, COMT and MnSOD): possible protective role of MnSOD gene polymorphism Val/Ala and Ala/Ala in women that never breast fed.	Valine	171-174	superoxide dismutase 2	Homo sapiens	147-152
18648594-11	2006	Recent findings suggest that employment of DR and multiple antioxidant agents (including, catalase, glutathione peroxidase, CuZn superoxide dismutase, and Mn superoxide dismutase = enzymes forming the primary defense against oxygen toxicity), and ozone therapy may mount an effective resistance to pathogenic factors relevant to the pathogenesis of cardiovascular episodes.	Oxygen	225-231	superoxide dismutase 2	Homo sapiens	155-178
16543247-9	2006	In an analysis of manganese superoxide dismutase (SOD2 Val16Ala, rs1799725) Ala/Ala homozygotes, we observed moderately increased risks for B-cell lymphomas (OR=1.3, 95% CI=1.0-1.6; referent=Val/Val and Val/Ala) that was consistent across the B-cell subtypes.	Alanine	60-63	superoxide dismutase 2	Homo sapiens	50-54
16543247-9	2006	In an analysis of manganese superoxide dismutase (SOD2 Val16Ala, rs1799725) Ala/Ala homozygotes, we observed moderately increased risks for B-cell lymphomas (OR=1.3, 95% CI=1.0-1.6; referent=Val/Val and Val/Ala) that was consistent across the B-cell subtypes.	Alanine	76-79	superoxide dismutase 2	Homo sapiens	50-54
16543247-9	2006	In an analysis of manganese superoxide dismutase (SOD2 Val16Ala, rs1799725) Ala/Ala homozygotes, we observed moderately increased risks for B-cell lymphomas (OR=1.3, 95% CI=1.0-1.6; referent=Val/Val and Val/Ala) that was consistent across the B-cell subtypes.	Valine	55-58	superoxide dismutase 2	Homo sapiens	50-54
16543247-9	2006	In an analysis of manganese superoxide dismutase (SOD2 Val16Ala, rs1799725) Ala/Ala homozygotes, we observed moderately increased risks for B-cell lymphomas (OR=1.3, 95% CI=1.0-1.6; referent=Val/Val and Val/Ala) that was consistent across the B-cell subtypes.	Alanine	76-79	superoxide dismutase 2	Homo sapiens	50-54
16807759-3	2006	Hence, we investigated the association of SOD2 polymorphisms with the development of methamphetamine psychosis, in two independent populations of Japan and Taiwan.	Methamphetamine	85-100	superoxide dismutase 2	Homo sapiens	42-46
16945136-11	2006	RESULTS: While neither allele alone shows any change in breast cancer risk, an increase in the risk of breast cancer (OR 1.87, 95% CI 1.09 - 3.19) is observed in individuals who carry both the Ala16Ala genotype of MnSOD and the Leu198Leu genotype of GPX-1.	ala16ala	193-201	superoxide dismutase 2	Homo sapiens	214-219
16807759-7	2006	Our results suggest that Ala/Val polymorphism of the SOD2 gene could be associated with the risk of developing methamphetamine psychosis.	Alanine	25-28	superoxide dismutase 2	Homo sapiens	53-57
16807759-7	2006	Our results suggest that Ala/Val polymorphism of the SOD2 gene could be associated with the risk of developing methamphetamine psychosis.	Valine	29-32	superoxide dismutase 2	Homo sapiens	53-57
16807759-7	2006	Our results suggest that Ala/Val polymorphism of the SOD2 gene could be associated with the risk of developing methamphetamine psychosis.	Methamphetamine	111-126	superoxide dismutase 2	Homo sapiens	53-57
16765446-3	2006	The only evidence for any Mn(3+) complex is found in a spectrum essentially identical to that of mitochondrial manganese superoxide dismutase (MnSOD).	manganese(III) acetate dihydrate	26-32	superoxide dismutase 2	Homo sapiens	143-148
17217237-4	2006	Manganese superoxide dismutase (MnSOD) plays a key role in protection against ROS.	Reactive Oxygen Species	78-81	superoxide dismutase 2	Homo sapiens	0-30
17217237-4	2006	Manganese superoxide dismutase (MnSOD) plays a key role in protection against ROS.	Reactive Oxygen Species	78-81	superoxide dismutase 2	Homo sapiens	32-37
17217237-12	2006	CONCLUSION: In the Polish population there is a statistically substantial association between schizophrenia incidence and the Val-9Val genotype in a gene for MnSOD.	Valine	126-129	superoxide dismutase 2	Homo sapiens	158-163
17217237-13	2006	Schizophrenic patients having a Val-9Val genotype in the gene for MnSOD have nearly a ten times higher risk for developing TD than schizophrenics not having this genotype.	Valine	32-35	superoxide dismutase 2	Homo sapiens	66-71
17217237-14	2006	Risk for developing schizophrenia for people having the Val-9Val genotype in the gene for MnSOD is over three times higher than for people lacking this genotype.	Valine	56-59	superoxide dismutase 2	Homo sapiens	90-95
16910769-4	2006	Because of its mitochondrial location, superoxide dismutase (SOD2) is the principal defense against the toxicity of superoxide anions generated by the oxidative phosphorylation.	Superoxides	116-133	superoxide dismutase 2	Homo sapiens	61-65
16837928-11	2006	Supplementation of SOD activity with EUK-8 reduced ROS, and interleukin-6 protein expression was suppressed by both mitochondrial inhibition and SOD augmentation.	Reactive Oxygen Species	51-54	superoxide dismutase 2	Homo sapiens	19-22
16819819-3	2006	Human MnSOD was prepared in which all nine tyrosine residues in each subunit are replaced with 3-fluorotyrosine.	Tyrosine	43-51	superoxide dismutase 2	Homo sapiens	6-11
16819819-3	2006	Human MnSOD was prepared in which all nine tyrosine residues in each subunit are replaced with 3-fluorotyrosine.	3-fluorotyrosine	95-111	superoxide dismutase 2	Homo sapiens	6-11
16819819-8	2006	Using this approach, amide hydrogen exchange kinetics were measured for regions comprising 78% of the MnSOD backbone.	Amides	21-26	superoxide dismutase 2	Homo sapiens	102-107
16819819-8	2006	Using this approach, amide hydrogen exchange kinetics were measured for regions comprising 78% of the MnSOD backbone.	Hydrogen	27-35	superoxide dismutase 2	Homo sapiens	102-107
16740634-10	2006	Using ChIP assays and immunoprecipitation, we further demonstrated that p53 interacts with Sp1 to suppress both the constitutive and 12-O-tetradecanoylphorbol-13-acetate-stimulated expression of the MnSOD gene.	Tetradecanoylphorbol Acetate	133-169	superoxide dismutase 2	Homo sapiens	199-204
18489268-7	2006	As MnSOD is a major inducible free-radical scavenger in skin, these results suggest that the Vfe could induce skin cells to produce their own endogenous protective defences in vivo against both exogenous environmental stressors such as UV irradiation or microflora as well as to combat endogenous sources of deleterious free radicals involved in skin ageing.	Free Radicals	320-333	superoxide dismutase 2	Homo sapiens	3-8
16814103-1	2006	We have studied the effects of overexpression of superoxide dismutase (SOD), a tumor suppressor protein that dismutes superoxide radical to H2O2, on breast cancer cell growth in vitro and xenograft growth in vivo.	Superoxides	118-136	superoxide dismutase 2	Homo sapiens	71-74
16814103-1	2006	We have studied the effects of overexpression of superoxide dismutase (SOD), a tumor suppressor protein that dismutes superoxide radical to H2O2, on breast cancer cell growth in vitro and xenograft growth in vivo.	Hydrogen Peroxide	140-144	superoxide dismutase 2	Homo sapiens	71-74
16910769-6	2006	We became interested in the role SOD2 plays in the metabolism of superoxide anions during erythroid development, as anemia is the major phenotype in transplanted animals.	Superoxides	65-82	superoxide dismutase 2	Homo sapiens	33-37
16910775-8	2006	MnSOD overexpression did prevent radiation-induced decreases in total glutathione content, which correlated with radioresistance and enhanced G(2) accumulation.	Glutathione	70-81	superoxide dismutase 2	Homo sapiens	0-5
16910776-4	2006	To examine this question, we used site-directed mutagenesis to produce a mutant form of human MnSOD that has a leucine at amino acid 26 in the active site rather than the usual histidine.	Leucine	111-118	superoxide dismutase 2	Homo sapiens	94-99
16910776-4	2006	To examine this question, we used site-directed mutagenesis to produce a mutant form of human MnSOD that has a leucine at amino acid 26 in the active site rather than the usual histidine.	Histidine	177-186	superoxide dismutase 2	Homo sapiens	94-99
16910777-2	2006	Here we demonstrate that the antiapoptotic effects of SOD2 are attributed to its ability to generate H(2)O(2) and that its efficient removal resensitizes cells to tumor necrosis factor (TNF)-alpha-induced apoptosis.	Hydrogen Peroxide	101-109	superoxide dismutase 2	Homo sapiens	54-58
16910777-3	2006	SOD2 overexpression in HT-1080 cells leads to a decrease in the fluorescence of the superoxidesensitive fluorophore, dihydroethidium, and a concomitant increase in oxidation of the H2O2-sensitive dye, dichlorodihydrofluorescein diacetate (DCFDA).	dihydroethidium	117-132	superoxide dismutase 2	Homo sapiens	0-4
16910777-3	2006	SOD2 overexpression in HT-1080 cells leads to a decrease in the fluorescence of the superoxidesensitive fluorophore, dihydroethidium, and a concomitant increase in oxidation of the H2O2-sensitive dye, dichlorodihydrofluorescein diacetate (DCFDA).	Hydrogen Peroxide	181-185	superoxide dismutase 2	Homo sapiens	0-4
16910777-3	2006	SOD2 overexpression in HT-1080 cells leads to a decrease in the fluorescence of the superoxidesensitive fluorophore, dihydroethidium, and a concomitant increase in oxidation of the H2O2-sensitive dye, dichlorodihydrofluorescein diacetate (DCFDA).	dichlorodihydrofluorescein diacetate	201-237	superoxide dismutase 2	Homo sapiens	0-4
16910777-3	2006	SOD2 overexpression in HT-1080 cells leads to a decrease in the fluorescence of the superoxidesensitive fluorophore, dihydroethidium, and a concomitant increase in oxidation of the H2O2-sensitive dye, dichlorodihydrofluorescein diacetate (DCFDA).	diacetyldichlorofluorescein	239-244	superoxide dismutase 2	Homo sapiens	0-4
16910777-4	2006	The rate of aminotriazole-inhibited catalase activity also was increased when SOD2 is overexpressed and reflects a 1.6-fold increase in the steady-state production of H(2)O(2).	Amitrole	12-25	superoxide dismutase 2	Homo sapiens	78-82
16910777-4	2006	The rate of aminotriazole-inhibited catalase activity also was increased when SOD2 is overexpressed and reflects a 1.6-fold increase in the steady-state production of H(2)O(2).	Water	167-172	superoxide dismutase 2	Homo sapiens	78-82
16828895-8	2006	In the case of mitochondrial MnSOD of eukaryotes (SOD2), metal insertion cannot occur post-translationally, but requires new synthesis and mitochondrial import of the SOD2 polypeptide.	Metals	57-62	superoxide dismutase 2	Homo sapiens	50-54
16910777-8	2006	These findings indicate that increases in the intracellular steady-state production of H(2)O(2) by SOD2 can block the activation of key processes fundamental to the process of programmed cell death.	Hydrogen Peroxide	87-95	superoxide dismutase 2	Homo sapiens	99-103
16828895-8	2006	In the case of mitochondrial MnSOD of eukaryotes (SOD2), metal insertion cannot occur post-translationally, but requires new synthesis and mitochondrial import of the SOD2 polypeptide.	Metals	57-62	superoxide dismutase 2	Homo sapiens	167-171
16571366-0	2006	Comments on "Association between Ala-9Val polymorphism of MnSOD gene and schizophrenia" by O. Akyol et al.	ala-9val	33-41	superoxide dismutase 2	Homo sapiens	58-63
16828895-9	2006	SOD2 can also bind iron in vivo, but is inactive with iron.	Iron	19-23	superoxide dismutase 2	Homo sapiens	0-4
16828895-10	2006	Such metal ion mis-incorporation with SOD2 can become prevalent upon disruption of mitochondrial metal homeostasis.	Metals	5-10	superoxide dismutase 2	Homo sapiens	38-42
16828895-10	2006	Such metal ion mis-incorporation with SOD2 can become prevalent upon disruption of mitochondrial metal homeostasis.	Metals	97-102	superoxide dismutase 2	Homo sapiens	38-42
16785027-5	2006	Furthermore, we found that activation of PKCdelta by bistratene A increased the intracellular levels of H(2)O(2) and MnSOD protein expression.	bistratene A	53-65	superoxide dismutase 2	Homo sapiens	117-122
16785027-6	2006	By contrast, suppression of PKCdelta by rottlerin decreased the intracellular levels of H(2)O(2) and MnSOD protein expression.	rottlerin	40-49	superoxide dismutase 2	Homo sapiens	101-106
29313210-6	2006	Consequently, induction of MnSOD by TNF-alpha primes neuronal cells to develop resistance against subsequent exposure to beta-amyloid and FeSO4.	ferrous sulfate	138-143	superoxide dismutase 2	Homo sapiens	27-32
16785034-6	2006	Overexpression of human manganese superoxide dismutase in PAEC reduced O(2)*(-) levels and attenuated cytotoxicity resulting from treatment with H(2)O(2).	Water	145-150	superoxide dismutase 2	Homo sapiens	24-54
16769586-1	2006	Manganese superoxide dismutase (MnSOD) protects cells against oxidative stress by eliminating superoxides.	Superoxides	94-105	superoxide dismutase 2	Homo sapiens	0-30
16769586-1	2006	Manganese superoxide dismutase (MnSOD) protects cells against oxidative stress by eliminating superoxides.	Superoxides	94-105	superoxide dismutase 2	Homo sapiens	32-37
16644673-4	2006	Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	89-92	superoxide dismutase 2	Homo sapiens	186-216
16644673-4	2006	Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	89-92	superoxide dismutase 2	Homo sapiens	218-223
16636651-12	2006	In addition, TBHP induced the expression of MTIIa, heme oxygenase-1, thioredoxin reductase-1, and MnSOD in both normal and MTIIa over-expressed cell lines.	tert-Butylhydroperoxide	13-17	superoxide dismutase 2	Homo sapiens	98-103
16506247-3	2006	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Superoxides	94-111	superoxide dismutase 2	Homo sapiens	23-53
16506247-3	2006	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Superoxides	94-111	superoxide dismutase 2	Homo sapiens	55-59
16506247-3	2006	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Hydrogen Peroxide	117-134	superoxide dismutase 2	Homo sapiens	23-53
16506247-3	2006	The antioxidant enzyme manganese superoxide dismutase (SOD2) catalyzes the dismutation of the superoxide anions into hydrogen peroxide.	Hydrogen Peroxide	117-134	superoxide dismutase 2	Homo sapiens	55-59
16510607-1	2006	Manganese superoxide dismutase (MnSOD) converts the superoxide anion into H(2)O(2), which, unless it is detoxified by glutathione peroxidase 1 (GPx1), can increase hepatic iron and can react with iron to form genotoxic compounds.	Superoxides	52-68	superoxide dismutase 2	Homo sapiens	32-37
16618754-7	2006	Our results showed that the production of hydrogen peroxide derived from MnSOD dismutation activated caspase-8, which might down-regulate Bcl-2 expression and induce Bax translocation to mitochondria.	Hydrogen Peroxide	42-59	superoxide dismutase 2	Homo sapiens	73-78
16428241-7	2006	This important amount of Mn-SOD is a primary antioxidant defense system against superoxide radicals, but its product, H(2)O(2), is also deleterious for cells.	Superoxides	80-90	superoxide dismutase 2	Homo sapiens	25-31
16599945-3	2006	Both the deformed astrocytes and the GFSBs contained ferric iron and were intensely immunolabelled with antibodies against the antioxidant proteins ferritin and manganese superoxide dismutase (Mn SOD).	gfsbs	37-42	superoxide dismutase 2	Homo sapiens	161-191
16599945-3	2006	Both the deformed astrocytes and the GFSBs contained ferric iron and were intensely immunolabelled with antibodies against the antioxidant proteins ferritin and manganese superoxide dismutase (Mn SOD).	gfsbs	37-42	superoxide dismutase 2	Homo sapiens	193-199
16599945-5	2006	The intense immunolabelling of ferritin and Mn SOD most likely reflects a defensive response to iron-mediated oxidative stress.	Iron	96-100	superoxide dismutase 2	Homo sapiens	44-50
16540396-17	2006	A persistent marked elevation of MnSOD in cells following their exposure to a thiol-containing reducing agent such as WR1065 can result in an elevated resistance to the cytotoxic effects of ionizing radiation and represents a novel radioprotection paradigm.	Sulfhydryl Compounds	78-83	superoxide dismutase 2	Homo sapiens	33-38
16412983-5	2006	Exogenously added catalase also protected cells from Cu[DEDTC]2, suggesting that this complex may kill after the levels of superoxide anion [O2*-] dismutated by MnSOD increase hydrogen peroxide-related stress.	Superoxides	123-139	superoxide dismutase 2	Homo sapiens	161-166
16412983-5	2006	Exogenously added catalase also protected cells from Cu[DEDTC]2, suggesting that this complex may kill after the levels of superoxide anion [O2*-] dismutated by MnSOD increase hydrogen peroxide-related stress.	Superoxides	141-143	superoxide dismutase 2	Homo sapiens	161-166
16412983-5	2006	Exogenously added catalase also protected cells from Cu[DEDTC]2, suggesting that this complex may kill after the levels of superoxide anion [O2*-] dismutated by MnSOD increase hydrogen peroxide-related stress.	Hydrogen Peroxide	176-193	superoxide dismutase 2	Homo sapiens	161-166
16510607-1	2006	Manganese superoxide dismutase (MnSOD) converts the superoxide anion into H(2)O(2), which, unless it is detoxified by glutathione peroxidase 1 (GPx1), can increase hepatic iron and can react with iron to form genotoxic compounds.	Superoxides	52-68	superoxide dismutase 2	Homo sapiens	0-30
16458347-1	2006	INTRODUCTION AND OBJECTIVE: Manganese superoxide dismutase (MnSOD), an enzyme that catalyzes superoxide radical quenching, is hypothesized to protect against premature aging.	Superoxides	38-48	superoxide dismutase 2	Homo sapiens	60-65
16510607-1	2006	Manganese superoxide dismutase (MnSOD) converts the superoxide anion into H(2)O(2), which, unless it is detoxified by glutathione peroxidase 1 (GPx1), can increase hepatic iron and can react with iron to form genotoxic compounds.	Hydrogen Peroxide	74-82	superoxide dismutase 2	Homo sapiens	0-30
16510607-1	2006	Manganese superoxide dismutase (MnSOD) converts the superoxide anion into H(2)O(2), which, unless it is detoxified by glutathione peroxidase 1 (GPx1), can increase hepatic iron and can react with iron to form genotoxic compounds.	Hydrogen Peroxide	74-82	superoxide dismutase 2	Homo sapiens	32-37
16510607-1	2006	Manganese superoxide dismutase (MnSOD) converts the superoxide anion into H(2)O(2), which, unless it is detoxified by glutathione peroxidase 1 (GPx1), can increase hepatic iron and can react with iron to form genotoxic compounds.	Iron	172-176	superoxide dismutase 2	Homo sapiens	0-30
16510607-1	2006	Manganese superoxide dismutase (MnSOD) converts the superoxide anion into H(2)O(2), which, unless it is detoxified by glutathione peroxidase 1 (GPx1), can increase hepatic iron and can react with iron to form genotoxic compounds.	Iron	172-176	superoxide dismutase 2	Homo sapiens	32-37
16510607-1	2006	Manganese superoxide dismutase (MnSOD) converts the superoxide anion into H(2)O(2), which, unless it is detoxified by glutathione peroxidase 1 (GPx1), can increase hepatic iron and can react with iron to form genotoxic compounds.	Iron	196-200	superoxide dismutase 2	Homo sapiens	0-30
16510607-1	2006	Manganese superoxide dismutase (MnSOD) converts the superoxide anion into H(2)O(2), which, unless it is detoxified by glutathione peroxidase 1 (GPx1), can increase hepatic iron and can react with iron to form genotoxic compounds.	Iron	196-200	superoxide dismutase 2	Homo sapiens	32-37
16489745-10	2006	A Ca(2+) dose-dependent dephosphorylation of MnSOD was associated with an approximately 2-fold maximum increase in activity; neither the dephosphorylation nor activity changes were induced by ROS production in the absence of Ca(2+).	Reactive Oxygen Species	192-195	superoxide dismutase 2	Homo sapiens	45-50
16780268-2	2006	ROS concentration in cells is maintained on a low level due to manganese superoxide dismutase activity (MnSOD).	Reactive Oxygen Species	0-3	superoxide dismutase 2	Homo sapiens	104-109
16780268-3	2006	THE AIM OF THE WORK: An attempt of evaluation of Ala-9Val polymorphism in gene for MnSOD in schizophrenic patients and control group was undertaken.	ala-9val	49-57	superoxide dismutase 2	Homo sapiens	83-88
16780268-14	2006	The lack of association between selected social - demographic and clinical factors of schizophrenic patients and Ala-9Val polymorphism in a gene for MnSOD.	ala-9val	113-121	superoxide dismutase 2	Homo sapiens	149-154
16780268-16	2006	Risk for developing schizophrenia in people having Val-9Val genotype in a gene for MnSOD is over three times higher than for people not having this very genotype.	Valine	51-54	superoxide dismutase 2	Homo sapiens	83-88
16423340-1	2006	OBJECTIVES: To investigate the possible association between functional variant Ala-9Val in the MnSOD gene and asthma in the case-control study comprising 626 Caucasian subjects.	ala-9val	79-87	superoxide dismutase 2	Homo sapiens	95-100
16780268-2	2006	ROS concentration in cells is maintained on a low level due to manganese superoxide dismutase activity (MnSOD).	Reactive Oxygen Species	0-3	superoxide dismutase 2	Homo sapiens	63-93
16390819-6	2006	Oestradiol induces glutathione peroxidase-1 and MnSOD by processes requiring the cell surface oestrogen receptor (ER) and the activation of pathways usually involved in oxidative stress response.	Estradiol	0-10	superoxide dismutase 2	Homo sapiens	48-53
16173037-12	2006	Superoxide is a by-product of selenite metabolism and normal cells showed increased MnSOD expression and SOD activity compared to the cancer-derived cells.	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	84-89
16443160-2	2006	Reaction of peroxynitrite with manganese superoxide dismutase (MnSOD) causes nitration of the active-site residue Tyr34 and nearly complete inhibition of catalysis.	Peroxynitrous Acid	12-25	superoxide dismutase 2	Homo sapiens	31-61
16443160-2	2006	Reaction of peroxynitrite with manganese superoxide dismutase (MnSOD) causes nitration of the active-site residue Tyr34 and nearly complete inhibition of catalysis.	Peroxynitrous Acid	12-25	superoxide dismutase 2	Homo sapiens	63-68
16443160-3	2006	We report the crystal structures at 2.4 A resolution of human MnSOD nitrated by peroxynitrite and the unmodified MnSOD.	Peroxynitrous Acid	80-93	superoxide dismutase 2	Homo sapiens	62-67
16173037-12	2006	Superoxide is a by-product of selenite metabolism and normal cells showed increased MnSOD expression and SOD activity compared to the cancer-derived cells.	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	86-89
16173037-12	2006	Superoxide is a by-product of selenite metabolism and normal cells showed increased MnSOD expression and SOD activity compared to the cancer-derived cells.	Selenious Acid	30-38	superoxide dismutase 2	Homo sapiens	84-89
16173037-12	2006	Superoxide is a by-product of selenite metabolism and normal cells showed increased MnSOD expression and SOD activity compared to the cancer-derived cells.	Selenious Acid	30-38	superoxide dismutase 2	Homo sapiens	86-89
16173037-13	2006	Prostate cancer cells treated with the MnSOD mimetic, MnTMPyP, were protected against the cytotoxic effects of selenite.	Selenious Acid	111-119	superoxide dismutase 2	Homo sapiens	39-44
16173037-14	2006	CONCLUSIONS: Higher MnSOD expression in normal cells may play an important role in eliminating superoxide radicals produced as a result of selenite metabolism and contribute to the tumor-selective killing by selenite in prostate cancer.	Superoxides	95-105	superoxide dismutase 2	Homo sapiens	20-25
16859522-1	2006	BACKGROUND: Manganese superoxide dismutase (MnSOD) plays a critical role in the detoxification of mitochondrial reactive oxygen species, constituting a major cellular defense mechanism against agents that induce oxidative stress.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	12-42
16084535-7	2006	We suggest that the oxidative injury caused by PAH exposure is modulated by genetic polymorphisms such as MnSOD and MPO.	p-Aminohippuric Acid	47-50	superoxide dismutase 2	Homo sapiens	106-111
16141349-5	2006	Essentially all of these events were reversed by free radical scavengers such as the manganese superoxide dismutase (MnSOD) mimetic TBAP and catalase.	Free Radicals	49-61	superoxide dismutase 2	Homo sapiens	85-115
16141349-5	2006	Essentially all of these events were reversed by free radical scavengers such as the manganese superoxide dismutase (MnSOD) mimetic TBAP and catalase.	Free Radicals	49-61	superoxide dismutase 2	Homo sapiens	117-122
16141349-5	2006	Essentially all of these events were reversed by free radical scavengers such as the manganese superoxide dismutase (MnSOD) mimetic TBAP and catalase.	tbap	132-136	superoxide dismutase 2	Homo sapiens	85-115
16141349-5	2006	Essentially all of these events were reversed by free radical scavengers such as the manganese superoxide dismutase (MnSOD) mimetic TBAP and catalase.	tbap	132-136	superoxide dismutase 2	Homo sapiens	117-122
16141349-6	2006	Notably, treatment with 2-ME/HDACIs resulted in down-regulation of thioredoxin, MnSOD, and glutathione peroxidase.	Mercaptoethanol	24-28	superoxide dismutase 2	Homo sapiens	80-85
16084535-0	2006	Effect of genetic polymorphisms of MnSOD and MPO on the relationship between PAH exposure and oxidative DNA damage.	p-Aminohippuric Acid	77-80	superoxide dismutase 2	Homo sapiens	35-40
16084535-4	2006	However, significant differences of regression coefficient were found for the relation between urinary log 1-OHP and urinary 8-OHdG concentrations in the presence of different MnSOD or MPO genotypes by multiple regression after controlling for age, sex, body mass index, cotinine, and smoking.	Oxaliplatin	107-112	superoxide dismutase 2	Homo sapiens	176-181
16084535-4	2006	However, significant differences of regression coefficient were found for the relation between urinary log 1-OHP and urinary 8-OHdG concentrations in the presence of different MnSOD or MPO genotypes by multiple regression after controlling for age, sex, body mass index, cotinine, and smoking.	8-ohdg	125-131	superoxide dismutase 2	Homo sapiens	176-181
16084535-5	2006	In those with the MnSOD Val/Ala or Ala/Ala genotypes this regression coefficient was 1.480 (p=0.040), whereas for the MnSOD Val/Val genotype it was 0.088 (p=0.859).	Valine	24-27	superoxide dismutase 2	Homo sapiens	18-23
16084535-5	2006	In those with the MnSOD Val/Ala or Ala/Ala genotypes this regression coefficient was 1.480 (p=0.040), whereas for the MnSOD Val/Val genotype it was 0.088 (p=0.859).	Alanine	28-31	superoxide dismutase 2	Homo sapiens	18-23
16084535-6	2006	The higher regression coefficient was obtained for the subject group with the MnSOD Val/Ala or Ala/Ala genotype in combination with the MPO G/G genotype (p=0.012).	Valine	84-87	superoxide dismutase 2	Homo sapiens	78-83
16084535-6	2006	The higher regression coefficient was obtained for the subject group with the MnSOD Val/Ala or Ala/Ala genotype in combination with the MPO G/G genotype (p=0.012).	Alanine	88-91	superoxide dismutase 2	Homo sapiens	78-83
16859522-1	2006	BACKGROUND: Manganese superoxide dismutase (MnSOD) plays a critical role in the detoxification of mitochondrial reactive oxygen species, constituting a major cellular defense mechanism against agents that induce oxidative stress.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	44-49
16380484-4	2006	Treatment with metformin and AICAR inhibited hyperglycemia-induced intracellular and mtROS production, stimulated AMP-activated protein kinase (AMPK) activity, and increased the expression of peroxisome proliferator-activated response-gamma coactivator-1alpha (PGC-1alpha) and manganese superoxide dismutase (MnSOD) mRNAs.	Metformin	15-24	superoxide dismutase 2	Homo sapiens	277-307
16380484-4	2006	Treatment with metformin and AICAR inhibited hyperglycemia-induced intracellular and mtROS production, stimulated AMP-activated protein kinase (AMPK) activity, and increased the expression of peroxisome proliferator-activated response-gamma coactivator-1alpha (PGC-1alpha) and manganese superoxide dismutase (MnSOD) mRNAs.	Metformin	15-24	superoxide dismutase 2	Homo sapiens	309-314
16380484-8	2006	These results suggest that metformin normalizes hyperglycemia-induced mtROS production by induction of MnSOD and promotion of mitochondrial biogenesis through the activation of AMPK-PGC-1alpha pathway.	Metformin	27-36	superoxide dismutase 2	Homo sapiens	103-108
15904944-7	2005	After incubation for 16 h, rotenone significantly increased the expression and activity of MnSOD, GPx, and catalase.	Rotenone	27-35	superoxide dismutase 2	Homo sapiens	91-96
16571274-5	2006	Significantly higher levels of NF-kappaB and Mn-SOD (both their protein level and their activity) were found in breast cancer patients before and after CAF therapy, in comparison with healthy women.	cafestol palmitate	152-155	superoxide dismutase 2	Homo sapiens	45-51
16369462-1	2006	BACKGROUND: Manganese-dependent superoxide dismutase (MnSOD) is a major defense mechanism against potential cellular damage by reactive oxygen species (ROS).	Reactive Oxygen Species	127-150	superoxide dismutase 2	Homo sapiens	12-52
16369462-1	2006	BACKGROUND: Manganese-dependent superoxide dismutase (MnSOD) is a major defense mechanism against potential cellular damage by reactive oxygen species (ROS).	Reactive Oxygen Species	127-150	superoxide dismutase 2	Homo sapiens	54-59
16369462-1	2006	BACKGROUND: Manganese-dependent superoxide dismutase (MnSOD) is a major defense mechanism against potential cellular damage by reactive oxygen species (ROS).	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	12-52
16369462-1	2006	BACKGROUND: Manganese-dependent superoxide dismutase (MnSOD) is a major defense mechanism against potential cellular damage by reactive oxygen species (ROS).	Reactive Oxygen Species	152-155	superoxide dismutase 2	Homo sapiens	54-59
16847469-2	2006	In this study, we aim to investigate the manganese superoxide dismutase (MnSOD) polymorphism at nucleotide 47 as a result of the change of Ala to Val on the protein sequence in CPPS patients.	Alanine	139-142	superoxide dismutase 2	Homo sapiens	41-71
16847469-2	2006	In this study, we aim to investigate the manganese superoxide dismutase (MnSOD) polymorphism at nucleotide 47 as a result of the change of Ala to Val on the protein sequence in CPPS patients.	Alanine	139-142	superoxide dismutase 2	Homo sapiens	73-78
16847469-2	2006	In this study, we aim to investigate the manganese superoxide dismutase (MnSOD) polymorphism at nucleotide 47 as a result of the change of Ala to Val on the protein sequence in CPPS patients.	Valine	146-149	superoxide dismutase 2	Homo sapiens	41-71
16847469-2	2006	In this study, we aim to investigate the manganese superoxide dismutase (MnSOD) polymorphism at nucleotide 47 as a result of the change of Ala to Val on the protein sequence in CPPS patients.	Valine	146-149	superoxide dismutase 2	Homo sapiens	73-78
15904944-8	2005	When cells were preincubated with fraxetin, there was a decrease in the protein levels and activity of both MnSOD and catalase, in comparison with the rotenone treatment.	fraxetin	34-42	superoxide dismutase 2	Homo sapiens	108-113
16170370-12	2005	Coexpression of mitochondrial hydrogen peroxide-removing proteins prevented the accumulation of HIF-1alpha protein in cells with high levels of MnSOD; this effect demonstrates that the restabilization of HIF-1alpha observed in high MnSOD overexpressors is probably due to hydrogen peroxide, most likely produced from MnSOD.	Hydrogen Peroxide	30-47	superoxide dismutase 2	Homo sapiens	144-149
16170370-12	2005	Coexpression of mitochondrial hydrogen peroxide-removing proteins prevented the accumulation of HIF-1alpha protein in cells with high levels of MnSOD; this effect demonstrates that the restabilization of HIF-1alpha observed in high MnSOD overexpressors is probably due to hydrogen peroxide, most likely produced from MnSOD.	Hydrogen Peroxide	30-47	superoxide dismutase 2	Homo sapiens	232-237
16170370-12	2005	Coexpression of mitochondrial hydrogen peroxide-removing proteins prevented the accumulation of HIF-1alpha protein in cells with high levels of MnSOD; this effect demonstrates that the restabilization of HIF-1alpha observed in high MnSOD overexpressors is probably due to hydrogen peroxide, most likely produced from MnSOD.	Hydrogen Peroxide	30-47	superoxide dismutase 2	Homo sapiens	232-237
16170370-12	2005	Coexpression of mitochondrial hydrogen peroxide-removing proteins prevented the accumulation of HIF-1alpha protein in cells with high levels of MnSOD; this effect demonstrates that the restabilization of HIF-1alpha observed in high MnSOD overexpressors is probably due to hydrogen peroxide, most likely produced from MnSOD.	Hydrogen Peroxide	272-289	superoxide dismutase 2	Homo sapiens	144-149
16281056-1	2005	We have created P1 artificial chromosome transgenic mice expressing the human mitochondrial superoxide dismutase 2 (SOD2) and thus generated mice with a physiologically controlled augmentation of SOD2 expression leading to increased SOD2 enzyme activities and lowered superoxide levels.	Superoxides	92-102	superoxide dismutase 2	Homo sapiens	116-120
16170370-12	2005	Coexpression of mitochondrial hydrogen peroxide-removing proteins prevented the accumulation of HIF-1alpha protein in cells with high levels of MnSOD; this effect demonstrates that the restabilization of HIF-1alpha observed in high MnSOD overexpressors is probably due to hydrogen peroxide, most likely produced from MnSOD.	Hydrogen Peroxide	272-289	superoxide dismutase 2	Homo sapiens	232-237
16170370-12	2005	Coexpression of mitochondrial hydrogen peroxide-removing proteins prevented the accumulation of HIF-1alpha protein in cells with high levels of MnSOD; this effect demonstrates that the restabilization of HIF-1alpha observed in high MnSOD overexpressors is probably due to hydrogen peroxide, most likely produced from MnSOD.	Hydrogen Peroxide	272-289	superoxide dismutase 2	Homo sapiens	232-237
16485861-2	2005	Manganese superoxide dismutase (MnSOD) plays a major role in protecting the mitochondrion from oxidative damage due to superoxide radicals and other excited oxygen species.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
16485861-2	2005	Manganese superoxide dismutase (MnSOD) plays a major role in protecting the mitochondrion from oxidative damage due to superoxide radicals and other excited oxygen species.	Oxygen	157-163	superoxide dismutase 2	Homo sapiens	0-30
16485861-2	2005	Manganese superoxide dismutase (MnSOD) plays a major role in protecting the mitochondrion from oxidative damage due to superoxide radicals and other excited oxygen species.	Oxygen	157-163	superoxide dismutase 2	Homo sapiens	32-37
16485861-8	2005	CONCLUSIONS: Our data suggest that the Ala-9Val polymorphism in the MnSOD gene is not associated with genetic susceptibility in AD patients.	ala-9val	39-47	superoxide dismutase 2	Homo sapiens	68-73
16150974-0	2005	Hydrogen bonding in human manganese superoxide dismutase containing 3-fluorotyrosine.	Hydrogen	0-8	superoxide dismutase 2	Homo sapiens	26-56
16150974-0	2005	Hydrogen bonding in human manganese superoxide dismutase containing 3-fluorotyrosine.	3-fluorotyrosine	68-84	superoxide dismutase 2	Homo sapiens	26-56
16150974-1	2005	Incorporation of 3-fluorotyrosine and site-specific mutagenesis has been utilized with Fourier transform infrared (FTIR) spectroscopy and x-ray crystallography to elucidate active-site structure and the role of an active-site residue Tyr34 in human manganese superoxide dismutase (MnSOD).	3-fluorotyrosine	17-33	superoxide dismutase 2	Homo sapiens	249-279
16150974-1	2005	Incorporation of 3-fluorotyrosine and site-specific mutagenesis has been utilized with Fourier transform infrared (FTIR) spectroscopy and x-ray crystallography to elucidate active-site structure and the role of an active-site residue Tyr34 in human manganese superoxide dismutase (MnSOD).	3-fluorotyrosine	17-33	superoxide dismutase 2	Homo sapiens	281-286
16150974-3	2005	Each of the nine tyrosine residues in each of the four subunits of the homotetramer of human MnSOD was replaced with 3-fluorotyrosine.	Tyrosine	17-25	superoxide dismutase 2	Homo sapiens	93-98
16150974-3	2005	Each of the nine tyrosine residues in each of the four subunits of the homotetramer of human MnSOD was replaced with 3-fluorotyrosine.	3-fluorotyrosine	117-133	superoxide dismutase 2	Homo sapiens	93-98
16150974-4	2005	The crystal structures of the unfluorinated and fluorinated wild-type MnSOD are nearly superimposable with the root mean-square deviation for 198 alpha-carbon atoms at 0.3 A.	Carbon	152-158	superoxide dismutase 2	Homo sapiens	70-75
16150974-5	2005	The FTIR data show distinct vibrational modes arising from 3-fluorotyrosine in MnSOD.	3-fluorotyrosine	59-75	superoxide dismutase 2	Homo sapiens	79-84
16150974-6	2005	Comparison of spectra for wild-type and Y34F MnSOD showed that the phenolic hydroxyl of Tyr34 is hydrogen bonded, acting as a proton donor in the active site.	Hydrogen	97-105	superoxide dismutase 2	Homo sapiens	45-50
16214029-3	2005	It was shown that despite early increases in the steady-state levels of ROS upon MnSOD overexpression, cellular oxidative damage was decreased significantly at later time points.	Reactive Oxygen Species	72-75	superoxide dismutase 2	Homo sapiens	81-86
16179351-2	2005	The manganese-containing SOD (Mn-SOD) has been suggested to have tumor suppressor function and is located in the mitochondria where the majority of O(2)(-) is generated during respiration.	Superoxides	148-152	superoxide dismutase 2	Homo sapiens	4-28
16179351-2	2005	The manganese-containing SOD (Mn-SOD) has been suggested to have tumor suppressor function and is located in the mitochondria where the majority of O(2)(-) is generated during respiration.	Superoxides	148-152	superoxide dismutase 2	Homo sapiens	30-36
16179351-6	2005	In experimental systems, suppression of Mn-SOD expression by small interfering RNA caused a 70% increase of superoxide in ovarian cancer cells, leading to stimulation of cell proliferation in vitro and more aggressive tumor growth in vivo.	Superoxides	108-118	superoxide dismutase 2	Homo sapiens	40-46
16179351-7	2005	Furthermore, stimulation of mitochondrial O(2)(-) production induced an increase of Mn-SOD expression.	Superoxides	42-49	superoxide dismutase 2	Homo sapiens	84-90
16179351-8	2005	Our findings suggest that the increase in Mn-SOD expression in ovarian cancer is a cellular response to intrinsic ROS stress and that scavenging of superoxide by SOD may alleviate the ROS stress and thus reduce the simulating effect of ROS on cell growth.	Reactive Oxygen Species	114-117	superoxide dismutase 2	Homo sapiens	42-48
16179351-8	2005	Our findings suggest that the increase in Mn-SOD expression in ovarian cancer is a cellular response to intrinsic ROS stress and that scavenging of superoxide by SOD may alleviate the ROS stress and thus reduce the simulating effect of ROS on cell growth.	Superoxides	148-158	superoxide dismutase 2	Homo sapiens	42-48
16215873-2	2005	Manganese superoxide dismutase (MnSOD) is critical to management of oxidative stress by catalyzing the formation of hydrogen peroxide from two superoxide anions.	Hydrogen Peroxide	116-133	superoxide dismutase 2	Homo sapiens	0-30
16215873-2	2005	Manganese superoxide dismutase (MnSOD) is critical to management of oxidative stress by catalyzing the formation of hydrogen peroxide from two superoxide anions.	Hydrogen Peroxide	116-133	superoxide dismutase 2	Homo sapiens	32-37
16215873-2	2005	Manganese superoxide dismutase (MnSOD) is critical to management of oxidative stress by catalyzing the formation of hydrogen peroxide from two superoxide anions.	Superoxides	143-160	superoxide dismutase 2	Homo sapiens	0-30
16215873-2	2005	Manganese superoxide dismutase (MnSOD) is critical to management of oxidative stress by catalyzing the formation of hydrogen peroxide from two superoxide anions.	Superoxides	143-160	superoxide dismutase 2	Homo sapiens	32-37
16214029-5	2005	A time course study demonstrated that increases in MnSOD activity prior to the onset of apoptosis correlated with alterations in the levels of nitration of tyrosine residue(s) of MnSOD protein.	Tyrosine	156-164	superoxide dismutase 2	Homo sapiens	51-56
16214029-5	2005	A time course study demonstrated that increases in MnSOD activity prior to the onset of apoptosis correlated with alterations in the levels of nitration of tyrosine residue(s) of MnSOD protein.	Tyrosine	156-164	superoxide dismutase 2	Homo sapiens	179-184
16099847-10	2005	In conclusion, without modifying MAO-B activity, selegiline augments the gene induction of Trx, leading to elevated expression of antioxidative MnSOD and antiapoptotic Bcl-2 proteins for protecting against MPP+-induced neurotoxicity.	Selegiline	49-59	superoxide dismutase 2	Homo sapiens	144-149
16198237-4	2005	Edaravone was administered to 27 randomly selected patients (GIa, n = 13; GIIa, n = 14) and its efficacy was studied by comparing their plasma OxLDL, S-100B, and MnSOD levels to those in patients without edaravone (GIb, n = 11, GIIb, n = 13).	Edaravone	0-9	superoxide dismutase 2	Homo sapiens	162-167
16142322-12	2005	Cells treated with radiation demonstrated an induction of MnSOD; however, the administration of MG-132 suppressed this induction These results support the hypothesis that proteasome inhibitors such as MG-132 can increase the efficacy of radiation therapy, in part, by suppression of cytoprotective NF-kappaB-mediated MnSOD expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-102	superoxide dismutase 2	Homo sapiens	317-322
16142322-6	2005	The purpose of this study is to evaluate the potential of the proteasome inhibitor, MG-132, to improve the efficacy of radiation therapy and to determine whether its effect is linked to the suppression of the antioxidant enzyme, manganese superoxide dismutase (MnSOD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-90	superoxide dismutase 2	Homo sapiens	229-259
16142322-12	2005	Cells treated with radiation demonstrated an induction of MnSOD; however, the administration of MG-132 suppressed this induction These results support the hypothesis that proteasome inhibitors such as MG-132 can increase the efficacy of radiation therapy, in part, by suppression of cytoprotective NF-kappaB-mediated MnSOD expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-207	superoxide dismutase 2	Homo sapiens	58-63
16142322-6	2005	The purpose of this study is to evaluate the potential of the proteasome inhibitor, MG-132, to improve the efficacy of radiation therapy and to determine whether its effect is linked to the suppression of the antioxidant enzyme, manganese superoxide dismutase (MnSOD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-90	superoxide dismutase 2	Homo sapiens	261-266
16142322-12	2005	Cells treated with radiation demonstrated an induction of MnSOD; however, the administration of MG-132 suppressed this induction These results support the hypothesis that proteasome inhibitors such as MG-132 can increase the efficacy of radiation therapy, in part, by suppression of cytoprotective NF-kappaB-mediated MnSOD expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-207	superoxide dismutase 2	Homo sapiens	317-322
16076760-6	2005	These results suggested that the NADPH oxidase, MnSOD, and e-NOS polymorphisms, but not catalase, might play a role in the development of arsenic-related hypertension, especially in subjects with high triglyceride levels.	Arsenic	138-145	superoxide dismutase 2	Homo sapiens	48-53
16166634-2	2005	Detoxification of mitochondrial ROS is regulated by induction of the nuclear SOD2 gene, which encodes the manganese-dependent superoxide dismutase (MnSOD).	Reactive Oxygen Species	32-35	superoxide dismutase 2	Homo sapiens	77-81
16166634-2	2005	Detoxification of mitochondrial ROS is regulated by induction of the nuclear SOD2 gene, which encodes the manganese-dependent superoxide dismutase (MnSOD).	Reactive Oxygen Species	32-35	superoxide dismutase 2	Homo sapiens	106-146
16166634-2	2005	Detoxification of mitochondrial ROS is regulated by induction of the nuclear SOD2 gene, which encodes the manganese-dependent superoxide dismutase (MnSOD).	Reactive Oxygen Species	32-35	superoxide dismutase 2	Homo sapiens	148-153
16160055-7	2005	In contrast, feeding ruminally protected vitamin C was not associated with greater (P = 0.59) mean plasma ascorbate concentration; however, feeding ruminally protected vitamin C was associated with lower (P = 0.03) mean blood total superoxide dismutase (Cu/Zn SOD and Mn SOD) concentration.	Ascorbic Acid	168-177	superoxide dismutase 2	Homo sapiens	268-274
16101137-4	2005	The expression of MnSOD and, less strongly, Cu/ZnSOD activity, as assessed by acrylamide gel electrophoresis, was inhibited by EUG, suggesting mitochondrial dysfunction.	Acrylamide	78-88	superoxide dismutase 2	Homo sapiens	18-23
16005485-11	2005	There are two distinct cGMP-mediated survival pathways: (i) the up-regulation of a redox protein thioredoxin (Trx) for elevating mitochondrial levels of antioxidant protein Mn superoxide dismutase (MnSOD) and antiapoptotic protein Bcl-2, and (ii) the activation of mitochondrial ATP-sensitive potassium channels [K(ATP)].	Cyclic GMP	23-27	superoxide dismutase 2	Homo sapiens	173-196
16005485-11	2005	There are two distinct cGMP-mediated survival pathways: (i) the up-regulation of a redox protein thioredoxin (Trx) for elevating mitochondrial levels of antioxidant protein Mn superoxide dismutase (MnSOD) and antiapoptotic protein Bcl-2, and (ii) the activation of mitochondrial ATP-sensitive potassium channels [K(ATP)].	Cyclic GMP	23-27	superoxide dismutase 2	Homo sapiens	198-203
16298938-8	2005	In vitro exposure to FGF-20 increased expression of the Nrf2 transcription factor and oxygen radical scavenging enzymes such as MnSOD, activated signal transduction pathways (ERK and Akt) and resulted in increased survival of irradiated cells in vitro.	Oxygen	86-92	superoxide dismutase 2	Homo sapiens	128-133
15951095-0	2005	MnSOD polymorphisms in sensitized patients with delayed-type hypersensitivity reactions to the chemical allergen para-phenylene diamine: a case-control study.	4-phenylenediamine	113-135	superoxide dismutase 2	Homo sapiens	0-5
15951095-5	2005	A valine (Val) to alanine (Ala) substitution at amino acid -9, occurring in the MnSOD gene, has been associated with various disease risk.	Valine	2-8	superoxide dismutase 2	Homo sapiens	80-85
15951095-5	2005	A valine (Val) to alanine (Ala) substitution at amino acid -9, occurring in the MnSOD gene, has been associated with various disease risk.	Valine	10-13	superoxide dismutase 2	Homo sapiens	80-85
15951095-5	2005	A valine (Val) to alanine (Ala) substitution at amino acid -9, occurring in the MnSOD gene, has been associated with various disease risk.	Alanine	18-25	superoxide dismutase 2	Homo sapiens	80-85
15951095-5	2005	A valine (Val) to alanine (Ala) substitution at amino acid -9, occurring in the MnSOD gene, has been associated with various disease risk.	Alanine	27-30	superoxide dismutase 2	Homo sapiens	80-85
15951095-6	2005	The aim of our study was to investigate possible associations of the MnSOD 47 T>C genotype in exon 2 (Ala-9Val) and the 339 T>C genotype in exon 3 (Ile58Thr) with contact sensitization to PPD in humans in a case-control study.	Alanine	105-108	superoxide dismutase 2	Homo sapiens	69-74
15993853-0	2005	Sequential induction of heme oxygenase-1 and manganese superoxide dismutase protects cultured astrocytes against nitric oxide.	Nitric Oxide	113-125	superoxide dismutase 2	Homo sapiens	45-75
15817612-11	2005	Compared with control cells, MnSOD-expressing DLD-1 POX cells generated a higher concentration of H2O2 owing to dismutation of superoxide radicals, which was elevated by POX.	Hydrogen Peroxide	98-102	superoxide dismutase 2	Homo sapiens	29-34
15817612-11	2005	Compared with control cells, MnSOD-expressing DLD-1 POX cells generated a higher concentration of H2O2 owing to dismutation of superoxide radicals, which was elevated by POX.	Superoxides	127-137	superoxide dismutase 2	Homo sapiens	29-34
15817612-12	2005	Thus, these data further suggest that the generation of superoxide radicals plays a crucial role in POX-induced apoptosis and the process is partially blocked by MnSOD.	Superoxides	56-75	superoxide dismutase 2	Homo sapiens	162-167
15894290-2	2005	Since PDT with the photosensitizer phthalocyanine Pc 4 induces mitochondrial damage and the superoxide scavenger manganese superoxide dismutase (MnSOD) is localized to mitochondria, here we tested genetically the role of MnSOD in apoptosis and ceramide accumulation after photosensitization with Pc 4.	Superoxides	92-102	superoxide dismutase 2	Homo sapiens	113-143
16024627-0	2005	Enforced expression of superoxide dismutase 2/manganese superoxide dismutase disrupts autocrine interleukin-6 stimulation in human multiple myeloma cells and enhances dexamethasone-induced apoptosis.	Dexamethasone	167-180	superoxide dismutase 2	Homo sapiens	46-76
16024627-3	2005	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme encoded by the SOD2 gene that attenuates oxidative free radicals in the mitochondria by catalyzing the formation of hydrogen peroxide from superoxide radicals.	Free Radicals	125-138	superoxide dismutase 2	Homo sapiens	0-30
16024627-3	2005	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme encoded by the SOD2 gene that attenuates oxidative free radicals in the mitochondria by catalyzing the formation of hydrogen peroxide from superoxide radicals.	Free Radicals	125-138	superoxide dismutase 2	Homo sapiens	32-37
16024627-3	2005	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme encoded by the SOD2 gene that attenuates oxidative free radicals in the mitochondria by catalyzing the formation of hydrogen peroxide from superoxide radicals.	Free Radicals	125-138	superoxide dismutase 2	Homo sapiens	89-93
16024627-3	2005	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme encoded by the SOD2 gene that attenuates oxidative free radicals in the mitochondria by catalyzing the formation of hydrogen peroxide from superoxide radicals.	Hydrogen Peroxide	190-207	superoxide dismutase 2	Homo sapiens	0-30
16024627-3	2005	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme encoded by the SOD2 gene that attenuates oxidative free radicals in the mitochondria by catalyzing the formation of hydrogen peroxide from superoxide radicals.	Hydrogen Peroxide	190-207	superoxide dismutase 2	Homo sapiens	32-37
16024627-3	2005	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme encoded by the SOD2 gene that attenuates oxidative free radicals in the mitochondria by catalyzing the formation of hydrogen peroxide from superoxide radicals.	Hydrogen Peroxide	190-207	superoxide dismutase 2	Homo sapiens	89-93
16024627-3	2005	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme encoded by the SOD2 gene that attenuates oxidative free radicals in the mitochondria by catalyzing the formation of hydrogen peroxide from superoxide radicals.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
16024627-3	2005	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme encoded by the SOD2 gene that attenuates oxidative free radicals in the mitochondria by catalyzing the formation of hydrogen peroxide from superoxide radicals.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	89-93
16024627-6	2005	Here, we show that SOD2 expression is epigenetically silenced in IM-9 cells, and replacement of MnSOD reduces cell proliferation and partially restores susceptibility to dexamethasone.	Dexamethasone	170-183	superoxide dismutase 2	Homo sapiens	96-101
15894290-2	2005	Since PDT with the photosensitizer phthalocyanine Pc 4 induces mitochondrial damage and the superoxide scavenger manganese superoxide dismutase (MnSOD) is localized to mitochondria, here we tested genetically the role of MnSOD in apoptosis and ceramide accumulation after photosensitization with Pc 4.	Superoxides	92-102	superoxide dismutase 2	Homo sapiens	145-150
15894290-4	2005	In Jurkat cells overexpressing mutant MnSOD, however, DEVDase activation and ceramide formation were promoted post-Pc 4-PDT.	Ceramides	77-85	superoxide dismutase 2	Homo sapiens	38-43
15894290-5	2005	Similarly, in MnSOD-null cells, Pc 4-PDT-induced apoptosis, as well as ceramide accumulation, were enhanced compared to their normal counterparts.	Ceramides	71-79	superoxide dismutase 2	Homo sapiens	14-19
15894290-6	2005	The data show that MnSOD affects sensitivity of cells to Pc 4-PDT-initiated apoptosis, and partly ceramide accumulation, suggesting that the processes are superoxide-mediated.	Ceramides	98-106	superoxide dismutase 2	Homo sapiens	19-24
15894290-6	2005	The data show that MnSOD affects sensitivity of cells to Pc 4-PDT-initiated apoptosis, and partly ceramide accumulation, suggesting that the processes are superoxide-mediated.	Superoxides	155-165	superoxide dismutase 2	Homo sapiens	19-24
15965087-11	2005	Preconditioning-induced adaptive tolerance may be signaling through a cGMP-dependent induction of cytosolic redox protein Trx1 and subsequently mitochondrial proteins such as Bcl-2, MnSOD, and perhaps Trx2 or HSP70.	Cyclic GMP	70-74	superoxide dismutase 2	Homo sapiens	182-187
16245254-6	2005	Treatment with CsA may lead to the nitration of specific proteins such as manganese superoxide dismutase (MnSOD).	Cyclosporine	15-18	superoxide dismutase 2	Homo sapiens	74-104
16245254-6	2005	Treatment with CsA may lead to the nitration of specific proteins such as manganese superoxide dismutase (MnSOD).	Cyclosporine	15-18	superoxide dismutase 2	Homo sapiens	106-111
15977906-5	2005	Inhibitor studies with purified recombinant Cu/ ZnSOD and MnSOD, both of which were functionally expressed in Escherichia coli, confirmed that they are copper/zinc and manganese-containing SOD, respectively.	Copper	152-158	superoxide dismutase 2	Homo sapiens	58-63
15977906-5	2005	Inhibitor studies with purified recombinant Cu/ ZnSOD and MnSOD, both of which were functionally expressed in Escherichia coli, confirmed that they are copper/zinc and manganese-containing SOD, respectively.	Manganese	168-177	superoxide dismutase 2	Homo sapiens	58-63
15884106-5	2005	Expression of Cu, ZnSOD, MnSOD and tyrosine-nitrated MnSOD were analyzed by Western blot and/or immunohistochemistry.	Tyrosine	35-43	superoxide dismutase 2	Homo sapiens	53-58
15883815-1	2005	PURPOSE: Manganese superoxide dismutase (MnSOD) is one of the major enzymes implicated in the cellular defence against reactive oxygen species.	Reactive Oxygen Species	119-142	superoxide dismutase 2	Homo sapiens	9-39
15883815-1	2005	PURPOSE: Manganese superoxide dismutase (MnSOD) is one of the major enzymes implicated in the cellular defence against reactive oxygen species.	Reactive Oxygen Species	119-142	superoxide dismutase 2	Homo sapiens	41-46
15883815-4	2005	A polymorphism (Ala-9Val) in the mitochondrial targeting sequence (MTS) of the MnSOD gene has been proposed to affect protein localization and thereby influence cellular defence against superoxide radicals.	ala-9val	16-24	superoxide dismutase 2	Homo sapiens	79-84
15883815-4	2005	A polymorphism (Ala-9Val) in the mitochondrial targeting sequence (MTS) of the MnSOD gene has been proposed to affect protein localization and thereby influence cellular defence against superoxide radicals.	Superoxides	186-196	superoxide dismutase 2	Homo sapiens	79-84
17491681-0	2005	Manganese superoxide dismutase alanine to valine polymorphism and risk of neuropathy and nephropathy in Egyptian type 1 diabetic patients.	Alanine	31-38	superoxide dismutase 2	Homo sapiens	0-30
17491681-0	2005	Manganese superoxide dismutase alanine to valine polymorphism and risk of neuropathy and nephropathy in Egyptian type 1 diabetic patients.	Valine	42-48	superoxide dismutase 2	Homo sapiens	0-30
15820221-0	2005	Overexpression of manganese superoxide dismutase protects against ATP depletion-mediated cell death of proximal tubule cells.	Adenosine Triphosphate	66-69	superoxide dismutase 2	Homo sapiens	18-48
15820221-3	2005	ATP depletion in wild-type cells induced an apoptotic cascade that involved caspase 9 activation; MnSOD overexpressing cells afforded protection against apoptosis.	Adenosine Triphosphate	0-3	superoxide dismutase 2	Homo sapiens	98-103
15867370-5	2005	In the mitochondria, p53 interacts with the primary antioxidant enzyme, manganese superoxide dismutase (MnSOD), consistent with the reduction of its superoxide scavenging activity, and a subsequent decrease of mitochondrial membrane potential.	Superoxides	82-92	superoxide dismutase 2	Homo sapiens	104-109
15820221-7	2005	Taken together, these results suggest that cysteine nitrosylation may be playing a role in caspase dysfunction in cells overexpressing MnSOD following ATP depletion.	Cysteine	43-51	superoxide dismutase 2	Homo sapiens	135-140
15820221-7	2005	Taken together, these results suggest that cysteine nitrosylation may be playing a role in caspase dysfunction in cells overexpressing MnSOD following ATP depletion.	Adenosine Triphosphate	151-154	superoxide dismutase 2	Homo sapiens	135-140
16080463-3	2005	In the present study, we tested the sensitivity of MCF-7 breast cancer cells overexpressing anti-apoptotic genes TRAF-1, c-FLIP, Bcl-xL, clAP-2 or Mn-SOD to paclitaxel and docetaxel.	Paclitaxel	157-167	superoxide dismutase 2	Homo sapiens	147-153
15862717-3	2005	In a seemingly contradictory role, it also is well documented that increased MnSOD expression suppresses the carcinogenesis effect of ROS.	Reactive Oxygen Species	134-137	superoxide dismutase 2	Homo sapiens	77-82
15862717-4	2005	Our recent studies demonstrated that overexpression of MnSOD reduced tumor incidence in the two-stage 7,12-dimethylbenz(a)-anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) skin carcinogenesis model.	9,10-Dimethyl-1,2-benzanthracene	102-133	superoxide dismutase 2	Homo sapiens	55-60
15862717-4	2005	Our recent studies demonstrated that overexpression of MnSOD reduced tumor incidence in the two-stage 7,12-dimethylbenz(a)-anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) skin carcinogenesis model.	9,10-Dimethyl-1,2-benzanthracene	135-139	superoxide dismutase 2	Homo sapiens	55-60
15862717-4	2005	Our recent studies demonstrated that overexpression of MnSOD reduced tumor incidence in the two-stage 7,12-dimethylbenz(a)-anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) skin carcinogenesis model.	Tetradecanoylphorbol Acetate	141-177	superoxide dismutase 2	Homo sapiens	55-60
15862717-4	2005	Our recent studies demonstrated that overexpression of MnSOD reduced tumor incidence in the two-stage 7,12-dimethylbenz(a)-anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) skin carcinogenesis model.	Tetradecanoylphorbol Acetate	179-182	superoxide dismutase 2	Homo sapiens	55-60
15862717-7	2005	This review will provide background information on the sequence of ROS-mediated events in the mitochondria and evidence that suggests that the antioxidant and tumor suppressor functions of MnSOD are indeed inter-related.	Reactive Oxygen Species	67-70	superoxide dismutase 2	Homo sapiens	189-194
15886469-5	2005	However, in HT-29 cells, the CPT-11/5-FU combination enhanced Mn-SOD activity when compared to cells treated with CPT-11 alone.	Irinotecan	29-35	superoxide dismutase 2	Homo sapiens	62-68
15869407-0	2005	Different roles of Sp family members in HIV-1 Tat-mediated manganese superoxide dismutase suppression in hepatocellular carcinoma cells.	TFF2 protein, human	19-21	superoxide dismutase 2	Homo sapiens	59-89
15886469-5	2005	However, in HT-29 cells, the CPT-11/5-FU combination enhanced Mn-SOD activity when compared to cells treated with CPT-11 alone.	Fluorouracil	36-40	superoxide dismutase 2	Homo sapiens	62-68
15886469-5	2005	However, in HT-29 cells, the CPT-11/5-FU combination enhanced Mn-SOD activity when compared to cells treated with CPT-11 alone.	Irinotecan	114-120	superoxide dismutase 2	Homo sapiens	62-68
15886469-7	2005	CONCLUSION: Treatment with the CPT-11/5-FU combination may promote in HT-29 cell apoptosis by enhancing Mn-SOD activity.	Irinotecan	31-37	superoxide dismutase 2	Homo sapiens	104-110
15886469-7	2005	CONCLUSION: Treatment with the CPT-11/5-FU combination may promote in HT-29 cell apoptosis by enhancing Mn-SOD activity.	Fluorouracil	38-42	superoxide dismutase 2	Homo sapiens	104-110
15908783-3	2005	There are numerous reports that levels of manganese superoxide dismutase enzyme (MnSOD), an antioxidant enzyme responsible for the attenuation of ROS, are lowered in cancer cells, but the reasons for this reduction are poorly defined.	Reactive Oxygen Species	146-149	superoxide dismutase 2	Homo sapiens	42-79
15908783-3	2005	There are numerous reports that levels of manganese superoxide dismutase enzyme (MnSOD), an antioxidant enzyme responsible for the attenuation of ROS, are lowered in cancer cells, but the reasons for this reduction are poorly defined.	Reactive Oxygen Species	146-149	superoxide dismutase 2	Homo sapiens	81-86
15908783-6	2005	The DNA methyltransferase inhibitor Zebularine reverses SOD-2 promoter methylation, increasing gene expression and enzyme levels.	pyrimidin-2-one beta-ribofuranoside	36-46	superoxide dismutase 2	Homo sapiens	56-61
15933380-2	2005	Recent evidences suggest that a genetic dimorphism that encodes for either alanine or valine in superoxide dismutase (SOD2) is involved with oxidative stress.	Alanine	75-82	superoxide dismutase 2	Homo sapiens	118-122
15809720-2	2005	With this system we quantitatively analyzed adriamycin (ADR)-induced cell death using manganese superoxide dismutase (MnSOD)- and wild-type p53-gene transfectants on SaOS(2), a p53-deficient human osteosarcoma cell line.	Doxorubicin	44-54	superoxide dismutase 2	Homo sapiens	118-123
15809720-7	2005	When isosorbide 5-mononitrate was combined with BSO, isosorbide 5-mononitrate increased ADR sensitivity of a moderately MnSOD-overexpressing cell line, SaOS(2)FM(L), decreased that of SaOS(2) FM(H), and did not change those of SaOS(2) and SaOS(2)wtp53 compared to BSO alone.	isosorbide-5-mononitrate	5-29	superoxide dismutase 2	Homo sapiens	120-125
15809720-7	2005	When isosorbide 5-mononitrate was combined with BSO, isosorbide 5-mononitrate increased ADR sensitivity of a moderately MnSOD-overexpressing cell line, SaOS(2)FM(L), decreased that of SaOS(2) FM(H), and did not change those of SaOS(2) and SaOS(2)wtp53 compared to BSO alone.	isosorbide-5-mononitrate	53-77	superoxide dismutase 2	Homo sapiens	120-125
15809720-13	2005	These findings indicate that hydrogen peroxide overload on p53-independent pathway due to MnSOD overexpression plus BSO might increase the apoptosis frequency without acceleration of apoptotic process of each cell, resulting in negating ADR-tolerance of MnSOD-overexpressing cell lines.	Hydrogen Peroxide	29-46	superoxide dismutase 2	Homo sapiens	90-95
15809720-13	2005	These findings indicate that hydrogen peroxide overload on p53-independent pathway due to MnSOD overexpression plus BSO might increase the apoptosis frequency without acceleration of apoptotic process of each cell, resulting in negating ADR-tolerance of MnSOD-overexpressing cell lines.	Hydrogen Peroxide	29-46	superoxide dismutase 2	Homo sapiens	254-259
16108378-4	2005	After 4 days of methanol induction, the expressed hMn-SOD was up to 32% of the total proteins in the supernatant by SDS-PAGE with specific activity of 247.7 u/mg.	Methanol	16-24	superoxide dismutase 2	Homo sapiens	50-57
16108378-4	2005	After 4 days of methanol induction, the expressed hMn-SOD was up to 32% of the total proteins in the supernatant by SDS-PAGE with specific activity of 247.7 u/mg.	Sodium Dodecyl Sulfate	116-119	superoxide dismutase 2	Homo sapiens	50-57
15864132-1	2005	A genetic dimorphism incorporates either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of manganese superoxide dismutase (MnSOD).	Alanine	41-48	superoxide dismutase 2	Homo sapiens	152-157
15864132-1	2005	A genetic dimorphism incorporates either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of manganese superoxide dismutase (MnSOD).	Alanine	50-53	superoxide dismutase 2	Homo sapiens	152-157
15864132-1	2005	A genetic dimorphism incorporates either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of manganese superoxide dismutase (MnSOD).	Valine	58-64	superoxide dismutase 2	Homo sapiens	152-157
15864132-1	2005	A genetic dimorphism incorporates either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of manganese superoxide dismutase (MnSOD).	Valine	66-69	superoxide dismutase 2	Homo sapiens	152-157
15864132-2	2005	The Ala-MTS confers a 40% higher MnSOD activity than the Val-MTS after import into isolated mitochondria in vitro.	Alanine	4-8	superoxide dismutase 2	Homo sapiens	33-38
15864132-4	2005	HuH7 human hepatoma cells were transfected with vectors encoding for the human Ala- or Val-MnSOD variants fused to a Myc-His-tag.	Valine	87-90	superoxide dismutase 2	Homo sapiens	91-96
15864132-5	2005	The Ala-variant resulted in four-fold higher levels of the mature exogenous protein and MnSOD activity than the Val-variant.	Alanine	4-7	superoxide dismutase 2	Homo sapiens	88-93
15864132-5	2005	The Ala-variant resulted in four-fold higher levels of the mature exogenous protein and MnSOD activity than the Val-variant.	Valine	112-115	superoxide dismutase 2	Homo sapiens	88-93
15864132-9	2005	Much larger differences in the activity of the human Val- and Ala-MnSOD variants are observed in whole cells rather than after import experiments performed in vitro.	Valine	53-56	superoxide dismutase 2	Homo sapiens	66-71
15864132-9	2005	Much larger differences in the activity of the human Val- and Ala-MnSOD variants are observed in whole cells rather than after import experiments performed in vitro.	Alanine	62-65	superoxide dismutase 2	Homo sapiens	66-71
15933380-2	2005	Recent evidences suggest that a genetic dimorphism that encodes for either alanine or valine in superoxide dismutase (SOD2) is involved with oxidative stress.	Valine	86-92	superoxide dismutase 2	Homo sapiens	118-122
15674333-3	2005	Here we show that three representative apoptotic stimuli, that is, serum starvation, a mitochondrial toxin, and a DNA-damaging agent (etoposide), rapidly induce several distinct classes of prosurvival molecules, in particular, Bcl-2/Bcl-X(L) and superoxide dismutase (SOD; including both MnSOD and Cu/ZnSOD).	Etoposide	134-143	superoxide dismutase 2	Homo sapiens	288-293
15674333-8	2005	Mechanistic studies indicate that reactive oxygen species (ROS) are rapidly induced upon apoptotic stimulation and that ROS inhibitors/scavengers block the induction of FOXO3a, MnSOD, and Bim.	Reactive Oxygen Species	34-57	superoxide dismutase 2	Homo sapiens	177-182
15674333-8	2005	Mechanistic studies indicate that reactive oxygen species (ROS) are rapidly induced upon apoptotic stimulation and that ROS inhibitors/scavengers block the induction of FOXO3a, MnSOD, and Bim.	Reactive Oxygen Species	59-62	superoxide dismutase 2	Homo sapiens	177-182
15674333-8	2005	Mechanistic studies indicate that reactive oxygen species (ROS) are rapidly induced upon apoptotic stimulation and that ROS inhibitors/scavengers block the induction of FOXO3a, MnSOD, and Bim.	Reactive Oxygen Species	120-123	superoxide dismutase 2	Homo sapiens	177-182
15765450-1	2005	BACKGROUND AND AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import.	Alanine	61-68	superoxide dismutase 2	Homo sapiens	134-164
15781667-2	2005	A polymorphism [valine (V) --> alanine (A)] of manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme in mitochondria, has been recently associated with prostate cancer.	Valine	16-22	superoxide dismutase 2	Homo sapiens	50-80
15781667-2	2005	A polymorphism [valine (V) --> alanine (A)] of manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme in mitochondria, has been recently associated with prostate cancer.	Valine	16-22	superoxide dismutase 2	Homo sapiens	82-87
15781667-2	2005	A polymorphism [valine (V) --> alanine (A)] of manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme in mitochondria, has been recently associated with prostate cancer.	Alanine	34-41	superoxide dismutase 2	Homo sapiens	50-80
15781667-2	2005	A polymorphism [valine (V) --> alanine (A)] of manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme in mitochondria, has been recently associated with prostate cancer.	Alanine	34-41	superoxide dismutase 2	Homo sapiens	82-87
15765450-1	2005	BACKGROUND AND AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import.	Alanine	61-68	superoxide dismutase 2	Homo sapiens	166-171
15765450-1	2005	BACKGROUND AND AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import.	Alanine	70-73	superoxide dismutase 2	Homo sapiens	134-164
15765450-1	2005	BACKGROUND AND AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import.	Alanine	70-73	superoxide dismutase 2	Homo sapiens	166-171
15765450-1	2005	BACKGROUND AND AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import.	Valine	78-84	superoxide dismutase 2	Homo sapiens	134-164
15765450-1	2005	BACKGROUND AND AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import.	Valine	78-84	superoxide dismutase 2	Homo sapiens	166-171
15765450-1	2005	BACKGROUND AND AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import.	Valine	86-89	superoxide dismutase 2	Homo sapiens	134-164
15765450-1	2005	BACKGROUND AND AIMS: A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD), and modulates its mitochondrial import.	Valine	86-89	superoxide dismutase 2	Homo sapiens	166-171
15734485-1	2005	BACKGROUND: Manganese superoxide dismutase (MnSOD) plays a critical role in the detoxification of mitochondrial reactive oxygen species, constituting a major cellular defense mechanism against agents that induce oxidative stress.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	12-42
15683720-1	2005	Overexpression of human manganese superoxide dismutase (MnSOD) in mouse NIH/3T3 cells using an inducible retroviral system led to alterations in the mitochondrial redox state since levels of reactive oxygen species rapidly increased after induction of human MnSOD (Antioxid.	Reactive Oxygen Species	191-214	superoxide dismutase 2	Homo sapiens	24-54
15683720-1	2005	Overexpression of human manganese superoxide dismutase (MnSOD) in mouse NIH/3T3 cells using an inducible retroviral system led to alterations in the mitochondrial redox state since levels of reactive oxygen species rapidly increased after induction of human MnSOD (Antioxid.	Reactive Oxygen Species	191-214	superoxide dismutase 2	Homo sapiens	56-61
15734485-1	2005	BACKGROUND: Manganese superoxide dismutase (MnSOD) plays a critical role in the detoxification of mitochondrial reactive oxygen species, constituting a major cellular defense mechanism against agents that induce oxidative stress.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	44-49
15725579-5	2005	However, in contrast to normal fibroblasts, exposure of psoriatic fibroblasts to 1 microM RA down-regulated Mn-SOD mRNA, and also decreased Mn-SOD activity by approximately 80% with no change in Mn-SOD protein levels.	Tretinoin	90-92	superoxide dismutase 2	Homo sapiens	140-146
15683235-6	2005	On the basis of our computational results as well as previously published kinetic data, we propose that the product-inhibited form of MnSOD is best described as a side-on peroxo-Mn3+ adduct possessing an axial H2O ligand.	peroxo-mn3+	171-182	superoxide dismutase 2	Homo sapiens	134-139
15683235-6	2005	On the basis of our computational results as well as previously published kinetic data, we propose that the product-inhibited form of MnSOD is best described as a side-on peroxo-Mn3+ adduct possessing an axial H2O ligand.	Water	210-213	superoxide dismutase 2	Homo sapiens	134-139
15705913-8	2005	When we combined genotypes associated with higher levels of reactive oxygen species for MnSOD and MPO, women with MnSOD CC and MPO GG genotypes had a 3-fold decrease in hazard of death (hazard ratio, 0.33; 95% confidence interval, 0.13-0.80; P = 0.01).	Reactive Oxygen Species	60-83	superoxide dismutase 2	Homo sapiens	88-93
15705913-8	2005	When we combined genotypes associated with higher levels of reactive oxygen species for MnSOD and MPO, women with MnSOD CC and MPO GG genotypes had a 3-fold decrease in hazard of death (hazard ratio, 0.33; 95% confidence interval, 0.13-0.80; P = 0.01).	Reactive Oxygen Species	60-83	superoxide dismutase 2	Homo sapiens	114-119
15725579-3	2005	As retinoic acid (RA) has been used in the treatment of psoriasis and a mechanism for its beneficial effects is not understood, we investigated the effects of RA on SOD mRNA and protein expression levels in human normal and psoriatic fibroblasts.	Tretinoin	159-161	superoxide dismutase 2	Homo sapiens	165-168
15725579-5	2005	However, in contrast to normal fibroblasts, exposure of psoriatic fibroblasts to 1 microM RA down-regulated Mn-SOD mRNA, and also decreased Mn-SOD activity by approximately 80% with no change in Mn-SOD protein levels.	Tretinoin	90-92	superoxide dismutase 2	Homo sapiens	140-146
15725579-5	2005	However, in contrast to normal fibroblasts, exposure of psoriatic fibroblasts to 1 microM RA down-regulated Mn-SOD mRNA, and also decreased Mn-SOD activity by approximately 80% with no change in Mn-SOD protein levels.	Tretinoin	90-92	superoxide dismutase 2	Homo sapiens	108-114
15725579-8	2005	These results indicate that RA can serve as a regulatory agent to down-regulate the steady-state levels of both Mn-SOD and Cu,Zn-SOD in psoriatic cells.	Tretinoin	28-30	superoxide dismutase 2	Homo sapiens	112-118
15650415-0	2005	Selenium attenuates expression of MnSOD and uncoupling protein 2 in J774.2 macrophages: molecular mechanism for its cell-death and antiinflammatory activity.	Selenium	0-8	superoxide dismutase 2	Homo sapiens	34-39
15634218-0	2005	Effects of calcium concentration on the SOD activity and UVB-induced cytotoxicity in cultured human keratinocytes.	Calcium	11-18	superoxide dismutase 2	Homo sapiens	40-43
15634218-3	2005	We examined the effects of Ca(2+) concentration of culture medium (DMEM (Dulbecco"s modified Eagle"s medium)) on the superoxide dismutase (SOD) activity and UVB-induced cytotoxicity in cultured human keratinocytes in order to investigate the relationship between cell differentiation and antioxidant defense.	dmem	67-71	superoxide dismutase 2	Homo sapiens	139-142
15543233-7	2005	Also, production of extracellular H(2)O(2) was increased in the MnSOD-overexpressing clones.	Hydrogen Peroxide	34-42	superoxide dismutase 2	Homo sapiens	64-69
15816534-1	2005	To clarify the mechanisms by which hydroquinone (HQ; 1,4-benzenediol) produces apoptosis, HQ-induced cytotoxicity, intemucleosomal DNA fragmentation, activation of superoxide dismutase (SOD), expression of Mn and Cu/ZnSOD mRNA and activation of caspase-3, -8 and -9 were investigated in the human promyelocytic leukemic cell line HL-60.	hydroquinone	35-47	superoxide dismutase 2	Homo sapiens	186-189
15650415-11	2005	Selenite prevented nuclear factor-kappaB (NF-kappaB) activation as a mechanism of its inhibitory activity on MnSOD expression in the immune-stimulated cells.	Selenious Acid	0-8	superoxide dismutase 2	Homo sapiens	109-114
15650415-13	2005	It is therefore concluded that selenium at high nanomolar to low micromolar concentrations shifts the balance between inflammatory response and cell death toward the latter, through a direct effect on the transcription factors Sp1 and NF-kappaB, and down-regulation of MnSOD and UCP2.	Selenium	31-39	superoxide dismutase 2	Homo sapiens	269-274
15386537-1	2005	Within mitochondria, manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species (ROS).	Reactive Oxygen Species	113-136	superoxide dismutase 2	Homo sapiens	21-51
15386537-1	2005	Within mitochondria, manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species (ROS).	Reactive Oxygen Species	113-136	superoxide dismutase 2	Homo sapiens	53-58
15386537-1	2005	Within mitochondria, manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species (ROS).	Reactive Oxygen Species	138-141	superoxide dismutase 2	Homo sapiens	21-51
15386537-1	2005	Within mitochondria, manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species (ROS).	Reactive Oxygen Species	138-141	superoxide dismutase 2	Homo sapiens	53-58
15386537-2	2005	An alanine-9valine (Ala-9Val) polymorphism in the mitochondrial targeting sequence of MnSOD has been described and has recently been associated with risk of human breast cancer.	ala-9val	20-28	superoxide dismutase 2	Homo sapiens	86-91
15386537-4	2005	Ala-9Val polymorphism in the signal sequence of the protein for MnSOD was determined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay in a study population.	ala-9val	0-8	superoxide dismutase 2	Homo sapiens	64-69
15386537-6	2005	When MnSOD Ala was combined with either cytochrome P450 1B1 CYP1B1*1 and catechol O-methyltransferase COMT-L (V158M) genotypes, the risk for developing breast cancer was significantly increased in patients with a body mass index (BMI) greater than 24 kg m(-2) (OR: 1.42 (95%CI=1.04-1.93)).	Alanine	11-14	superoxide dismutase 2	Homo sapiens	5-10
15610954-0	2005	Association between Ala-9Val polymorphism of Mn-SOD gene and schizophrenia.	ala-9val	20-28	superoxide dismutase 2	Homo sapiens	45-51
15610954-2	2005	The major intracellular antioxidant enzymes, copper-zinc superoxide dismutase in the cytoplasm and manganese superoxide dismutase (Mn-SOD) in the mitochondria, rapidly and specifically reduce superoxide radicals to hydrogen peroxide.	Superoxides	57-67	superoxide dismutase 2	Homo sapiens	99-129
15610954-2	2005	The major intracellular antioxidant enzymes, copper-zinc superoxide dismutase in the cytoplasm and manganese superoxide dismutase (Mn-SOD) in the mitochondria, rapidly and specifically reduce superoxide radicals to hydrogen peroxide.	Superoxides	57-67	superoxide dismutase 2	Homo sapiens	131-137
15610954-2	2005	The major intracellular antioxidant enzymes, copper-zinc superoxide dismutase in the cytoplasm and manganese superoxide dismutase (Mn-SOD) in the mitochondria, rapidly and specifically reduce superoxide radicals to hydrogen peroxide.	Hydrogen Peroxide	215-232	superoxide dismutase 2	Homo sapiens	99-129
15610954-2	2005	The major intracellular antioxidant enzymes, copper-zinc superoxide dismutase in the cytoplasm and manganese superoxide dismutase (Mn-SOD) in the mitochondria, rapidly and specifically reduce superoxide radicals to hydrogen peroxide.	Hydrogen Peroxide	215-232	superoxide dismutase 2	Homo sapiens	131-137
15610954-4	2005	The present study was performed to assess whether there is a genetic association between a functional polymorphism (Ala-9Val) in the human Mn-SOD gene in schizophrenic patients (n=153) and healthy controls (n=196) using a PCR/RFLP method.	ala-9val	116-124	superoxide dismutase 2	Homo sapiens	139-145
15330761-3	2004	Pre-treatment with CHX (cycloheximide) followed by PMA led to significantly higher levels of MnSOD mRNA compared with those with either agent alone, suggesting de novo synthesis of an inhibitory protein.	Cycloheximide	19-22	superoxide dismutase 2	Homo sapiens	93-98
15330761-3	2004	Pre-treatment with CHX (cycloheximide) followed by PMA led to significantly higher levels of MnSOD mRNA compared with those with either agent alone, suggesting de novo synthesis of an inhibitory protein.	Cycloheximide	24-37	superoxide dismutase 2	Homo sapiens	93-98
15534883-2	2004	Manganese superoxide dismutase (SOD2) catalyzes the dismutation of superoxide radicals, a major type of ROS, into hydrogen peroxide.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-36
15330761-1	2004	Cytokines, phorbol esters, radiation and chemotherapeutic drugs up-regulate the expression of MnSOD (manganese superoxide dismutase).	Phorbol Esters	11-25	superoxide dismutase 2	Homo sapiens	94-99
15534883-2	2004	Manganese superoxide dismutase (SOD2) catalyzes the dismutation of superoxide radicals, a major type of ROS, into hydrogen peroxide.	Reactive Oxygen Species	104-107	superoxide dismutase 2	Homo sapiens	32-36
15330761-1	2004	Cytokines, phorbol esters, radiation and chemotherapeutic drugs up-regulate the expression of MnSOD (manganese superoxide dismutase).	Phorbol Esters	11-25	superoxide dismutase 2	Homo sapiens	101-131
15330761-9	2004	Western blot analysis indicated the presence of several PKC isoforms in the VA-13 cell line; however, PMA pre-treatment specifically down-regulated alpha and betaI, suggesting a role for one or more of these proteins in SOD2 induction.	Tetradecanoylphorbol Acetate	102-105	superoxide dismutase 2	Homo sapiens	220-224
15330761-2	2004	Using the VA-13 cell line, we studied the regulation of SOD2 upon treatment with PMA.	Tetradecanoylphorbol Acetate	81-84	superoxide dismutase 2	Homo sapiens	56-60
15534883-2	2004	Manganese superoxide dismutase (SOD2) catalyzes the dismutation of superoxide radicals, a major type of ROS, into hydrogen peroxide.	Hydrogen Peroxide	114-131	superoxide dismutase 2	Homo sapiens	32-36
15589819-0	2004	The Ala-9Val polymorphism in the mitochondrial targeting sequence (MTS) of the manganese superoxide dismutase gene is not associated with juvenile-onset asthma.	ala-9val	4-12	superoxide dismutase 2	Homo sapiens	79-109
15604281-6	2004	Complementary DNA microarray expression profiling allowed us to identify a subset of genes specifically regulated by tamoxifen and CC-8490, and not by other apoptotic stimuli, including nuclear factor (NF)-kappaB with its target genes IEX-3, SOD2, IL6, and IL8.	Tamoxifen	117-126	superoxide dismutase 2	Homo sapiens	242-246
15598343-1	2004	BACKGROUND: Manganese superoxide dismutase (MnSOD) plays a critical role in the detoxification of mitochondrial reactive oxygen species constituting a major cellular defense mechanism against agents that induce oxidative stress.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	12-42
15598343-1	2004	BACKGROUND: Manganese superoxide dismutase (MnSOD) plays a critical role in the detoxification of mitochondrial reactive oxygen species constituting a major cellular defense mechanism against agents that induce oxidative stress.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	44-49
15611622-6	2004	Suppression of ROS by NF-kappaB is mediated by Ferritin heavy chain (FHC)--the primary iron-storage mechanism in cells--and possibly, by the mitochondrial enzyme Mn++ superoxide dismutase (Mn-SOD).	Reactive Oxygen Species	15-18	superoxide dismutase 2	Homo sapiens	162-187
15589819-2	2004	METHODS: Alanine or valine polymorphism in the signal peptide of Mn-SOD gene was evaluated using a primer pair to amplify a 107-bp fragment followed by digestion with NgoM IV.	Alanine	9-16	superoxide dismutase 2	Homo sapiens	65-71
15611622-6	2004	Suppression of ROS by NF-kappaB is mediated by Ferritin heavy chain (FHC)--the primary iron-storage mechanism in cells--and possibly, by the mitochondrial enzyme Mn++ superoxide dismutase (Mn-SOD).	Reactive Oxygen Species	15-18	superoxide dismutase 2	Homo sapiens	189-195
15589819-2	2004	METHODS: Alanine or valine polymorphism in the signal peptide of Mn-SOD gene was evaluated using a primer pair to amplify a 107-bp fragment followed by digestion with NgoM IV.	Valine	20-26	superoxide dismutase 2	Homo sapiens	65-71
15642323-9	2004	Furthermore, Sod2-deficient cells showed dramatic mitochondrial damage, cytochrome C leakage, caspase 3 activation and increased apoptotic cell death when they were challenged with O2-.	Oxygen	181-183	superoxide dismutase 2	Homo sapiens	13-17
15591282-1	2004	The A16V mitochondrial targeting sequence polymorphism influences the antioxidant activity of MnSOD, an enzyme involved in neutralising iron induced oxidative stress.	Iron	136-140	superoxide dismutase 2	Homo sapiens	94-99
15642322-9	2004	Analysis with real-time PCR showed a maximum 3-6-fold increase in mRNA levels 9 hr after the 3 hr O2-exposure for the enzymes heme oxygenase-1 (HO-1), MnSOD and TrxR1 (the cytoplasmic form of TrxR).	Oxygen	98-100	superoxide dismutase 2	Homo sapiens	151-156
15591282-10	2004	In patients with hereditary haemochromatosis, the MnSOD genotype affects the risk of cardiomyopathy related to iron overload and possibly to other known and unknown risk factors and could represent an iron toxicity modifier gene.	Iron	111-115	superoxide dismutase 2	Homo sapiens	50-55
15591282-10	2004	In patients with hereditary haemochromatosis, the MnSOD genotype affects the risk of cardiomyopathy related to iron overload and possibly to other known and unknown risk factors and could represent an iron toxicity modifier gene.	Iron	201-205	superoxide dismutase 2	Homo sapiens	50-55
16114557-0	2004	[Effect of EGCG on H2O2-induced MnSOD gene expression in cultured spiral ganglion cells].	epigallocatechin gallate	11-15	superoxide dismutase 2	Homo sapiens	32-37
16114557-0	2004	[Effect of EGCG on H2O2-induced MnSOD gene expression in cultured spiral ganglion cells].	Hydrogen Peroxide	19-23	superoxide dismutase 2	Homo sapiens	32-37
16114557-1	2004	OBJECTIVE: To investigate the influence of EGCG on H2O2-induced gene expression of manganese superoxide dismutase (MnSOD or SOD2) in cultured spiral ganglion cells (SGCs) in vitro.	epigallocatechin gallate	43-47	superoxide dismutase 2	Homo sapiens	115-120
16114557-1	2004	OBJECTIVE: To investigate the influence of EGCG on H2O2-induced gene expression of manganese superoxide dismutase (MnSOD or SOD2) in cultured spiral ganglion cells (SGCs) in vitro.	Hydrogen Peroxide	51-55	superoxide dismutase 2	Homo sapiens	115-120
16114557-1	2004	OBJECTIVE: To investigate the influence of EGCG on H2O2-induced gene expression of manganese superoxide dismutase (MnSOD or SOD2) in cultured spiral ganglion cells (SGCs) in vitro.	Hydrogen Peroxide	51-55	superoxide dismutase 2	Homo sapiens	124-128
16114557-3	2004	Semi-quantitative RT-PCR was applied to observe MnSOD gene expression in SGCs after H2O2 and EGCG treatment.	Hydrogen Peroxide	84-88	superoxide dismutase 2	Homo sapiens	48-53
16114557-3	2004	Semi-quantitative RT-PCR was applied to observe MnSOD gene expression in SGCs after H2O2 and EGCG treatment.	epigallocatechin gallate	93-97	superoxide dismutase 2	Homo sapiens	48-53
16114557-4	2004	RESULTS: The expression of MnSOD gene was up-regulated with the increase of the concentration of H2O2 in cultured SGCs, and MnSOD gene expression was significantly up-regulated at a dose of H2O2 > or =100 micromol/L.	Hydrogen Peroxide	97-101	superoxide dismutase 2	Homo sapiens	27-32
16114557-4	2004	RESULTS: The expression of MnSOD gene was up-regulated with the increase of the concentration of H2O2 in cultured SGCs, and MnSOD gene expression was significantly up-regulated at a dose of H2O2 > or =100 micromol/L.	Hydrogen Peroxide	190-194	superoxide dismutase 2	Homo sapiens	27-32
16114557-4	2004	RESULTS: The expression of MnSOD gene was up-regulated with the increase of the concentration of H2O2 in cultured SGCs, and MnSOD gene expression was significantly up-regulated at a dose of H2O2 > or =100 micromol/L.	Hydrogen Peroxide	190-194	superoxide dismutase 2	Homo sapiens	124-129
16114557-6	2004	CONCLUSION: EGCG suppresses H2O2-induced up-regulation of MnSOD gene expression in cultured SGCs by getting rid of oxygen free radicals, reinforcing the activity of antioxidant enzymes such as MnSOD, and protects cultured SGCs from H2O2-induced oxidizing damage.	epigallocatechin gallate	12-16	superoxide dismutase 2	Homo sapiens	58-63
16114557-6	2004	CONCLUSION: EGCG suppresses H2O2-induced up-regulation of MnSOD gene expression in cultured SGCs by getting rid of oxygen free radicals, reinforcing the activity of antioxidant enzymes such as MnSOD, and protects cultured SGCs from H2O2-induced oxidizing damage.	epigallocatechin gallate	12-16	superoxide dismutase 2	Homo sapiens	193-198
16114557-6	2004	CONCLUSION: EGCG suppresses H2O2-induced up-regulation of MnSOD gene expression in cultured SGCs by getting rid of oxygen free radicals, reinforcing the activity of antioxidant enzymes such as MnSOD, and protects cultured SGCs from H2O2-induced oxidizing damage.	Hydrogen Peroxide	28-32	superoxide dismutase 2	Homo sapiens	58-63
16114557-6	2004	CONCLUSION: EGCG suppresses H2O2-induced up-regulation of MnSOD gene expression in cultured SGCs by getting rid of oxygen free radicals, reinforcing the activity of antioxidant enzymes such as MnSOD, and protects cultured SGCs from H2O2-induced oxidizing damage.	Hydrogen Peroxide	28-32	superoxide dismutase 2	Homo sapiens	193-198
16114557-6	2004	CONCLUSION: EGCG suppresses H2O2-induced up-regulation of MnSOD gene expression in cultured SGCs by getting rid of oxygen free radicals, reinforcing the activity of antioxidant enzymes such as MnSOD, and protects cultured SGCs from H2O2-induced oxidizing damage.	oxygen free radicals	115-135	superoxide dismutase 2	Homo sapiens	58-63
16114557-6	2004	CONCLUSION: EGCG suppresses H2O2-induced up-regulation of MnSOD gene expression in cultured SGCs by getting rid of oxygen free radicals, reinforcing the activity of antioxidant enzymes such as MnSOD, and protects cultured SGCs from H2O2-induced oxidizing damage.	Hydrogen Peroxide	232-236	superoxide dismutase 2	Homo sapiens	58-63
15345661-3	2004	Therefore, genes involved in regulating the reactive oxygen species manganese-superoxide dismutase (SOD2) and the antioxidant paraoxonase (PON) could influence cochlea vulnerability to noise.	Reactive Oxygen Species	44-67	superoxide dismutase 2	Homo sapiens	100-104
15382061-5	2004	Release of mitochondrial cytochrome c and Mn-SOD suggest mitochondria as a target of RuCl2(KTZ)2.	rucl2(ktz)2	85-96	superoxide dismutase 2	Homo sapiens	42-48
15319267-8	2004	Moreover, cytotoxic effects of LY83583 on CAECs and HUVECs were reversed by adenoviral overexpression of MnSOD.	6-anilino-5,8-quinolinedione	31-38	superoxide dismutase 2	Homo sapiens	105-110
25175611-6	2004	The enzyme level of placental MnSOD was also significantly associated with MDA concentration (P=0.04) and neonatal birth weight (P< 0.01).	Adenosine Monophosphate	131-134	superoxide dismutase 2	Homo sapiens	30-35
15516670-3	2004	Superoxide dismutases (SOD)s are the only enzymes capable of consuming superoxide radicals.	Superoxides	71-81	superoxide dismutase 2	Homo sapiens	23-26
15624308-0	2004	Delayed radioprotection by NFkappaB-mediated induction of Sod2 (MnSOD) in SA-NH tumor cells after exposure to clinically used thiol-containing drugs.	Sulfhydryl Compounds	126-131	superoxide dismutase 2	Homo sapiens	58-62
15624308-9	2004	This delayed radioprotective effect correlated with elevated Sod2 protein levels in wild-type SA-NH tumor cells but was not observed in SA-NH+mIkappaBalpha1 cells, indicating that interference with thiol-induced NFKB activation abrogates this delayed radioprotective effect.	Sulfhydryl Compounds	198-203	superoxide dismutase 2	Homo sapiens	61-65
15624308-0	2004	Delayed radioprotection by NFkappaB-mediated induction of Sod2 (MnSOD) in SA-NH tumor cells after exposure to clinically used thiol-containing drugs.	Sulfhydryl Compounds	126-131	superoxide dismutase 2	Homo sapiens	64-69
15624308-2	2004	Manganese superoxide dismutase (Sod2) is one such gene whose expression levels have been shown to be elevated after exposure to the thiol compounds WR-1065 and N-acetyl-L-cysteine (NAC), resulting in an increase in radiation resistance.	Sulfhydryl Compounds	132-137	superoxide dismutase 2	Homo sapiens	32-36
15308628-7	2004	In contrast, VEGF-mediated induction of Mn-SOD was enhanced by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 and by dominant negative Akt and was decreased by constitutively active Akt.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	114-122	superoxide dismutase 2	Homo sapiens	40-46
15459441-4	2004	Sublethal ischemic insults release chemical signals (nitric oxide [NO], adenosine, and reactive oxygen species) that trigger a series of signaling events (eg, activation of protein kinase C, Src protein tyrosine kinases, Janus kinases 1/2, and nuclear factor-kappaB) and culminates in increased synthesis of inducible NO synthase, cyclooxygenase-2, heme oxygenase-1, aldose reductase, Mn superoxide dismutase, and probably other cardioprotective proteins.	Reactive Oxygen Species	87-110	superoxide dismutase 2	Homo sapiens	385-408
15205258-1	2004	SOD2 is an antioxidant protein that protects cells against mitochondrial superoxide.	Superoxides	73-83	superoxide dismutase 2	Homo sapiens	0-4
15205258-6	2004	Fluorescence-activated cell sorting (FACS) analysis of cells labeled with oxidation-sensitive dyes demonstrates enhanced production of superoxide and hydrogen peroxide by SOD2-deficient cells.	Superoxides	135-145	superoxide dismutase 2	Homo sapiens	171-175
15205258-6	2004	Fluorescence-activated cell sorting (FACS) analysis of cells labeled with oxidation-sensitive dyes demonstrates enhanced production of superoxide and hydrogen peroxide by SOD2-deficient cells.	Hydrogen Peroxide	150-167	superoxide dismutase 2	Homo sapiens	171-175
15205258-8	2004	Red cell proteome analysis demonstrates that several proteins involved in folding/chaperone function, redox regulation, adenosine triphosphate (ATP) synthesis, and red cell metabolism show altered expression in SOD2-deficient cells.	Adenosine Triphosphate	120-142	superoxide dismutase 2	Homo sapiens	211-215
15205258-8	2004	Red cell proteome analysis demonstrates that several proteins involved in folding/chaperone function, redox regulation, adenosine triphosphate (ATP) synthesis, and red cell metabolism show altered expression in SOD2-deficient cells.	Adenosine Triphosphate	144-147	superoxide dismutase 2	Homo sapiens	211-215
15308628-14	2004	Together, these data suggest that VEGF is uniquely coupled to Mn-SOD expression through growth factor-specific reactive oxygen species (ROS)-sensitive positive (protein kinase C-NF-kappaB) and negative (PI3K-Akt-forkhead) signaling pathways.	Reactive Oxygen Species	111-134	superoxide dismutase 2	Homo sapiens	62-68
15451059-2	2004	Here we show that a tris-malonic acid derivative of the fullerene C60 molecule (C3) is capable of removing the biologically important superoxide radical with a rate constant (k(C3)) of 2 x 10(6) mol(-1) s(-1), approximately 100-fold slower than the superoxide dismutases (SOD), a family of enzymes responsible for endogenous dismutation of superoxide.	tris-malonic acid	20-37	superoxide dismutase 2	Homo sapiens	272-275
15308628-14	2004	Together, these data suggest that VEGF is uniquely coupled to Mn-SOD expression through growth factor-specific reactive oxygen species (ROS)-sensitive positive (protein kinase C-NF-kappaB) and negative (PI3K-Akt-forkhead) signaling pathways.	Reactive Oxygen Species	136-139	superoxide dismutase 2	Homo sapiens	62-68
15451059-2	2004	Here we show that a tris-malonic acid derivative of the fullerene C60 molecule (C3) is capable of removing the biologically important superoxide radical with a rate constant (k(C3)) of 2 x 10(6) mol(-1) s(-1), approximately 100-fold slower than the superoxide dismutases (SOD), a family of enzymes responsible for endogenous dismutation of superoxide.	Fullerenes	56-65	superoxide dismutase 2	Homo sapiens	272-275
15451059-2	2004	Here we show that a tris-malonic acid derivative of the fullerene C60 molecule (C3) is capable of removing the biologically important superoxide radical with a rate constant (k(C3)) of 2 x 10(6) mol(-1) s(-1), approximately 100-fold slower than the superoxide dismutases (SOD), a family of enzymes responsible for endogenous dismutation of superoxide.	Superoxides	134-144	superoxide dismutase 2	Homo sapiens	272-275
15451059-2	2004	Here we show that a tris-malonic acid derivative of the fullerene C60 molecule (C3) is capable of removing the biologically important superoxide radical with a rate constant (k(C3)) of 2 x 10(6) mol(-1) s(-1), approximately 100-fold slower than the superoxide dismutases (SOD), a family of enzymes responsible for endogenous dismutation of superoxide.	Superoxides	249-259	superoxide dismutase 2	Homo sapiens	272-275
15331175-3	2004	For women carrying the MPO variant genotypes, the adjusted odds ratio of the SOD2 polymorphism (Val/Val vs. Ala/Ala) was 3.26 (95% CI, 1.55-6.83).	Valine	96-99	superoxide dismutase 2	Homo sapiens	77-81
15331175-3	2004	For women carrying the MPO variant genotypes, the adjusted odds ratio of the SOD2 polymorphism (Val/Val vs. Ala/Ala) was 3.26 (95% CI, 1.55-6.83).	Valine	100-103	superoxide dismutase 2	Homo sapiens	77-81
15331175-3	2004	For women carrying the MPO variant genotypes, the adjusted odds ratio of the SOD2 polymorphism (Val/Val vs. Ala/Ala) was 3.26 (95% CI, 1.55-6.83).	Alanine	108-111	superoxide dismutase 2	Homo sapiens	77-81
15331175-3	2004	For women carrying the MPO variant genotypes, the adjusted odds ratio of the SOD2 polymorphism (Val/Val vs. Ala/Ala) was 3.26 (95% CI, 1.55-6.83).	Alanine	112-115	superoxide dismutase 2	Homo sapiens	77-81
15554245-8	2004	2) An increase in H2O2 by downregulation or inhibition of catalase activity and/or upregulation of MnSOD activity inhibits apoptosis while a decrease in H2O2 by upregulation of catalase activity and/or downregulation of MnSOD activity supports apoptosis, possibly because of a supportive role of H2O2 in a survival pathway.	Hydrogen Peroxide	18-22	superoxide dismutase 2	Homo sapiens	220-225
15517870-8	2004	In addition, over expression of the human SOD2 gene (MnSOD) inhibited NF-kappaB and pGL3CB1EI1 activity, indicating that superoxide or some species derived from superoxide may have participated in the up-regulation of reporter activity in response to chronic exposure to fractionated ionizing radiation.	Superoxides	121-131	superoxide dismutase 2	Homo sapiens	42-46
15612529-8	2004	The increase in hydroxyl radical concentration was accompanied by an increase in antioxidant enzyme expression (SOD1 and SOD2), and an increase in nitrotyrosine expression was also observed, reflecting the increased production of NO and oxygen radicals.	Hydroxyl Radical	16-32	superoxide dismutase 2	Homo sapiens	121-125
15554245-7	2004	From the results reviewed here, two schemes for the involvement of MnSOD and catalase in the regulation of apoptosis can be extracted: 1) Both MnSOD and catalase inhibit apoptosis by removing superoxide anion radicals or H2O2, respectively, because these reactive oxygen species are mediators required for the apoptotic program or inhibit a survival pathway.	Superoxides	192-217	superoxide dismutase 2	Homo sapiens	67-72
15554245-7	2004	From the results reviewed here, two schemes for the involvement of MnSOD and catalase in the regulation of apoptosis can be extracted: 1) Both MnSOD and catalase inhibit apoptosis by removing superoxide anion radicals or H2O2, respectively, because these reactive oxygen species are mediators required for the apoptotic program or inhibit a survival pathway.	Superoxides	192-217	superoxide dismutase 2	Homo sapiens	143-148
15554245-7	2004	From the results reviewed here, two schemes for the involvement of MnSOD and catalase in the regulation of apoptosis can be extracted: 1) Both MnSOD and catalase inhibit apoptosis by removing superoxide anion radicals or H2O2, respectively, because these reactive oxygen species are mediators required for the apoptotic program or inhibit a survival pathway.	Hydrogen Peroxide	221-225	superoxide dismutase 2	Homo sapiens	67-72
15554245-7	2004	From the results reviewed here, two schemes for the involvement of MnSOD and catalase in the regulation of apoptosis can be extracted: 1) Both MnSOD and catalase inhibit apoptosis by removing superoxide anion radicals or H2O2, respectively, because these reactive oxygen species are mediators required for the apoptotic program or inhibit a survival pathway.	Hydrogen Peroxide	221-225	superoxide dismutase 2	Homo sapiens	143-148
15554245-7	2004	From the results reviewed here, two schemes for the involvement of MnSOD and catalase in the regulation of apoptosis can be extracted: 1) Both MnSOD and catalase inhibit apoptosis by removing superoxide anion radicals or H2O2, respectively, because these reactive oxygen species are mediators required for the apoptotic program or inhibit a survival pathway.	Reactive Oxygen Species	255-278	superoxide dismutase 2	Homo sapiens	67-72
15554245-7	2004	From the results reviewed here, two schemes for the involvement of MnSOD and catalase in the regulation of apoptosis can be extracted: 1) Both MnSOD and catalase inhibit apoptosis by removing superoxide anion radicals or H2O2, respectively, because these reactive oxygen species are mediators required for the apoptotic program or inhibit a survival pathway.	Reactive Oxygen Species	255-278	superoxide dismutase 2	Homo sapiens	143-148
15512801-5	2004	In contrast, PC-3 cells overexpressing MnSOD had less ROS production, less lipid peroxidation, and greater cell survival compared to PC-3 Wt cells.	Reactive Oxygen Species	54-57	superoxide dismutase 2	Homo sapiens	39-44
15512801-6	2004	Since MnSOD removes superoxide, these results suggest that superoxide free radical or its reaction products are responsible for part of the cytotoxicity associated with hyperthermia and that MnSOD can reduce cellular injury and thereby enhance heat tolerance.	Superoxides	20-30	superoxide dismutase 2	Homo sapiens	6-11
15512801-6	2004	Since MnSOD removes superoxide, these results suggest that superoxide free radical or its reaction products are responsible for part of the cytotoxicity associated with hyperthermia and that MnSOD can reduce cellular injury and thereby enhance heat tolerance.	Superoxides	59-69	superoxide dismutase 2	Homo sapiens	6-11
15375496-5	2004	There was a close relationship between the expression of nitrotyrosine and all three NOS isoforms (for all p<0.0005), catalase (p<0.0005) and MnSOD (p=0.043), in addition enlarged tumor size was in association with high nitrotyrosine (p=0.046), eNOS (p=0.005) and VEGF (p=0.046) levels.	3-nitrotyrosine	57-70	superoxide dismutase 2	Homo sapiens	148-153
15517870-8	2004	In addition, over expression of the human SOD2 gene (MnSOD) inhibited NF-kappaB and pGL3CB1EI1 activity, indicating that superoxide or some species derived from superoxide may have participated in the up-regulation of reporter activity in response to chronic exposure to fractionated ionizing radiation.	Superoxides	121-131	superoxide dismutase 2	Homo sapiens	53-58
15517870-8	2004	In addition, over expression of the human SOD2 gene (MnSOD) inhibited NF-kappaB and pGL3CB1EI1 activity, indicating that superoxide or some species derived from superoxide may have participated in the up-regulation of reporter activity in response to chronic exposure to fractionated ionizing radiation.	Superoxides	161-171	superoxide dismutase 2	Homo sapiens	42-46
15517870-8	2004	In addition, over expression of the human SOD2 gene (MnSOD) inhibited NF-kappaB and pGL3CB1EI1 activity, indicating that superoxide or some species derived from superoxide may have participated in the up-regulation of reporter activity in response to chronic exposure to fractionated ionizing radiation.	Superoxides	161-171	superoxide dismutase 2	Homo sapiens	53-58
15247771-1	2004	PURPOSE: The glutathione peroxidase 1 gene (GPX1) and the manganese superoxide dismutase gene (MnSOD) encode the main antioxidant enzymes that detoxify endogenous reactive oxygen species involved in carcinogenesis.	Reactive Oxygen Species	163-186	superoxide dismutase 2	Homo sapiens	58-88
15310847-4	2004	These processes are inhibited by Mn-superoxide dismutase, establishing the generation of O(2)(-) and its role as an essential reactant.	o(2)	89-93	superoxide dismutase 2	Homo sapiens	33-56
15039138-3	2004	One of the most important free radical scavenging enzymes, mitochondrial manganese superoxide dismutase (MnSOD), has been shown to be elevated in mesothelioma (K. Kahlos et al., 1998, Am.	Free Radicals	26-38	superoxide dismutase 2	Homo sapiens	73-103
15039138-3	2004	One of the most important free radical scavenging enzymes, mitochondrial manganese superoxide dismutase (MnSOD), has been shown to be elevated in mesothelioma (K. Kahlos et al., 1998, Am.	Free Radicals	26-38	superoxide dismutase 2	Homo sapiens	105-110
15039138-13	2004	Association with oxidative/nitrosative stress in mesothelioma using nitrotyrosine immunostaining pointed to a tendency for more intense reactivity in those mesotheliomas with higher MnSOD expression (P = 0.069).	3-nitrotyrosine	68-81	superoxide dismutase 2	Homo sapiens	182-187
15305022-1	2004	Manganese superoxide dismutase (MnSOD) is an antioxidative enzyme that scavenges superoxide radicals and is localized in the mitochondrial matrix.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
15337840-6	2004	The downregulation of the MnSOD expression may lead to an increase of free-radical production and thus explain why the cells in the chronic stress model were more vulnerable to other oxidative stress influences.	Free Radicals	70-82	superoxide dismutase 2	Homo sapiens	26-31
15247771-1	2004	PURPOSE: The glutathione peroxidase 1 gene (GPX1) and the manganese superoxide dismutase gene (MnSOD) encode the main antioxidant enzymes that detoxify endogenous reactive oxygen species involved in carcinogenesis.	Reactive Oxygen Species	163-186	superoxide dismutase 2	Homo sapiens	95-100
15247771-3	2004	MATERIALS AND METHODS: Genotypes of the leucine (Leu) to proline (Pro) polymorphism at codon 198 of GPX1, the alanine (Ala) to Valine (Val) polymorphism in exon 2 and the isoleucine to threonine polymorphism at codon 56 of MnSOD were determined by a polymerase chain reaction-restriction fragment length polymorphism technique in 213 patients and 209 normal controls.	Proline	66-69	superoxide dismutase 2	Homo sapiens	223-228
15247771-9	2004	CONCLUSIONS: The GPX1 Pro/Leu genotype may significantly increase the risk of bladder cancer and the increased risk may be modified by the Ala-9Val MnSOD polymorphism.	Alanine	139-142	superoxide dismutase 2	Homo sapiens	148-153
15247771-9	2004	CONCLUSIONS: The GPX1 Pro/Leu genotype may significantly increase the risk of bladder cancer and the increased risk may be modified by the Ala-9Val MnSOD polymorphism.	9val	143-147	superoxide dismutase 2	Homo sapiens	148-153
15170341-0	2004	Role of hydrogen bonding in the active site of human manganese superoxide dismutase.	Hydrogen	8-16	superoxide dismutase 2	Homo sapiens	53-83
15087454-2	2004	We have reported that NF-kappaB is essential but not sufficient for the synergistic induction of MnSOD by phorbol 12-myristate 13-acetate and cytokines.	Tetradecanoylphorbol Acetate	106-137	superoxide dismutase 2	Homo sapiens	97-102
15087454-10	2004	These results identify NPM as a partner of the NF-kappaB transcription complex in the induction of MnSOD by phorbol 12-myristate 13-acetate and cytokines.	Tetradecanoylphorbol Acetate	108-139	superoxide dismutase 2	Homo sapiens	99-104
15168344-3	2004	Within the mitochondria manganese superoxide dismutase (MnSOD) affords the major defense against ROS.	Reactive Oxygen Species	97-100	superoxide dismutase 2	Homo sapiens	24-54
15168344-3	2004	Within the mitochondria manganese superoxide dismutase (MnSOD) affords the major defense against ROS.	Reactive Oxygen Species	97-100	superoxide dismutase 2	Homo sapiens	56-61
15168344-10	2004	These results indicate that neoplastic cells in breast carcinomas retain their capability to produce MnSOD and thus protected from the possible cellular damage provoked by reactive oxygen species.	Reactive Oxygen Species	172-195	superoxide dismutase 2	Homo sapiens	101-106
15193990-2	2004	Two allelic variants have been described for the SOD2 gene (Ile58Thr involves a C to T substitution at nucleotide residue 339 and Ala-9Val involves a T to C substitution at nucleotide residue 1183).	ala-9val	130-138	superoxide dismutase 2	Homo sapiens	49-53
15193990-9	2004	CONCLUSIONS: We have extended a method of SOD2 polymorphism (Ala-9Val) in mitochondrial sequence.	Alanine	61-64	superoxide dismutase 2	Homo sapiens	42-46
15170341-1	2004	The side chain of Gln143, a conserved residue in manganese superoxide dismutase (MnSOD), forms a hydrogen bond with the manganese-bound solvent and is critical in maintaining catalytic activity.	Hydrogen	97-105	superoxide dismutase 2	Homo sapiens	49-79
15170341-1	2004	The side chain of Gln143, a conserved residue in manganese superoxide dismutase (MnSOD), forms a hydrogen bond with the manganese-bound solvent and is critical in maintaining catalytic activity.	Hydrogen	97-105	superoxide dismutase 2	Homo sapiens	81-86
15170341-1	2004	The side chain of Gln143, a conserved residue in manganese superoxide dismutase (MnSOD), forms a hydrogen bond with the manganese-bound solvent and is critical in maintaining catalytic activity.	Manganese	49-58	superoxide dismutase 2	Homo sapiens	81-86
15170341-6	2004	The crystal structure of Y34F/W123F human MnSOD at 1.95 A resolution suggests that this effect is not related to a conformational change in the side chain of Gln143, which does not change orientation in Y34F/W123F, but rather to more subtle electronic effects due to the loss of hydrogen bonding to the carboxamide side chain of Gln143.	Hydrogen	279-287	superoxide dismutase 2	Homo sapiens	42-47
15170341-6	2004	The crystal structure of Y34F/W123F human MnSOD at 1.95 A resolution suggests that this effect is not related to a conformational change in the side chain of Gln143, which does not change orientation in Y34F/W123F, but rather to more subtle electronic effects due to the loss of hydrogen bonding to the carboxamide side chain of Gln143.	carboxamide	303-314	superoxide dismutase 2	Homo sapiens	42-47
15170341-7	2004	Wild-type MnSOD containing Trp123 and Tyr34 has approximately the same thermal stability compared with mutants containing Phe at these positions, suggesting the hydrogen bonds formed by these residues have functional rather than structural roles.	Phenylalanine	122-125	superoxide dismutase 2	Homo sapiens	10-15
15170341-7	2004	Wild-type MnSOD containing Trp123 and Tyr34 has approximately the same thermal stability compared with mutants containing Phe at these positions, suggesting the hydrogen bonds formed by these residues have functional rather than structural roles.	Hydrogen	161-169	superoxide dismutase 2	Homo sapiens	10-15
15130278-4	2004	Overexpression of MnSOD resulted in a seven- to eightfold increase in reduced glutathione (GSH), 18- to 26-fold increase in oxidized glutathione (GSSG), and a two- to threefold decrease in the ratio of GSH to GSSG.	Glutathione	78-89	superoxide dismutase 2	Homo sapiens	18-23
15130278-4	2004	Overexpression of MnSOD resulted in a seven- to eightfold increase in reduced glutathione (GSH), 18- to 26-fold increase in oxidized glutathione (GSSG), and a two- to threefold decrease in the ratio of GSH to GSSG.	Glutathione	91-94	superoxide dismutase 2	Homo sapiens	18-23
15130278-4	2004	Overexpression of MnSOD resulted in a seven- to eightfold increase in reduced glutathione (GSH), 18- to 26-fold increase in oxidized glutathione (GSSG), and a two- to threefold decrease in the ratio of GSH to GSSG.	Glutathione	133-144	superoxide dismutase 2	Homo sapiens	18-23
15130278-4	2004	Overexpression of MnSOD resulted in a seven- to eightfold increase in reduced glutathione (GSH), 18- to 26-fold increase in oxidized glutathione (GSSG), and a two- to threefold decrease in the ratio of GSH to GSSG.	Glutathione Disulfide	146-150	superoxide dismutase 2	Homo sapiens	18-23
15130278-4	2004	Overexpression of MnSOD resulted in a seven- to eightfold increase in reduced glutathione (GSH), 18- to 26-fold increase in oxidized glutathione (GSSG), and a two- to threefold decrease in the ratio of GSH to GSSG.	Glutathione	202-205	superoxide dismutase 2	Homo sapiens	18-23
15130278-4	2004	Overexpression of MnSOD resulted in a seven- to eightfold increase in reduced glutathione (GSH), 18- to 26-fold increase in oxidized glutathione (GSSG), and a two- to threefold decrease in the ratio of GSH to GSSG.	Glutathione Disulfide	209-213	superoxide dismutase 2	Homo sapiens	18-23
15130278-5	2004	MnSOD-overexpressing cells showed an increase in sensitivity to the cytotoxicity of buthionine sulfoximine, a glutathione-depleting agent, and vitamin C, but a decrease in sensitivity to sodium selenite.	Buthionine Sulfoximine	84-106	superoxide dismutase 2	Homo sapiens	0-5
15130278-5	2004	MnSOD-overexpressing cells showed an increase in sensitivity to the cytotoxicity of buthionine sulfoximine, a glutathione-depleting agent, and vitamin C, but a decrease in sensitivity to sodium selenite.	Glutathione	110-121	superoxide dismutase 2	Homo sapiens	0-5
15130278-5	2004	MnSOD-overexpressing cells showed an increase in sensitivity to the cytotoxicity of buthionine sulfoximine, a glutathione-depleting agent, and vitamin C, but a decrease in sensitivity to sodium selenite.	Ascorbic Acid	143-152	superoxide dismutase 2	Homo sapiens	0-5
15130278-5	2004	MnSOD-overexpressing cells showed an increase in sensitivity to the cytotoxicity of buthionine sulfoximine, a glutathione-depleting agent, and vitamin C, but a decrease in sensitivity to sodium selenite.	Sodium Selenite	187-202	superoxide dismutase 2	Homo sapiens	0-5
15130278-6	2004	Treatment with a superoxide dismutase (SOD) mimic MnTMPyP resulted in similar effects of MnSOD overexpression on cell responses to vitamin C and selenium.	Ascorbic Acid	131-140	superoxide dismutase 2	Homo sapiens	89-94
15130279-2	2004	Manganese superoxide dismutase (MnSOD) is a nuclear-encoded mitochondrial enzyme, which scavenges superoxide generated from the electron-transport chain in mitochondria.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
15130279-8	2004	These results suggest that only when MnSOD is located in mitochondria is it efficient in protecting against cellular injuries by H/R, and they also indicate that mitochondria are primary sites of H/R-induced cellular oxidative injuries.	r	131-132	superoxide dismutase 2	Homo sapiens	37-42
14729580-12	2004	MnSOD Val/Val genotype increased the risk of bladder cancer with OR of 1.91 (95% CI = 1.20-3.04), and there was a combined effect with smoking (OR = 7.20, 95% CI = 3.23-16.1) and PAH (OR = 3.02, 95% CI = 1.35-6.74).	Polycyclic Aromatic Hydrocarbons	179-182	superoxide dismutase 2	Homo sapiens	0-5
15118344-0	2004	Induction of manganese-superoxide dismutase by YS 51, a synthetic 1-(beta-naphtylmethyl)6,7-dihydroxy- 1,2,3,4-tetrahydroisoquinoline alkaloid: implication for anti-inflammatory actions.	Yttrium	47-49	superoxide dismutase 2	Homo sapiens	13-43
15184255-3	2004	A valine (Val) to alanine (Ala) substitution at amino acid 16, occurring in the mitochondrial targeting sequence of the MnSOD gene, has been associated with an increase in breast cancer risk.	Valine	2-8	superoxide dismutase 2	Homo sapiens	120-125
15184255-3	2004	A valine (Val) to alanine (Ala) substitution at amino acid 16, occurring in the mitochondrial targeting sequence of the MnSOD gene, has been associated with an increase in breast cancer risk.	Valine	10-13	superoxide dismutase 2	Homo sapiens	120-125
15184255-3	2004	A valine (Val) to alanine (Ala) substitution at amino acid 16, occurring in the mitochondrial targeting sequence of the MnSOD gene, has been associated with an increase in breast cancer risk.	Alanine	18-25	superoxide dismutase 2	Homo sapiens	120-125
15184255-3	2004	A valine (Val) to alanine (Ala) substitution at amino acid 16, occurring in the mitochondrial targeting sequence of the MnSOD gene, has been associated with an increase in breast cancer risk.	Alanine	27-30	superoxide dismutase 2	Homo sapiens	120-125
15184255-8	2004	We did observe evidence that the MnSOD Ala allele may modify the relation of cigarette smoking with breast cancer risk.	Alanine	39-42	superoxide dismutase 2	Homo sapiens	33-38
15196853-5	2004	RESULTS: For SOD2, women with the TC (val/ala) or CC (ala/ala) genotypes were at increased risk [odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1-4.0].	Technetium	34-36	superoxide dismutase 2	Homo sapiens	13-17
15196853-5	2004	RESULTS: For SOD2, women with the TC (val/ala) or CC (ala/ala) genotypes were at increased risk [odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1-4.0].	Valine	38-41	superoxide dismutase 2	Homo sapiens	13-17
15196853-5	2004	RESULTS: For SOD2, women with the TC (val/ala) or CC (ala/ala) genotypes were at increased risk [odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1-4.0].	Alanine	42-45	superoxide dismutase 2	Homo sapiens	13-17
15196853-5	2004	RESULTS: For SOD2, women with the TC (val/ala) or CC (ala/ala) genotypes were at increased risk [odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1-4.0].	Alanine	54-57	superoxide dismutase 2	Homo sapiens	13-17
15196853-5	2004	RESULTS: For SOD2, women with the TC (val/ala) or CC (ala/ala) genotypes were at increased risk [odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1-4.0].	Alanine	54-57	superoxide dismutase 2	Homo sapiens	13-17
15213518-4	2004	The homozygous variant MnSOD genotype was associated with increased lung cancer risk among individuals with zero or "low" AES (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.52-3.01) and no association (OR = 1.00; 95% CI = 0.36-2.73) among the "high" AES group.	aes	122-125	superoxide dismutase 2	Homo sapiens	23-28
15213518-4	2004	The homozygous variant MnSOD genotype was associated with increased lung cancer risk among individuals with zero or "low" AES (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.52-3.01) and no association (OR = 1.00; 95% CI = 0.36-2.73) among the "high" AES group.	aes	259-262	superoxide dismutase 2	Homo sapiens	23-28
15118344-1	2004	The effect of YS 51, a synthetic 1-(beta-naphtylmethyl)6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline alkaloid, on the expression of manganese-superoxide dismutase (Mn-SOD), an antioxidant enzyme, was examined in sheep pulmonary artery endothelial cells (SPAEC) and a human cervical carcinoma cell line (Hela).	1-(beta-naphtylmethyl)6,7-dihydroxy	33-68	superoxide dismutase 2	Homo sapiens	163-169
15118344-3	2004	YS 51 also showed synergistic effects on the induction of Mn-SOD mRNA with phorbol-12-myristate-13-acetate (TPA) and/or tumor necrosis factor-alpha (TNF-alpha).	Yttrium	0-2	superoxide dismutase 2	Homo sapiens	58-64
15118344-3	2004	YS 51 also showed synergistic effects on the induction of Mn-SOD mRNA with phorbol-12-myristate-13-acetate (TPA) and/or tumor necrosis factor-alpha (TNF-alpha).	Tetradecanoylphorbol Acetate	75-106	superoxide dismutase 2	Homo sapiens	58-64
15118344-3	2004	YS 51 also showed synergistic effects on the induction of Mn-SOD mRNA with phorbol-12-myristate-13-acetate (TPA) and/or tumor necrosis factor-alpha (TNF-alpha).	Tetradecanoylphorbol Acetate	108-111	superoxide dismutase 2	Homo sapiens	58-64
15118344-0	2004	Induction of manganese-superoxide dismutase by YS 51, a synthetic 1-(beta-naphtylmethyl)6,7-dihydroxy- 1,2,3,4-tetrahydroisoquinoline alkaloid: implication for anti-inflammatory actions.	1-(beta-naphtylmethyl)6,7-dihydroxy- 1,2,3,4-tetrahydroisoquinoline alkaloid	66-142	superoxide dismutase 2	Homo sapiens	13-43
15118344-4	2004	In Hela cells, the induction of Mn-SOD mRNA by YS 51 was in a time- and dose-dependent manner and the expression of Mn-SOD mRNA was increased to a maximum of 4-fold in 9 h. Enhancement of Mn-SOD mRNA by YS 51 was completely abolished by actinomycin D but not cycloheximide, suggesting that the induction of Mn-SOD mRNA byYS 51 is independent of new protein synthesis.	Dactinomycin	237-250	superoxide dismutase 2	Homo sapiens	32-38
15118344-4	2004	In Hela cells, the induction of Mn-SOD mRNA by YS 51 was in a time- and dose-dependent manner and the expression of Mn-SOD mRNA was increased to a maximum of 4-fold in 9 h. Enhancement of Mn-SOD mRNA by YS 51 was completely abolished by actinomycin D but not cycloheximide, suggesting that the induction of Mn-SOD mRNA byYS 51 is independent of new protein synthesis.	Dactinomycin	237-250	superoxide dismutase 2	Homo sapiens	116-122
15118344-4	2004	In Hela cells, the induction of Mn-SOD mRNA by YS 51 was in a time- and dose-dependent manner and the expression of Mn-SOD mRNA was increased to a maximum of 4-fold in 9 h. Enhancement of Mn-SOD mRNA by YS 51 was completely abolished by actinomycin D but not cycloheximide, suggesting that the induction of Mn-SOD mRNA byYS 51 is independent of new protein synthesis.	Dactinomycin	237-250	superoxide dismutase 2	Homo sapiens	116-122
15118344-4	2004	In Hela cells, the induction of Mn-SOD mRNA by YS 51 was in a time- and dose-dependent manner and the expression of Mn-SOD mRNA was increased to a maximum of 4-fold in 9 h. Enhancement of Mn-SOD mRNA by YS 51 was completely abolished by actinomycin D but not cycloheximide, suggesting that the induction of Mn-SOD mRNA byYS 51 is independent of new protein synthesis.	Dactinomycin	237-250	superoxide dismutase 2	Homo sapiens	116-122
15118344-4	2004	In Hela cells, the induction of Mn-SOD mRNA by YS 51 was in a time- and dose-dependent manner and the expression of Mn-SOD mRNA was increased to a maximum of 4-fold in 9 h. Enhancement of Mn-SOD mRNA by YS 51 was completely abolished by actinomycin D but not cycloheximide, suggesting that the induction of Mn-SOD mRNA byYS 51 is independent of new protein synthesis.	Cycloheximide	259-272	superoxide dismutase 2	Homo sapiens	32-38
15118344-1	2004	The effect of YS 51, a synthetic 1-(beta-naphtylmethyl)6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline alkaloid, on the expression of manganese-superoxide dismutase (Mn-SOD), an antioxidant enzyme, was examined in sheep pulmonary artery endothelial cells (SPAEC) and a human cervical carcinoma cell line (Hela).	1-(beta-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetra-hydroisoquinoline	14-19	superoxide dismutase 2	Homo sapiens	131-161
15118344-1	2004	The effect of YS 51, a synthetic 1-(beta-naphtylmethyl)6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline alkaloid, on the expression of manganese-superoxide dismutase (Mn-SOD), an antioxidant enzyme, was examined in sheep pulmonary artery endothelial cells (SPAEC) and a human cervical carcinoma cell line (Hela).	1-(beta-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetra-hydroisoquinoline	14-19	superoxide dismutase 2	Homo sapiens	163-169
15118344-4	2004	In Hela cells, the induction of Mn-SOD mRNA by YS 51 was in a time- and dose-dependent manner and the expression of Mn-SOD mRNA was increased to a maximum of 4-fold in 9 h. Enhancement of Mn-SOD mRNA by YS 51 was completely abolished by actinomycin D but not cycloheximide, suggesting that the induction of Mn-SOD mRNA byYS 51 is independent of new protein synthesis.	Cycloheximide	259-272	superoxide dismutase 2	Homo sapiens	116-122
15118344-1	2004	The effect of YS 51, a synthetic 1-(beta-naphtylmethyl)6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline alkaloid, on the expression of manganese-superoxide dismutase (Mn-SOD), an antioxidant enzyme, was examined in sheep pulmonary artery endothelial cells (SPAEC) and a human cervical carcinoma cell line (Hela).	1-(beta-naphtylmethyl)6,7-dihydroxy	33-68	superoxide dismutase 2	Homo sapiens	131-161
15118344-4	2004	In Hela cells, the induction of Mn-SOD mRNA by YS 51 was in a time- and dose-dependent manner and the expression of Mn-SOD mRNA was increased to a maximum of 4-fold in 9 h. Enhancement of Mn-SOD mRNA by YS 51 was completely abolished by actinomycin D but not cycloheximide, suggesting that the induction of Mn-SOD mRNA byYS 51 is independent of new protein synthesis.	Cycloheximide	259-272	superoxide dismutase 2	Homo sapiens	116-122
15128298-6	2004	The coding sequences were expressed in Escherichia coli as six-histidine tagged recombinant proteins and generated products with molecular masses of 86.1 kDa for HSP and 22.4 kDa for MnSOD.	Histidine	63-72	superoxide dismutase 2	Homo sapiens	183-188
15118344-4	2004	In Hela cells, the induction of Mn-SOD mRNA by YS 51 was in a time- and dose-dependent manner and the expression of Mn-SOD mRNA was increased to a maximum of 4-fold in 9 h. Enhancement of Mn-SOD mRNA by YS 51 was completely abolished by actinomycin D but not cycloheximide, suggesting that the induction of Mn-SOD mRNA byYS 51 is independent of new protein synthesis.	Cycloheximide	259-272	superoxide dismutase 2	Homo sapiens	116-122
15118344-5	2004	Pretreatment of curcumin, an inhibitor of c-jun N-terminal kinase (JNK), dose-dependently suppressed the induction of Mn-SOD mRNA by YS 51, but not by 2"-amino-3"-methoxyflavone (PD98059) and 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)imidazol (SB203580), inhibitors of mitogen-activated protein kinase.	Curcumin	16-24	superoxide dismutase 2	Homo sapiens	118-124
15118344-5	2004	Pretreatment of curcumin, an inhibitor of c-jun N-terminal kinase (JNK), dose-dependently suppressed the induction of Mn-SOD mRNA by YS 51, but not by 2"-amino-3"-methoxyflavone (PD98059) and 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)imidazol (SB203580), inhibitors of mitogen-activated protein kinase.	Yttrium	133-135	superoxide dismutase 2	Homo sapiens	118-124
15118344-5	2004	Pretreatment of curcumin, an inhibitor of c-jun N-terminal kinase (JNK), dose-dependently suppressed the induction of Mn-SOD mRNA by YS 51, but not by 2"-amino-3"-methoxyflavone (PD98059) and 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)imidazol (SB203580), inhibitors of mitogen-activated protein kinase.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	179-186	superoxide dismutase 2	Homo sapiens	118-124
15118344-5	2004	Pretreatment of curcumin, an inhibitor of c-jun N-terminal kinase (JNK), dose-dependently suppressed the induction of Mn-SOD mRNA by YS 51, but not by 2"-amino-3"-methoxyflavone (PD98059) and 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)imidazol (SB203580), inhibitors of mitogen-activated protein kinase.	4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)imidazol	192-259	superoxide dismutase 2	Homo sapiens	118-124
15118344-5	2004	Pretreatment of curcumin, an inhibitor of c-jun N-terminal kinase (JNK), dose-dependently suppressed the induction of Mn-SOD mRNA by YS 51, but not by 2"-amino-3"-methoxyflavone (PD98059) and 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)imidazol (SB203580), inhibitors of mitogen-activated protein kinase.	SB 203580	261-269	superoxide dismutase 2	Homo sapiens	118-124
15118344-7	2004	These results implicated that the JNK pathway appears to play a crucial role in mediating the YS 51-induced Mn-SOD gene expression, and that up-regulation of Mn-SOD would contribute to the anti-inflammatory actions mediated by YS 51.	Yttrium	94-96	superoxide dismutase 2	Homo sapiens	108-114
15118344-7	2004	These results implicated that the JNK pathway appears to play a crucial role in mediating the YS 51-induced Mn-SOD gene expression, and that up-regulation of Mn-SOD would contribute to the anti-inflammatory actions mediated by YS 51.	Yttrium	227-229	superoxide dismutase 2	Homo sapiens	158-164
14967442-0	2004	Ascorbate as a "redox sensor" and protector against irradiation-induced oxidative stress in 32D CL 3 hematopoietic cells and subclones overexpressing human manganese superoxide dismutase.	Ascorbic Acid	0-9	superoxide dismutase 2	Homo sapiens	156-186
15059885-2	2004	Microarray expression analysis of doxorubicin exposed, related human lymphoblasts, p53 wild-type (WT) Tk6, and p53 mutant WTK1 identified the p53-dependent up-regulation of manganese superoxide dismutase (MnSOD) and glutathione peroxidase 1 (GPx).	Doxorubicin	34-45	superoxide dismutase 2	Homo sapiens	173-203
15059885-4	2004	A 3-fold increase in the MnSOD promoter activity was observed after the induction of p53 in Li-Fraumeni syndrome (LFS) fibroblast, TR9-7, expressing p53 under the control of a tetracycline-regulated promoter.	Tetracycline	176-188	superoxide dismutase 2	Homo sapiens	25-30
15059885-10	2004	We observed both the release of cytochrome C and Ca(2+) from the mitochondria into the cytoplasm and an increased frequency of apoptotic cells after p53 induction in the TR9-7 cells that coincided with an increased expression of MnSOD and GPx, and the level of reactive oxygen species.	Reactive Oxygen Species	261-284	superoxide dismutase 2	Homo sapiens	229-234
14688256-2	2004	Mn-SOD serves as the primary cellular defense against oxidative damage by converting superoxide radicals (O(2)(-)) to O(2) and H(2)O(2).	Superoxides	85-95	superoxide dismutase 2	Homo sapiens	0-6
14688256-2	2004	Mn-SOD serves as the primary cellular defense against oxidative damage by converting superoxide radicals (O(2)(-)) to O(2) and H(2)O(2).	Superoxides	106-110	superoxide dismutase 2	Homo sapiens	0-6
14688256-2	2004	Mn-SOD serves as the primary cellular defense against oxidative damage by converting superoxide radicals (O(2)(-)) to O(2) and H(2)O(2).	Superoxides	118-122	superoxide dismutase 2	Homo sapiens	0-6
14688256-2	2004	Mn-SOD serves as the primary cellular defense against oxidative damage by converting superoxide radicals (O(2)(-)) to O(2) and H(2)O(2).	h(2)	127-131	superoxide dismutase 2	Homo sapiens	0-6
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Superoxides	121-139	superoxide dismutase 2	Homo sapiens	66-96
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Superoxides	121-139	superoxide dismutase 2	Homo sapiens	98-103
14656937-9	2004	Co-localization studies established that the mitochondria are a primary site for 3-nitrotyrosine localization and immunoprecipitation/immunoblotting experiments confirmed that MnSOD tyrosine nitration occurs in AIDS-KS cells.	Tyrosine	88-96	superoxide dismutase 2	Homo sapiens	176-181
14656937-9	2004	Co-localization studies established that the mitochondria are a primary site for 3-nitrotyrosine localization and immunoprecipitation/immunoblotting experiments confirmed that MnSOD tyrosine nitration occurs in AIDS-KS cells.	Potassium	216-218	superoxide dismutase 2	Homo sapiens	176-181
14656937-10	2004	Functional SOD assays showed that AIDS-KS cells possess significantly lower MnSOD activity relative to matched control cells; findings which correspond with ongoing MnSOD tyrosine nitration and subsequent inactivation within AIDS-KS cells.	Tyrosine	171-179	superoxide dismutase 2	Homo sapiens	165-170
14656937-10	2004	Functional SOD assays showed that AIDS-KS cells possess significantly lower MnSOD activity relative to matched control cells; findings which correspond with ongoing MnSOD tyrosine nitration and subsequent inactivation within AIDS-KS cells.	Potassium	39-41	superoxide dismutase 2	Homo sapiens	11-14
14656937-10	2004	Functional SOD assays showed that AIDS-KS cells possess significantly lower MnSOD activity relative to matched control cells; findings which correspond with ongoing MnSOD tyrosine nitration and subsequent inactivation within AIDS-KS cells.	Potassium	39-41	superoxide dismutase 2	Homo sapiens	76-81
14656937-10	2004	Functional SOD assays showed that AIDS-KS cells possess significantly lower MnSOD activity relative to matched control cells; findings which correspond with ongoing MnSOD tyrosine nitration and subsequent inactivation within AIDS-KS cells.	Potassium	39-41	superoxide dismutase 2	Homo sapiens	165-170
14670077-9	2004	MnSOD activation was blocked by inhibitors of JNK (JNKI1) and p38 MAPK (SB203580), but not by an ERK (extracellular-signal-regulated kinase) inhibitor (U0126), in HCV-replicating and Ad-NS5A-transduced cells.	SB 203580	72-80	superoxide dismutase 2	Homo sapiens	0-5
14672935-1	2004	The iron- and manganese-containing superoxide dismutases (Fe/Mn-SOD) share the same chemical function and spatial structure but can be distinguished according to their modes of oligomerization and their metal ion specificity.	Iron	4-8	superoxide dismutase 2	Homo sapiens	61-67
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Superoxides	141-145	superoxide dismutase 2	Homo sapiens	66-96
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Superoxides	141-145	superoxide dismutase 2	Homo sapiens	98-103
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Hydrogen Peroxide	156-173	superoxide dismutase 2	Homo sapiens	66-96
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Hydrogen Peroxide	156-173	superoxide dismutase 2	Homo sapiens	98-103
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Hydrogen Peroxide	175-182	superoxide dismutase 2	Homo sapiens	66-96
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Hydrogen Peroxide	175-182	superoxide dismutase 2	Homo sapiens	98-103
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Hydrogen Peroxide	175-183	superoxide dismutase 2	Homo sapiens	66-96
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Hydrogen Peroxide	175-183	superoxide dismutase 2	Homo sapiens	98-103
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Water	249-254	superoxide dismutase 2	Homo sapiens	66-96
15018733-1	2004	Pancreatic cancer has low levels of antioxidant enzymes including manganese superoxide dismutase (MnSOD), which converts superoxide radical (O(2)(*-)) into hydrogen peroxide (H(2)O(2)), and glutathione peroxidase (GPx), which converts H(2)O(2) into water.	Water	249-254	superoxide dismutase 2	Homo sapiens	98-103
14967442-5	2004	RESULTS: Manganese superoxide dismutase-overexpressing 2C6 cells maintained higher levels of ascorbate (5.4 +/- 0.5 and 2.6 +/- 0.5 nmol/10(6) cells, respectively) and thiols (14.0 +/- 0.1 and 11.1 +/- 0.2 nmol/10(6) cells) compared to 32D cl 3 parent cells.	Ascorbic Acid	93-102	superoxide dismutase 2	Homo sapiens	9-39
14967442-5	2004	RESULTS: Manganese superoxide dismutase-overexpressing 2C6 cells maintained higher levels of ascorbate (5.4 +/- 0.5 and 2.6 +/- 0.5 nmol/10(6) cells, respectively) and thiols (14.0 +/- 0.1 and 11.1 +/- 0.2 nmol/10(6) cells) compared to 32D cl 3 parent cells.	Sulfhydryl Compounds	168-174	superoxide dismutase 2	Homo sapiens	9-39
14967442-5	2004	RESULTS: Manganese superoxide dismutase-overexpressing 2C6 cells maintained higher levels of ascorbate (5.4 +/- 0.5 and 2.6 +/- 0.5 nmol/10(6) cells, respectively) and thiols (14.0 +/- 0.1 and 11.1 +/- 0.2 nmol/10(6) cells) compared to 32D cl 3 parent cells.	32d cl	236-242	superoxide dismutase 2	Homo sapiens	9-39
14967442-8	2004	CONCLUSIONS: Manganese superoxide dismutase overexpression protects 2C6 cells from irradiation damage by scavenging ROS that readily interact with major endogenous antioxidants--ascorbate and GSH--in nontransfected hematopoietic 32D cl 3 cells.	Reactive Oxygen Species	116-119	superoxide dismutase 2	Homo sapiens	13-43
14967442-8	2004	CONCLUSIONS: Manganese superoxide dismutase overexpression protects 2C6 cells from irradiation damage by scavenging ROS that readily interact with major endogenous antioxidants--ascorbate and GSH--in nontransfected hematopoietic 32D cl 3 cells.	Ascorbic Acid	178-187	superoxide dismutase 2	Homo sapiens	13-43
14967442-8	2004	CONCLUSIONS: Manganese superoxide dismutase overexpression protects 2C6 cells from irradiation damage by scavenging ROS that readily interact with major endogenous antioxidants--ascorbate and GSH--in nontransfected hematopoietic 32D cl 3 cells.	Glutathione	192-195	superoxide dismutase 2	Homo sapiens	13-43
14638684-1	2004	The side chains of His30 and Tyr166 from adjacent subunits in the homotetramer human manganese superoxide dismutase (Mn-SOD) form a hydrogen bond across the dimer interface and participate in a hydrogen-bonded network that extends to the active site.	Hydrogen	132-140	superoxide dismutase 2	Homo sapiens	85-115
14660625-11	2004	Heme oxygenase-1 expression was increased in rho(0) cells, and a heme oxygenase-1 inhibitor decreased the induction of MnSOD in rho(0) cells and their resistance against ROS donors.	ros	170-173	superoxide dismutase 2	Homo sapiens	119-124
14638684-1	2004	The side chains of His30 and Tyr166 from adjacent subunits in the homotetramer human manganese superoxide dismutase (Mn-SOD) form a hydrogen bond across the dimer interface and participate in a hydrogen-bonded network that extends to the active site.	Hydrogen	132-140	superoxide dismutase 2	Homo sapiens	117-123
14638684-1	2004	The side chains of His30 and Tyr166 from adjacent subunits in the homotetramer human manganese superoxide dismutase (Mn-SOD) form a hydrogen bond across the dimer interface and participate in a hydrogen-bonded network that extends to the active site.	Hydrogen	194-202	superoxide dismutase 2	Homo sapiens	85-115
14638684-1	2004	The side chains of His30 and Tyr166 from adjacent subunits in the homotetramer human manganese superoxide dismutase (Mn-SOD) form a hydrogen bond across the dimer interface and participate in a hydrogen-bonded network that extends to the active site.	Hydrogen	194-202	superoxide dismutase 2	Homo sapiens	117-123
14678790-4	2004	Cytochrome c catalyzes both self- and adjacent-molecule (hydroxyphenylacetic acid, Mn-superoxide dismutase) nitration via heme-dependent mechanisms involving tyrosyl radical and *NO2 production, as for phagocyte peroxidases.	Heme	122-126	superoxide dismutase 2	Homo sapiens	83-106
15051313-4	2004	A network of intramitochondrial antioxidants consisting of the enzymes Mn-superoxide dismutase and glutathione peroxidase and of the reductants NADH(2), ubiquinol and reduced glutathione, is operative in minimizing the potentially harmful effects of O(2)(-), NO, H(2)O(2) and ONOO(-).	nadh(2)	144-151	superoxide dismutase 2	Homo sapiens	71-94
15051313-4	2004	A network of intramitochondrial antioxidants consisting of the enzymes Mn-superoxide dismutase and glutathione peroxidase and of the reductants NADH(2), ubiquinol and reduced glutathione, is operative in minimizing the potentially harmful effects of O(2)(-), NO, H(2)O(2) and ONOO(-).	ubiquinol	153-162	superoxide dismutase 2	Homo sapiens	71-94
15051313-4	2004	A network of intramitochondrial antioxidants consisting of the enzymes Mn-superoxide dismutase and glutathione peroxidase and of the reductants NADH(2), ubiquinol and reduced glutathione, is operative in minimizing the potentially harmful effects of O(2)(-), NO, H(2)O(2) and ONOO(-).	Glutathione	99-110	superoxide dismutase 2	Homo sapiens	71-94
15051313-4	2004	A network of intramitochondrial antioxidants consisting of the enzymes Mn-superoxide dismutase and glutathione peroxidase and of the reductants NADH(2), ubiquinol and reduced glutathione, is operative in minimizing the potentially harmful effects of O(2)(-), NO, H(2)O(2) and ONOO(-).	Superoxides	250-254	superoxide dismutase 2	Homo sapiens	71-94
15051313-4	2004	A network of intramitochondrial antioxidants consisting of the enzymes Mn-superoxide dismutase and glutathione peroxidase and of the reductants NADH(2), ubiquinol and reduced glutathione, is operative in minimizing the potentially harmful effects of O(2)(-), NO, H(2)O(2) and ONOO(-).	Hydrogen Peroxide	263-271	superoxide dismutase 2	Homo sapiens	71-94
15051313-4	2004	A network of intramitochondrial antioxidants consisting of the enzymes Mn-superoxide dismutase and glutathione peroxidase and of the reductants NADH(2), ubiquinol and reduced glutathione, is operative in minimizing the potentially harmful effects of O(2)(-), NO, H(2)O(2) and ONOO(-).	onoo	276-280	superoxide dismutase 2	Homo sapiens	71-94
15051327-4	2004	The consistent induction of the mitochondrial antioxidant enzyme manganese superoxide dismutase (Mn-SOD) observed in experimental animals after acute and chronic ethanol administration has all the characteristics of a "stress response" to an oxidative insult.	Ethanol	162-169	superoxide dismutase 2	Homo sapiens	65-95
15051327-4	2004	The consistent induction of the mitochondrial antioxidant enzyme manganese superoxide dismutase (Mn-SOD) observed in experimental animals after acute and chronic ethanol administration has all the characteristics of a "stress response" to an oxidative insult.	Ethanol	162-169	superoxide dismutase 2	Homo sapiens	97-103
15673194-8	2004	The data demonstrate that YHT induces the apoptosis of human cervical carcinoma HeLa cells by intervening Mn-SOD.	yht	26-29	superoxide dismutase 2	Homo sapiens	106-112
14678790-4	2004	Cytochrome c catalyzes both self- and adjacent-molecule (hydroxyphenylacetic acid, Mn-superoxide dismutase) nitration via heme-dependent mechanisms involving tyrosyl radical and *NO2 production, as for phagocyte peroxidases.	Tyrosyl radical	158-173	superoxide dismutase 2	Homo sapiens	83-106
14678790-4	2004	Cytochrome c catalyzes both self- and adjacent-molecule (hydroxyphenylacetic acid, Mn-superoxide dismutase) nitration via heme-dependent mechanisms involving tyrosyl radical and *NO2 production, as for phagocyte peroxidases.	Nitrogen Dioxide	179-182	superoxide dismutase 2	Homo sapiens	83-106
14678790-7	2004	Extensive tyrosine nitration of Mn-superoxide dismutase occurred when exposed to either cytochrome c or MPx-11 in the presence of H2O2 and NO2-, with no apparent decrease in catalytic activity.	Tyrosine	10-18	superoxide dismutase 2	Homo sapiens	32-55
14678790-7	2004	Extensive tyrosine nitration of Mn-superoxide dismutase occurred when exposed to either cytochrome c or MPx-11 in the presence of H2O2 and NO2-, with no apparent decrease in catalytic activity.	Hydrogen Peroxide	130-134	superoxide dismutase 2	Homo sapiens	32-55
14678790-7	2004	Extensive tyrosine nitration of Mn-superoxide dismutase occurred when exposed to either cytochrome c or MPx-11 in the presence of H2O2 and NO2-, with no apparent decrease in catalytic activity.	Nitrogen Dioxide	139-142	superoxide dismutase 2	Homo sapiens	32-55
15535847-2	2004	Manganese superoxide dismutase (MnSOD) is a major enzyme that is responsible for the detoxification of reactive oxygen species in the mitochondria.	Reactive Oxygen Species	103-126	superoxide dismutase 2	Homo sapiens	0-30
14531733-0	2004	Accumulation of manganese superoxide dismutase under metal-depleted conditions: proposed role for zinc ions in cellular redox balance.	Metals	53-58	superoxide dismutase 2	Homo sapiens	16-46
14531733-3	2004	MnSOD activity increased 5-7-fold during incubation in a medium supplemented with metal-depleted fetal bovine serum, with a corresponding elevation of its mRNA levels.	Metals	82-87	superoxide dismutase 2	Homo sapiens	0-5
14531733-9	2004	This was further supported by the observation that curcumin suppressed both the DNA-binding activity of NF-kappaB and the induction of MnSOD mRNA in cells cultivated under metal-depleted conditions.	Curcumin	51-59	superoxide dismutase 2	Homo sapiens	135-140
14531733-9	2004	This was further supported by the observation that curcumin suppressed both the DNA-binding activity of NF-kappaB and the induction of MnSOD mRNA in cells cultivated under metal-depleted conditions.	Metals	172-177	superoxide dismutase 2	Homo sapiens	135-140
14531733-11	2004	It is possible that a deficiency of zinc in the low-copper diet may be primarily involved in MnSOD induction.	Copper	52-58	superoxide dismutase 2	Homo sapiens	93-98
15217492-1	2004	INTRODUCTION: A polymorphism in the manganese superoxide dismutase (MnSOD) gene, Ala-9Val, has been examined in association with breast cancer risk in several epidemiologic studies.	ala-9val	81-89	superoxide dismutase 2	Homo sapiens	68-73
15217492-3	2004	METHODS: We examined the role of the MnSOD Ala-9Val polymorphism in a population-based case-control study of invasive and in situ breast cancer in North Carolina.	ala-9val	43-51	superoxide dismutase 2	Homo sapiens	37-42
15217492-5	2004	RESULTS: The odds ratio for MnSOD Ala/Ala versus any MnSOD Val genotypes was not elevated in African Americans (odds ratio = 0.9, 95% confidence interval = 0.7-1.2) or in whites (odds ratio = 1.0, 95% confidence interval = 0.8-1.2).	Alanine	34-37	superoxide dismutase 2	Homo sapiens	28-33
15777015-1	2004	The release of cytochrome c from mitochondria during apoptosis results in the enhanced production of superoxide radicals, which are converted to H2O2 by Mn-superoxide dismutase.	Superoxides	101-120	superoxide dismutase 2	Homo sapiens	153-176
15777015-1	2004	The release of cytochrome c from mitochondria during apoptosis results in the enhanced production of superoxide radicals, which are converted to H2O2 by Mn-superoxide dismutase.	Hydrogen Peroxide	145-149	superoxide dismutase 2	Homo sapiens	153-176
15217492-0	2004	Manganese superoxide dismutase Ala-9Val polymorphism and risk of breast cancer in a population-based case-control study of African Americans and whites.	ala-9val	31-39	superoxide dismutase 2	Homo sapiens	0-30
15217492-1	2004	INTRODUCTION: A polymorphism in the manganese superoxide dismutase (MnSOD) gene, Ala-9Val, has been examined in association with breast cancer risk in several epidemiologic studies.	ala-9val	81-89	superoxide dismutase 2	Homo sapiens	36-66
15535847-2	2004	Manganese superoxide dismutase (MnSOD) is a major enzyme that is responsible for the detoxification of reactive oxygen species in the mitochondria.	Reactive Oxygen Species	103-126	superoxide dismutase 2	Homo sapiens	32-37
15535847-3	2004	A T --> C substitution in the MnSOD gene results in a Val --> Ala change at the -9 position of the mitochondrial targeting sequence (Val-9Ala), which alters the protein secondary structure and thus affects transport of MnSOD into the mitochondria.	Alanine	68-71	superoxide dismutase 2	Homo sapiens	33-38
15535847-3	2004	A T --> C substitution in the MnSOD gene results in a Val --> Ala change at the -9 position of the mitochondrial targeting sequence (Val-9Ala), which alters the protein secondary structure and thus affects transport of MnSOD into the mitochondria.	Alanine	68-71	superoxide dismutase 2	Homo sapiens	225-230
14690515-8	2004	While the presence of Mn3+ complexes cannot be proven in the spectrum of endogenous mitochondrial manganese, the shape of this spectrum could suggest the presence of Mn3+ near the limit of detection, probably as MnSOD.	manganese(III) acetate dihydrate	166-170	superoxide dismutase 2	Homo sapiens	212-217
14661095-6	2003	Examples of peroxynitrite-dependent nitration catalysts are the Mn-superoxide dismutase, some cytochromes and several metalloporphyrins.	Peroxynitrous Acid	12-25	superoxide dismutase 2	Homo sapiens	64-87
14675044-6	2004	As a control, FK506-induced cell death was also measured in the presence of superoxide anion inhibitor, 4,5-dihydroxy-1,2-benzene disulfonic acid (Tiron), TEMPO, or overexpressed human manganese superoxide dismutase (MnSOD).	Tacrolimus	14-19	superoxide dismutase 2	Homo sapiens	185-215
14675044-6	2004	As a control, FK506-induced cell death was also measured in the presence of superoxide anion inhibitor, 4,5-dihydroxy-1,2-benzene disulfonic acid (Tiron), TEMPO, or overexpressed human manganese superoxide dismutase (MnSOD).	Tacrolimus	14-19	superoxide dismutase 2	Homo sapiens	217-222
14675044-12	2004	In fact, TEMPO or expression of MnSOD enhanced the effect of FK506.	Tacrolimus	61-66	superoxide dismutase 2	Homo sapiens	32-37
14704872-4	2003	We examined polymorphic markers Ala(-9)Val in SOD2 gene and Arg213Gly in SOD3 gene for possible relation to DPN in Russian type 1 diabetic patients.	Valine	39-42	superoxide dismutase 2	Homo sapiens	46-50
14981915-7	2003	The MnSOD mRNA expression in HL-60 cells assayed by reverse transcriptase-polymerase chain reaction was highly inhibited by BHA/BHT or BMP, accompanied by the change in the electrophoretic mobility of MnSOD on polyacryamide gel.	Butylated Hydroxyanisole	124-127	superoxide dismutase 2	Homo sapiens	4-9
14654562-6	2003	MnSOD expression was related with the resistance to DOX and mitomycin C but not with that to 5-fluorouracil and vinblastine.	Doxorubicin	52-55	superoxide dismutase 2	Homo sapiens	0-5
14654562-6	2003	MnSOD expression was related with the resistance to DOX and mitomycin C but not with that to 5-fluorouracil and vinblastine.	Mitomycin	60-71	superoxide dismutase 2	Homo sapiens	0-5
14654562-9	2003	In addition, MnSOD overexpression increased the resistance of gastric carcinoma cells to DOX.	Doxorubicin	89-92	superoxide dismutase 2	Homo sapiens	13-18
14654562-10	2003	CONCLUSIONS: MnSOD is an important factor of drug response to reactive oxygen species-generating anticancer drugs in the gastric cancer cells.	Reactive Oxygen Species	62-85	superoxide dismutase 2	Homo sapiens	13-18
12871859-3	2003	Given the link between pyocyanin-mediated epithelial cell injury and oxidative stress, we assessed pyocyanin"s effect on MnSOD, CuZnSOD, and catalase levels in the A549 human alveolar epithelial cell line and in normal human bronchial epithelial cells.	Pyocyanine	99-108	superoxide dismutase 2	Homo sapiens	121-126
12871859-6	2003	Overexpression of MnSOD in A549 cells prevented pyocyanin-mediated loss of catalase protein, but catalase activity still declined.	Pyocyanine	48-57	superoxide dismutase 2	Homo sapiens	18-23
14981915-7	2003	The MnSOD mRNA expression in HL-60 cells assayed by reverse transcriptase-polymerase chain reaction was highly inhibited by BHA/BHT or BMP, accompanied by the change in the electrophoretic mobility of MnSOD on polyacryamide gel.	Butylated Hydroxyanisole	124-127	superoxide dismutase 2	Homo sapiens	201-206
14981915-7	2003	The MnSOD mRNA expression in HL-60 cells assayed by reverse transcriptase-polymerase chain reaction was highly inhibited by BHA/BHT or BMP, accompanied by the change in the electrophoretic mobility of MnSOD on polyacryamide gel.	Butylated Hydroxytoluene	128-131	superoxide dismutase 2	Homo sapiens	4-9
14981915-7	2003	The MnSOD mRNA expression in HL-60 cells assayed by reverse transcriptase-polymerase chain reaction was highly inhibited by BHA/BHT or BMP, accompanied by the change in the electrophoretic mobility of MnSOD on polyacryamide gel.	Butylated Hydroxytoluene	128-131	superoxide dismutase 2	Homo sapiens	201-206
14981915-7	2003	The MnSOD mRNA expression in HL-60 cells assayed by reverse transcriptase-polymerase chain reaction was highly inhibited by BHA/BHT or BMP, accompanied by the change in the electrophoretic mobility of MnSOD on polyacryamide gel.	2-tert-butyl-4-methylphenol	135-138	superoxide dismutase 2	Homo sapiens	4-9
14981915-7	2003	The MnSOD mRNA expression in HL-60 cells assayed by reverse transcriptase-polymerase chain reaction was highly inhibited by BHA/BHT or BMP, accompanied by the change in the electrophoretic mobility of MnSOD on polyacryamide gel.	polyacryamide	210-223	superoxide dismutase 2	Homo sapiens	4-9
14981915-7	2003	The MnSOD mRNA expression in HL-60 cells assayed by reverse transcriptase-polymerase chain reaction was highly inhibited by BHA/BHT or BMP, accompanied by the change in the electrophoretic mobility of MnSOD on polyacryamide gel.	polyacryamide	210-223	superoxide dismutase 2	Homo sapiens	201-206
14578299-6	2003	Similar results were obtained with the MnSOD mimetic Mn(III)tetrakis(4-benzoic acid)porphyrin chloride that normalized nitrotyrosine, 8-OHdG, and apoptosis and inhibited PKC activation.	mn(iii)tetrakis(4-benzoic acid)porphyrin chloride	53-102	superoxide dismutase 2	Homo sapiens	39-44
14578299-6	2003	Similar results were obtained with the MnSOD mimetic Mn(III)tetrakis(4-benzoic acid)porphyrin chloride that normalized nitrotyrosine, 8-OHdG, and apoptosis and inhibited PKC activation.	3-nitrotyrosine	119-132	superoxide dismutase 2	Homo sapiens	39-44
14578299-6	2003	Similar results were obtained with the MnSOD mimetic Mn(III)tetrakis(4-benzoic acid)porphyrin chloride that normalized nitrotyrosine, 8-OHdG, and apoptosis and inhibited PKC activation.	8-ohdg	134-140	superoxide dismutase 2	Homo sapiens	39-44
12963120-1	2003	A polymorphism in the signal sequence (Ala-9Val) of the gene encoding the free radical-quenching manganese superoxide dismutase (MnSOD) has been reported to alter the risk for breast cancer.	Alanine	39-42	superoxide dismutase 2	Homo sapiens	97-127
12966547-2	2003	As a consequence, the production of the oxygen radical scavenger manganese superoxide dismutase (MnSOD) is increased.	Oxygen	40-46	superoxide dismutase 2	Homo sapiens	97-102
14499631-5	2003	MnSOD activity was strongly induced in virally transformed WI-38 cells by treatment with the herbicide paraquat or inhibition of GSH synthesis with BSO.	Paraquat	103-111	superoxide dismutase 2	Homo sapiens	0-5
14499631-5	2003	MnSOD activity was strongly induced in virally transformed WI-38 cells by treatment with the herbicide paraquat or inhibition of GSH synthesis with BSO.	Glutathione	129-132	superoxide dismutase 2	Homo sapiens	0-5
14499631-8	2003	These results reveal differences in tumor and normal cell responses to changes in ambient oxygen tension and show that MnSOD activity is inducible when an appropriate stimulus is applied.	Oxygen	90-96	superoxide dismutase 2	Homo sapiens	119-124
14578853-6	2003	Arachidonic acid (AA) plus iron-induced cell death was partially prevented in both Ad.SOD1- and Ad.SOD2-infected E47 cells.	Arachidonic Acid	0-16	superoxide dismutase 2	Homo sapiens	99-103
14578853-6	2003	Arachidonic acid (AA) plus iron-induced cell death was partially prevented in both Ad.SOD1- and Ad.SOD2-infected E47 cells.	Iron	27-31	superoxide dismutase 2	Homo sapiens	99-103
14578853-7	2003	Overexpression of Cu/Zn-SOD and Mn-SOD also partially protected E47 cells from the increase in reactive oxygen production and lipid peroxidation and the loss of mitochondrial membrane potential induced by AA and iron.	reactive oxygen	95-110	superoxide dismutase 2	Homo sapiens	32-38
14578853-7	2003	Overexpression of Cu/Zn-SOD and Mn-SOD also partially protected E47 cells from the increase in reactive oxygen production and lipid peroxidation and the loss of mitochondrial membrane potential induced by AA and iron.	Iron	212-216	superoxide dismutase 2	Homo sapiens	32-38
14578853-8	2003	Infection with Cu/Zn-SOD and Mn-SOD also protected the E47 cells against AA toxicity or buthionine sulfoximine (BSO)-dependent toxicity.	Buthionine Sulfoximine	88-110	superoxide dismutase 2	Homo sapiens	29-35
14578853-8	2003	Infection with Cu/Zn-SOD and Mn-SOD also protected the E47 cells against AA toxicity or buthionine sulfoximine (BSO)-dependent toxicity.	Buthionine Sulfoximine	112-115	superoxide dismutase 2	Homo sapiens	29-35
12963120-1	2003	A polymorphism in the signal sequence (Ala-9Val) of the gene encoding the free radical-quenching manganese superoxide dismutase (MnSOD) has been reported to alter the risk for breast cancer.	Alanine	39-42	superoxide dismutase 2	Homo sapiens	129-134
14503839-3	2003	We hypothesized that the inducibility of Mn-SOD and MT mRNA by paraquat, an intracellular superoxide generator, might be altered in lymphocytes of gastric cancer patients.	Paraquat	63-71	superoxide dismutase 2	Homo sapiens	41-47
12826016-4	2003	DPI prevented expression of MnSOD by oxLDL, whereas inhibitors of cytochrome P450 (methoxalen) or xanthine oxidase (allopurinol) did not, thus pointing to a role of NADPH-oxidase-derived ROS in oxLDL-induced MnSOD expression.	diphenyleneiodonium	0-3	superoxide dismutase 2	Homo sapiens	28-33
12826016-5	2003	Transfection of cells with MnSOD antisense, but not scrambled antisense, oligonucleotides significantly attenuated oxLDL-mediated MnSOD expression and hindered cytoprotective effects of non-toxic oxLDL concentrations.	Oligonucleotides	73-89	superoxide dismutase 2	Homo sapiens	27-32
12826016-5	2003	Transfection of cells with MnSOD antisense, but not scrambled antisense, oligonucleotides significantly attenuated oxLDL-mediated MnSOD expression and hindered cytoprotective effects of non-toxic oxLDL concentrations.	Oligonucleotides	73-89	superoxide dismutase 2	Homo sapiens	130-135
14503839-3	2003	We hypothesized that the inducibility of Mn-SOD and MT mRNA by paraquat, an intracellular superoxide generator, might be altered in lymphocytes of gastric cancer patients.	Superoxides	90-100	superoxide dismutase 2	Homo sapiens	41-47
12788471-5	2003	Oxidative stress elicited by crystalline silica is also evidenced by increased expression of antioxidant enzymes such as manganese superoxide dismutase (Mn-SOD) and glutathione peroxidase, and the enzyme inducible nitric oxide synthase (iNOS).	Silicon Dioxide	41-47	superoxide dismutase 2	Homo sapiens	121-151
12893274-4	2003	Here, we show that Cu/Zn-SOD is translocated into the nucleus of HeLa cells in the presence of expanded ataxin-1, whereas Mn-SOD is localized in the cytoplasm: the longer the expansion of polyglutamine, the higher the level of translocation of Cu/Zn-SOD.	polyglutamine	188-201	superoxide dismutase 2	Homo sapiens	122-128
12816884-6	2003	Nuclear run-on assays demonstrated that 17beta-estradiol increases MnSOD and ecSOD transcription rate.	Estradiol	40-56	superoxide dismutase 2	Homo sapiens	67-72
12862482-1	2003	Mn-superoxide dismutase (Mn-SOD), which protects the cell from the toxic potential of superoxide radicals (O(2)(-*)), is the only type of SOD which resides in eukaryotic mitochondria.	Superoxides	3-13	superoxide dismutase 2	Homo sapiens	25-31
12862482-1	2003	Mn-superoxide dismutase (Mn-SOD), which protects the cell from the toxic potential of superoxide radicals (O(2)(-*)), is the only type of SOD which resides in eukaryotic mitochondria.	Superoxides	3-13	superoxide dismutase 2	Homo sapiens	28-31
12862482-1	2003	Mn-superoxide dismutase (Mn-SOD), which protects the cell from the toxic potential of superoxide radicals (O(2)(-*)), is the only type of SOD which resides in eukaryotic mitochondria.	o(2)	107-111	superoxide dismutase 2	Homo sapiens	0-23
12862482-1	2003	Mn-superoxide dismutase (Mn-SOD), which protects the cell from the toxic potential of superoxide radicals (O(2)(-*)), is the only type of SOD which resides in eukaryotic mitochondria.	o(2)	107-111	superoxide dismutase 2	Homo sapiens	25-31
12862482-1	2003	Mn-superoxide dismutase (Mn-SOD), which protects the cell from the toxic potential of superoxide radicals (O(2)(-*)), is the only type of SOD which resides in eukaryotic mitochondria.	o(2)	107-111	superoxide dismutase 2	Homo sapiens	28-31
12862482-18	2003	Similar coordination and stabilization of the (*)OOH radical by the Mn center may be key steps in the enzymatic dismutation of superoxide radicals by Mn-SOD.	OOH	49-52	superoxide dismutase 2	Homo sapiens	150-156
12862482-18	2003	Similar coordination and stabilization of the (*)OOH radical by the Mn center may be key steps in the enzymatic dismutation of superoxide radicals by Mn-SOD.	Superoxides	127-137	superoxide dismutase 2	Homo sapiens	150-156
12948282-6	2003	RESULTS: Men homozygous for the MnSOD ala allele had a 70% increase in risk over men homozygous for the val allele (odds ratio, OR = 1.72, 95% confidence interval, CI = 0.96-3.08, p = 0.07).	Alanine	38-41	superoxide dismutase 2	Homo sapiens	32-37
12948282-6	2003	RESULTS: Men homozygous for the MnSOD ala allele had a 70% increase in risk over men homozygous for the val allele (odds ratio, OR = 1.72, 95% confidence interval, CI = 0.96-3.08, p = 0.07).	Valine	104-107	superoxide dismutase 2	Homo sapiens	32-37
12948282-8	2003	Although there was no difference in the association with disease stage, men homozygous for MnSOD ala (compared to MnSOD val/val or val/ala) showed a three-fold risk increase for high-grade tumors (OR = 2.72, 95% CI: 1.15-6.40, p = 0.02).	Alanine	97-100	superoxide dismutase 2	Homo sapiens	91-96
12948282-8	2003	Although there was no difference in the association with disease stage, men homozygous for MnSOD ala (compared to MnSOD val/val or val/ala) showed a three-fold risk increase for high-grade tumors (OR = 2.72, 95% CI: 1.15-6.40, p = 0.02).	Alanine	97-100	superoxide dismutase 2	Homo sapiens	114-119
12948282-8	2003	Although there was no difference in the association with disease stage, men homozygous for MnSOD ala (compared to MnSOD val/val or val/ala) showed a three-fold risk increase for high-grade tumors (OR = 2.72, 95% CI: 1.15-6.40, p = 0.02).	Valine	120-123	superoxide dismutase 2	Homo sapiens	91-96
12948282-8	2003	Although there was no difference in the association with disease stage, men homozygous for MnSOD ala (compared to MnSOD val/val or val/ala) showed a three-fold risk increase for high-grade tumors (OR = 2.72, 95% CI: 1.15-6.40, p = 0.02).	Valine	120-123	superoxide dismutase 2	Homo sapiens	114-119
12948282-8	2003	Although there was no difference in the association with disease stage, men homozygous for MnSOD ala (compared to MnSOD val/val or val/ala) showed a three-fold risk increase for high-grade tumors (OR = 2.72, 95% CI: 1.15-6.40, p = 0.02).	Valine	124-127	superoxide dismutase 2	Homo sapiens	91-96
12948282-8	2003	Although there was no difference in the association with disease stage, men homozygous for MnSOD ala (compared to MnSOD val/val or val/ala) showed a three-fold risk increase for high-grade tumors (OR = 2.72, 95% CI: 1.15-6.40, p = 0.02).	Valine	124-127	superoxide dismutase 2	Homo sapiens	114-119
12948282-9	2003	CONCLUSION: These data suggest an effect of the MnSOD ala/ala genotype on the development of prostate cancer.	Alanine	54-57	superoxide dismutase 2	Homo sapiens	48-53
12948282-9	2003	CONCLUSION: These data suggest an effect of the MnSOD ala/ala genotype on the development of prostate cancer.	Alanine	58-61	superoxide dismutase 2	Homo sapiens	48-53
12882796-9	2003	MnSOD-deficient cells showed dramatic mitochondrial damage when exposed to 50 micro M H(2)O(2) for 1 hour.	Hydrogen Peroxide	86-94	superoxide dismutase 2	Homo sapiens	0-5
12882796-10	2003	Similarly, oxidative challenge by H(2)O(2), photochemically generated reactive oxygen species, or UVB irradiation produced greater DNA strand breaks in MnSOD-deficient cells than in those in which the enzyme was upregulated.	Hydrogen Peroxide	34-42	superoxide dismutase 2	Homo sapiens	152-157
12882796-10	2003	Similarly, oxidative challenge by H(2)O(2), photochemically generated reactive oxygen species, or UVB irradiation produced greater DNA strand breaks in MnSOD-deficient cells than in those in which the enzyme was upregulated.	Reactive Oxygen Species	70-93	superoxide dismutase 2	Homo sapiens	152-157
12799643-8	2003	These results suggest that cyclin E overexpression might reduce tumour cells sensitivity to doxorubicin by affecting the expression of MnSOD and that determination of cyclin E expression levels might help to select patients to be treated with an anthracycline-based antineoplastic therapy.	Doxorubicin	92-103	superoxide dismutase 2	Homo sapiens	135-140
12788471-5	2003	Oxidative stress elicited by crystalline silica is also evidenced by increased expression of antioxidant enzymes such as manganese superoxide dismutase (Mn-SOD) and glutathione peroxidase, and the enzyme inducible nitric oxide synthase (iNOS).	Silicon Dioxide	41-47	superoxide dismutase 2	Homo sapiens	153-159
12894522-4	2003	In addition, morphine increased the activity of mitochondrial Mn-containing superoxide dismutase (MnSOD) in HL-60 cells, but decreased the MnSOD activity in A549 and MCF7 cells.	Morphine	13-21	superoxide dismutase 2	Homo sapiens	62-96
12777700-7	2003	Furthermore, our recent observations provide new molecular biologic and pharmacologic evidence suggesting that physiologic concentrations of 17beta-estradiol (<10 nM) activate ERs (ERbeta > ERalpha) and upregulate a cyclic guanosine 5"- monophosphate (cGMP)-dependent thioredoxin (Trx) and MnSOD expression following the induction of NOS1 in human brain-derived SH-SY5Y cells.	Estradiol	141-157	superoxide dismutase 2	Homo sapiens	296-301
12862208-0	2003	Nifedipine upregulates manganese superoxide dismutase expression in vascular smooth muscle cells via endothelial cell-dependent pathways.	Nifedipine	0-10	superoxide dismutase 2	Homo sapiens	23-53
12862208-3	2003	Here, we show that the calcium antagonist nifedipine upregulates the expression of manganese superoxide dismutase (Mn SOD), an endogenous antioxidant enzyme, in vascular smooth muscle cells (VSMC) via cellular interactions between VSMC and endothelial cells (EC).	Calcium	23-30	superoxide dismutase 2	Homo sapiens	83-113
12862208-3	2003	Here, we show that the calcium antagonist nifedipine upregulates the expression of manganese superoxide dismutase (Mn SOD), an endogenous antioxidant enzyme, in vascular smooth muscle cells (VSMC) via cellular interactions between VSMC and endothelial cells (EC).	Calcium	23-30	superoxide dismutase 2	Homo sapiens	115-121
12862208-3	2003	Here, we show that the calcium antagonist nifedipine upregulates the expression of manganese superoxide dismutase (Mn SOD), an endogenous antioxidant enzyme, in vascular smooth muscle cells (VSMC) via cellular interactions between VSMC and endothelial cells (EC).	Nifedipine	42-52	superoxide dismutase 2	Homo sapiens	83-113
12862208-3	2003	Here, we show that the calcium antagonist nifedipine upregulates the expression of manganese superoxide dismutase (Mn SOD), an endogenous antioxidant enzyme, in vascular smooth muscle cells (VSMC) via cellular interactions between VSMC and endothelial cells (EC).	Nifedipine	42-52	superoxide dismutase 2	Homo sapiens	115-121
12862208-4	2003	Nifedipine induced upregulation of Mn SOD activity and expression in VSMC when cocultured with EC but not when cultured individually.	Nifedipine	0-10	superoxide dismutase 2	Homo sapiens	35-41
12862208-5	2003	NG-Monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthesis, inhibited the upregulation of Mn SOD expression induced by nifedipine.	omega-N-Methylarginine	0-24	superoxide dismutase 2	Homo sapiens	110-116
12862208-5	2003	NG-Monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthesis, inhibited the upregulation of Mn SOD expression induced by nifedipine.	omega-N-Methylarginine	26-32	superoxide dismutase 2	Homo sapiens	110-116
12862208-5	2003	NG-Monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthesis, inhibited the upregulation of Mn SOD expression induced by nifedipine.	Nitric Oxide	51-63	superoxide dismutase 2	Homo sapiens	110-116
12862208-5	2003	NG-Monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthesis, inhibited the upregulation of Mn SOD expression induced by nifedipine.	Nifedipine	139-149	superoxide dismutase 2	Homo sapiens	110-116
12862208-6	2003	Additionally, N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino) ethanamine, a NO donor, reversed this inhibition by L-NMMA, indicating that NO may be involved in the mechanism underlying the nifedipine-induced upregulation of Mn SOD in VSMC.	n-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino) ethanamine	14-73	superoxide dismutase 2	Homo sapiens	225-231
12862208-6	2003	Additionally, N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino) ethanamine, a NO donor, reversed this inhibition by L-NMMA, indicating that NO may be involved in the mechanism underlying the nifedipine-induced upregulation of Mn SOD in VSMC.	omega-N-Methylarginine	115-121	superoxide dismutase 2	Homo sapiens	225-231
12862208-6	2003	Additionally, N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino) ethanamine, a NO donor, reversed this inhibition by L-NMMA, indicating that NO may be involved in the mechanism underlying the nifedipine-induced upregulation of Mn SOD in VSMC.	Nifedipine	190-200	superoxide dismutase 2	Homo sapiens	225-231
12862208-7	2003	Preincubation of VSMC with Mn SOD antisense oligodeoxyribonucleotides (ODN) blocked the suppressive effects of nifedipine on DNA synthesis in VSMC cocultured with EC, whereas sense ODN had no effect.	vsmc	17-21	superoxide dismutase 2	Homo sapiens	27-33
12862208-7	2003	Preincubation of VSMC with Mn SOD antisense oligodeoxyribonucleotides (ODN) blocked the suppressive effects of nifedipine on DNA synthesis in VSMC cocultured with EC, whereas sense ODN had no effect.	Oligodeoxyribonucleotides	44-69	superoxide dismutase 2	Homo sapiens	27-33
12862208-7	2003	Preincubation of VSMC with Mn SOD antisense oligodeoxyribonucleotides (ODN) blocked the suppressive effects of nifedipine on DNA synthesis in VSMC cocultured with EC, whereas sense ODN had no effect.	Nifedipine	111-121	superoxide dismutase 2	Homo sapiens	27-33
12862208-8	2003	We conclude that the calcium antagonist nifedipine induces upregulation of Mn SOD expression in VSMC via NO derived from EC.	Nifedipine	40-50	superoxide dismutase 2	Homo sapiens	75-81
12736188-2	2003	We constructed a fusion gene encoding a chimeric SOD consisting of the mature human mitochondrial SOD2 plus the COOH-terminal 26-amino acid heparin-binding "tail" from SOD3.	Carbonic Acid	112-116	superoxide dismutase 2	Homo sapiens	49-52
12736188-2	2003	We constructed a fusion gene encoding a chimeric SOD consisting of the mature human mitochondrial SOD2 plus the COOH-terminal 26-amino acid heparin-binding "tail" from SOD3.	amino acid heparin	129-147	superoxide dismutase 2	Homo sapiens	49-52
12894522-4	2003	In addition, morphine increased the activity of mitochondrial Mn-containing superoxide dismutase (MnSOD) in HL-60 cells, but decreased the MnSOD activity in A549 and MCF7 cells.	Morphine	13-21	superoxide dismutase 2	Homo sapiens	98-103
12894522-4	2003	In addition, morphine increased the activity of mitochondrial Mn-containing superoxide dismutase (MnSOD) in HL-60 cells, but decreased the MnSOD activity in A549 and MCF7 cells.	Morphine	13-21	superoxide dismutase 2	Homo sapiens	139-144
12646264-1	2003	Endogenous tyrosine nitration and inactivation of manganese superoxide dismutase (MnSOD) has previously been shown to occur in both human and rat chronic renal allograft rejection.	Tyrosine	11-19	superoxide dismutase 2	Homo sapiens	50-80
12815947-0	2003	[Association of the SOD2 Ala(-9)Val and SOD3 Arg213Gly polymorphisms with diabetic polyneuropathy in patients with diabetes mellitus type 1].	Alanine	25-28	superoxide dismutase 2	Homo sapiens	20-24
12815947-0	2003	[Association of the SOD2 Ala(-9)Val and SOD3 Arg213Gly polymorphisms with diabetic polyneuropathy in patients with diabetes mellitus type 1].	Valine	32-35	superoxide dismutase 2	Homo sapiens	20-24
12646264-1	2003	Endogenous tyrosine nitration and inactivation of manganese superoxide dismutase (MnSOD) has previously been shown to occur in both human and rat chronic renal allograft rejection.	Tyrosine	11-19	superoxide dismutase 2	Homo sapiens	82-87
12646264-4	2003	Tyrosine nitration of specific mitochondrial proteins, MnSOD and cytochrome c, occurred at the earliest time point examined, an event that preceded significant renal injury.	Tyrosine	0-8	superoxide dismutase 2	Homo sapiens	55-60
12700280-10	2003	Cell growth, plating efficiency, and growth in soft agar decreased with increasing amounts of the adenovirus MnSOD construct.	Agar	52-56	superoxide dismutase 2	Homo sapiens	109-114
12627943-0	2003	Catalytic and structural effects of amino acid substitution at histidine 30 in human manganese superoxide dismutase: insertion of valine C gamma into the substrate access channel.	Histidine	63-72	superoxide dismutase 2	Homo sapiens	85-115
12651009-3	2003	Translation of MnSOD monomers could be detected by SDS-PAGE, and assembly of the active homotetramer by native PAGE.	Sodium Dodecyl Sulfate	51-54	superoxide dismutase 2	Homo sapiens	15-20
12651009-6	2003	The purification of MnSOD was performed by chromatography applying the His-tag technology.	Histidine	71-74	superoxide dismutase 2	Homo sapiens	20-25
12627943-0	2003	Catalytic and structural effects of amino acid substitution at histidine 30 in human manganese superoxide dismutase: insertion of valine C gamma into the substrate access channel.	valine c	130-138	superoxide dismutase 2	Homo sapiens	85-115
12627943-1	2003	Catalysis of the disproportionation of superoxide by human manganese superoxide dismutase (MnSOD) is characterized by an initial burst of catalysis followed by a much slower region that is zero order in superoxide and due to a product inhibition by peroxide anion.	Superoxides	39-49	superoxide dismutase 2	Homo sapiens	59-89
12627943-1	2003	Catalysis of the disproportionation of superoxide by human manganese superoxide dismutase (MnSOD) is characterized by an initial burst of catalysis followed by a much slower region that is zero order in superoxide and due to a product inhibition by peroxide anion.	Superoxides	39-49	superoxide dismutase 2	Homo sapiens	91-96
12627943-1	2003	Catalysis of the disproportionation of superoxide by human manganese superoxide dismutase (MnSOD) is characterized by an initial burst of catalysis followed by a much slower region that is zero order in superoxide and due to a product inhibition by peroxide anion.	Superoxides	69-79	superoxide dismutase 2	Homo sapiens	91-96
12627943-1	2003	Catalysis of the disproportionation of superoxide by human manganese superoxide dismutase (MnSOD) is characterized by an initial burst of catalysis followed by a much slower region that is zero order in superoxide and due to a product inhibition by peroxide anion.	peroxide anion	249-263	superoxide dismutase 2	Homo sapiens	59-89
12627943-1	2003	Catalysis of the disproportionation of superoxide by human manganese superoxide dismutase (MnSOD) is characterized by an initial burst of catalysis followed by a much slower region that is zero order in superoxide and due to a product inhibition by peroxide anion.	peroxide anion	249-263	superoxide dismutase 2	Homo sapiens	91-96
12627943-3	2003	Using pulse radiolysis to generate superoxide, we have determined that kcat/K(m) was decreased and product inhibition increased for H30V MnSOD, both by 1-2 orders of magnitude, compared with wild type, H30N, and H30Q MnSOD.	Superoxides	35-45	superoxide dismutase 2	Homo sapiens	137-142
12627943-7	2003	This is supported by comparison of the crystal structure of H30V MnSOD with that of azide bound to Mn(III)SOD from Thermus thermophilus and by visible absorption spectra showing that azide binding to the metal in H30V Mn(III)SOD is abolished.	Azides	84-89	superoxide dismutase 2	Homo sapiens	65-70
12627943-7	2003	This is supported by comparison of the crystal structure of H30V MnSOD with that of azide bound to Mn(III)SOD from Thermus thermophilus and by visible absorption spectra showing that azide binding to the metal in H30V Mn(III)SOD is abolished.	Azides	183-188	superoxide dismutase 2	Homo sapiens	65-70
12627943-7	2003	This is supported by comparison of the crystal structure of H30V MnSOD with that of azide bound to Mn(III)SOD from Thermus thermophilus and by visible absorption spectra showing that azide binding to the metal in H30V Mn(III)SOD is abolished.	Metals	204-209	superoxide dismutase 2	Homo sapiens	65-70
12590982-3	2003	The polymorphism of MnSOD 5777T, threonine at the 58th amino acid, cannot be found in RA patients and controls in Taiwan.	Threonine	33-42	superoxide dismutase 2	Homo sapiens	20-25
12683635-9	2003	In Mn-SOD mRNA, Val at -9 position was varied to Ala in lymphocytes from two donors and three OSC cell lines, respectively.	Valine	16-19	superoxide dismutase 2	Homo sapiens	3-9
12618592-1	2003	A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of human manganese superoxide dismutase (MnSOD) and has been reported to modulate the risk of some cancers, neurodegenerative diseases and severe alcoholic liver disease.	Alanine	40-47	superoxide dismutase 2	Homo sapiens	125-155
12618592-1	2003	A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of human manganese superoxide dismutase (MnSOD) and has been reported to modulate the risk of some cancers, neurodegenerative diseases and severe alcoholic liver disease.	Alanine	40-47	superoxide dismutase 2	Homo sapiens	157-162
12618592-1	2003	A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of human manganese superoxide dismutase (MnSOD) and has been reported to modulate the risk of some cancers, neurodegenerative diseases and severe alcoholic liver disease.	Alanine	49-52	superoxide dismutase 2	Homo sapiens	125-155
12618592-1	2003	A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of human manganese superoxide dismutase (MnSOD) and has been reported to modulate the risk of some cancers, neurodegenerative diseases and severe alcoholic liver disease.	Alanine	49-52	superoxide dismutase 2	Homo sapiens	157-162
12618592-1	2003	A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of human manganese superoxide dismutase (MnSOD) and has been reported to modulate the risk of some cancers, neurodegenerative diseases and severe alcoholic liver disease.	Valine	57-63	superoxide dismutase 2	Homo sapiens	125-155
12618592-1	2003	A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of human manganese superoxide dismutase (MnSOD) and has been reported to modulate the risk of some cancers, neurodegenerative diseases and severe alcoholic liver disease.	Valine	57-63	superoxide dismutase 2	Homo sapiens	157-162
12618592-1	2003	A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of human manganese superoxide dismutase (MnSOD) and has been reported to modulate the risk of some cancers, neurodegenerative diseases and severe alcoholic liver disease.	Valine	65-68	superoxide dismutase 2	Homo sapiens	125-155
12618592-1	2003	A genetic dimorphism encodes for either alanine (Ala) or valine (Val) in the mitochondrial targeting sequence (MTS) of human manganese superoxide dismutase (MnSOD) and has been reported to modulate the risk of some cancers, neurodegenerative diseases and severe alcoholic liver disease.	Valine	65-68	superoxide dismutase 2	Homo sapiens	157-162
12414438-7	2003	Overexpression of MnSOD, but not CuZnSOD or catalase, protected cellular aconitase, but not ATP, from pyocyanin-mediated depletion.	Adenosine Triphosphate	92-95	superoxide dismutase 2	Homo sapiens	18-23
12414438-7	2003	Overexpression of MnSOD, but not CuZnSOD or catalase, protected cellular aconitase, but not ATP, from pyocyanin-mediated depletion.	Pyocyanine	102-111	superoxide dismutase 2	Homo sapiens	18-23
12580960-0	2003	Overexpression of manganese superoxide dismutase promotes survival in cell lines after doxorubicin treatment.	Doxorubicin	87-98	superoxide dismutase 2	Homo sapiens	18-48
12388080-1	2003	Manganese superoxide dismutase (MnSOD) is a critical antioxidant enzyme that protects against superoxide anion generated as a consequence of normal cellular respiration, as well as during the inflammatory response.	Superoxides	94-110	superoxide dismutase 2	Homo sapiens	0-30
12388080-1	2003	Manganese superoxide dismutase (MnSOD) is a critical antioxidant enzyme that protects against superoxide anion generated as a consequence of normal cellular respiration, as well as during the inflammatory response.	Superoxides	94-110	superoxide dismutase 2	Homo sapiens	32-37
12388080-2	2003	By employing dimethyl sulfate in vivo footprinting, we have previously identified ten basal protein binding sites within the MnSOD promoter.	dimethyl sulfate	13-29	superoxide dismutase 2	Homo sapiens	125-130
12580960-3	2003	The present study was performed to determine whether over-expression of MnSOD may play a role in resistance to doxorubicin.	Doxorubicin	111-122	superoxide dismutase 2	Homo sapiens	72-77
12683635-9	2003	In Mn-SOD mRNA, Val at -9 position was varied to Ala in lymphocytes from two donors and three OSC cell lines, respectively.	Alanine	49-52	superoxide dismutase 2	Homo sapiens	3-9
12580960-8	2003	In contrast, A375 and U937 cells transduced with the MNSOD gene consistently demonstrate increased colony formation in the presence of increasing concentrations of doxorubicin.	Doxorubicin	164-175	superoxide dismutase 2	Homo sapiens	53-58
12580960-10	2003	These results indicate that overexpression of MnSOD can enhance resistance to doxorubicin treatment.	Doxorubicin	78-89	superoxide dismutase 2	Homo sapiens	46-51
12517793-8	2003	Because the I58T variant of human SOD2 is thiol-sensitive, we measured SOD in Jurkat cells grown in the presence of thiol agents, observing markedly less SOD activity.	Sulfhydryl Compounds	42-47	superoxide dismutase 2	Homo sapiens	34-38
14515147-1	2003	In the retinoic acid-differentiated neuroblastoma SH-SY5Y cells, IL-1 induced binding activity of NFkappaB and up-regulated the expression and activity of MnSOD.	Tretinoin	7-20	superoxide dismutase 2	Homo sapiens	155-160
12543247-1	2003	We hypothesized that inhibitors of peroxide removal, such as BCNU, an indirect inhibitor of glutathione peroxidase (GPx), and 3-amino-1,2,4-triazole (AT), a direct inhibitor of catalase (CAT), should cause toxicity to cancer cells after manganese superoxide dismutase (MnSOD) overexpression due to elevated peroxide levels.	Peroxides	35-43	superoxide dismutase 2	Homo sapiens	237-267
12543247-1	2003	We hypothesized that inhibitors of peroxide removal, such as BCNU, an indirect inhibitor of glutathione peroxidase (GPx), and 3-amino-1,2,4-triazole (AT), a direct inhibitor of catalase (CAT), should cause toxicity to cancer cells after manganese superoxide dismutase (MnSOD) overexpression due to elevated peroxide levels.	Peroxides	35-43	superoxide dismutase 2	Homo sapiens	269-274
14515147-5	2003	Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NFkappaB activation, down-regulated the expression and activity of MnSOD, which may suggest that the regulation of MnSOD by IL-1 in retinoic acid-differentiated neuroblastoma cells was mediated by the nuclear factor kappaB.	pyrrolidine dithiocarbamic acid	0-27	superoxide dismutase 2	Homo sapiens	119-124
14515147-5	2003	Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NFkappaB activation, down-regulated the expression and activity of MnSOD, which may suggest that the regulation of MnSOD by IL-1 in retinoic acid-differentiated neuroblastoma cells was mediated by the nuclear factor kappaB.	pyrrolidine dithiocarbamic acid	0-27	superoxide dismutase 2	Homo sapiens	167-172
14515147-5	2003	Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NFkappaB activation, down-regulated the expression and activity of MnSOD, which may suggest that the regulation of MnSOD by IL-1 in retinoic acid-differentiated neuroblastoma cells was mediated by the nuclear factor kappaB.	pyrrolidine dithiocarbamic acid	29-33	superoxide dismutase 2	Homo sapiens	119-124
14515147-5	2003	Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NFkappaB activation, down-regulated the expression and activity of MnSOD, which may suggest that the regulation of MnSOD by IL-1 in retinoic acid-differentiated neuroblastoma cells was mediated by the nuclear factor kappaB.	pyrrolidine dithiocarbamic acid	29-33	superoxide dismutase 2	Homo sapiens	167-172
12517793-8	2003	Because the I58T variant of human SOD2 is thiol-sensitive, we measured SOD in Jurkat cells grown in the presence of thiol agents, observing markedly less SOD activity.	Sulfhydryl Compounds	116-121	superoxide dismutase 2	Homo sapiens	34-38
12517793-9	2003	In cell-free extracts, thiols quickly eliminated the SOD2 activity.	Sulfhydryl Compounds	23-29	superoxide dismutase 2	Homo sapiens	53-57
12624725-1	2003	We evaluated the relationship of an alanine or valine polymorphism at amino acid sequence 16 [Val(16)Ala] of manganese superoxide dismutase (Mn-SOD) with diabetes and diabetic nephropathy in Japanese type 2 diabetic patients.	Alanine	36-43	superoxide dismutase 2	Homo sapiens	109-139
12624725-1	2003	We evaluated the relationship of an alanine or valine polymorphism at amino acid sequence 16 [Val(16)Ala] of manganese superoxide dismutase (Mn-SOD) with diabetes and diabetic nephropathy in Japanese type 2 diabetic patients.	Alanine	36-43	superoxide dismutase 2	Homo sapiens	141-147
12624725-1	2003	We evaluated the relationship of an alanine or valine polymorphism at amino acid sequence 16 [Val(16)Ala] of manganese superoxide dismutase (Mn-SOD) with diabetes and diabetic nephropathy in Japanese type 2 diabetic patients.	Valine	47-53	superoxide dismutase 2	Homo sapiens	109-139
12624725-1	2003	We evaluated the relationship of an alanine or valine polymorphism at amino acid sequence 16 [Val(16)Ala] of manganese superoxide dismutase (Mn-SOD) with diabetes and diabetic nephropathy in Japanese type 2 diabetic patients.	Valine	47-53	superoxide dismutase 2	Homo sapiens	141-147
12426235-3	2002	We tested whether overexpression of MnSOD could decrease superoxide levels and protect the bladder from radiation damage.	Superoxides	57-67	superoxide dismutase 2	Homo sapiens	36-41
12469142-1	2003	Manganese superoxide dismutase (MnSOD) is an important superoxide anion scavenger located in mitochondria and protects cells from the damage caused by reactive oxygen species.	Superoxides	55-71	superoxide dismutase 2	Homo sapiens	0-30
12469142-1	2003	Manganese superoxide dismutase (MnSOD) is an important superoxide anion scavenger located in mitochondria and protects cells from the damage caused by reactive oxygen species.	Superoxides	55-71	superoxide dismutase 2	Homo sapiens	32-37
12469142-1	2003	Manganese superoxide dismutase (MnSOD) is an important superoxide anion scavenger located in mitochondria and protects cells from the damage caused by reactive oxygen species.	Reactive Oxygen Species	151-174	superoxide dismutase 2	Homo sapiens	0-30
12469142-1	2003	Manganese superoxide dismutase (MnSOD) is an important superoxide anion scavenger located in mitochondria and protects cells from the damage caused by reactive oxygen species.	Reactive Oxygen Species	151-174	superoxide dismutase 2	Homo sapiens	32-37
12417255-6	2002	This pathway is sensitive to inhibitors of Ca(2+) uptake in the mitochondria (ruthenium red), Ca(2+) chelators (TMB-8, EGTA-AM), and antioxidants (PDTC, NAC, Mn-SOD).	Ruthenium Red	78-91	superoxide dismutase 2	Homo sapiens	158-164
12540033-7	2002	When the cells were exposed to 0.194 mM CPFX for 48 hours, the level of lipid peroxidation increased and the content of total GSH decreased significantly; activities of total SOD, Mn SOD and CuZn SOD did not change; the decrease observed in the activity of Cat was not significant; and the activity of GPx was highly variable.	Ciprofloxacin	40-44	superoxide dismutase 2	Homo sapiens	175-178
12540033-7	2002	When the cells were exposed to 0.194 mM CPFX for 48 hours, the level of lipid peroxidation increased and the content of total GSH decreased significantly; activities of total SOD, Mn SOD and CuZn SOD did not change; the decrease observed in the activity of Cat was not significant; and the activity of GPx was highly variable.	Ciprofloxacin	40-44	superoxide dismutase 2	Homo sapiens	180-186
12540033-8	2002	Vitamin E pretreatment of the cells provided significant protection against CPFX-induced cytotoxicity; lowered the level of lipid peroxidation significantly, but increased the total GSH content only moderately; no change was observed in the activities of Cat and total SOD, but a significant increase in Mn SOD and a significant decrease in CuZn SOD were noticed.	Vitamin E	0-9	superoxide dismutase 2	Homo sapiens	269-272
12540033-8	2002	Vitamin E pretreatment of the cells provided significant protection against CPFX-induced cytotoxicity; lowered the level of lipid peroxidation significantly, but increased the total GSH content only moderately; no change was observed in the activities of Cat and total SOD, but a significant increase in Mn SOD and a significant decrease in CuZn SOD were noticed.	Vitamin E	0-9	superoxide dismutase 2	Homo sapiens	304-310
12496360-0	2002	Role of reactive oxygen species in cells overexpressing manganese superoxide dismutase: mechanism for induction of radioresistance.	Reactive Oxygen Species	8-31	superoxide dismutase 2	Homo sapiens	56-86
12496360-1	2002	Manganese superoxide dismutase (MnSOD) catalyzes the dismutation of superoxide anions (O(2)(-)) into hydrogen peroxide (H(2)O(2)).	Superoxides	68-85	superoxide dismutase 2	Homo sapiens	0-30
12496360-1	2002	Manganese superoxide dismutase (MnSOD) catalyzes the dismutation of superoxide anions (O(2)(-)) into hydrogen peroxide (H(2)O(2)).	Superoxides	68-85	superoxide dismutase 2	Homo sapiens	32-37
12496360-1	2002	Manganese superoxide dismutase (MnSOD) catalyzes the dismutation of superoxide anions (O(2)(-)) into hydrogen peroxide (H(2)O(2)).	Superoxides	87-91	superoxide dismutase 2	Homo sapiens	0-30
12496360-1	2002	Manganese superoxide dismutase (MnSOD) catalyzes the dismutation of superoxide anions (O(2)(-)) into hydrogen peroxide (H(2)O(2)).	Superoxides	87-91	superoxide dismutase 2	Homo sapiens	32-37
12496360-1	2002	Manganese superoxide dismutase (MnSOD) catalyzes the dismutation of superoxide anions (O(2)(-)) into hydrogen peroxide (H(2)O(2)).	Hydrogen Peroxide	101-118	superoxide dismutase 2	Homo sapiens	0-30
12496360-1	2002	Manganese superoxide dismutase (MnSOD) catalyzes the dismutation of superoxide anions (O(2)(-)) into hydrogen peroxide (H(2)O(2)).	Hydrogen Peroxide	101-118	superoxide dismutase 2	Homo sapiens	32-37
12496360-2	2002	We altered the intracellular status of reactive oxygen species by introducing human MnSOD cDNA into the human ovarian cancer cell line SK-OV-3.	Reactive Oxygen Species	39-62	superoxide dismutase 2	Homo sapiens	84-89
12496360-6	2002	Either inhibition of p38 mitogen-activated protein kinase (p38MAPK) or scavenging free radicals blocked the induction of radioresistance by MnSOD and also abolished the shortening of the G(2)-M duration with concomitant inhibition of p38MAPK phosphorylation.	free	82-86	superoxide dismutase 2	Homo sapiens	140-145
12496360-8	2002	These results suggest that the accumulated H(2)O(2) potentiated the activation of p38MAPK after irradiation in cells overexpressing MnSOD, which led to the protection of cells from irradiation-mediated cell death through the G(2)-M checkpoint.	Hydrogen Peroxide	43-51	superoxide dismutase 2	Homo sapiens	132-137
12447859-2	2002	Recently, it has been reported that homozygosity for a valine to alanine substitution in the mitochondrial targeting sequence of manganese superoxide dismutase (Mn-SOD) represents a risk factor for severe ALD.	Valine	55-61	superoxide dismutase 2	Homo sapiens	129-159
12447859-2	2002	Recently, it has been reported that homozygosity for a valine to alanine substitution in the mitochondrial targeting sequence of manganese superoxide dismutase (Mn-SOD) represents a risk factor for severe ALD.	Valine	55-61	superoxide dismutase 2	Homo sapiens	161-167
12447859-2	2002	Recently, it has been reported that homozygosity for a valine to alanine substitution in the mitochondrial targeting sequence of manganese superoxide dismutase (Mn-SOD) represents a risk factor for severe ALD.	Alanine	65-72	superoxide dismutase 2	Homo sapiens	129-159
12447859-2	2002	Recently, it has been reported that homozygosity for a valine to alanine substitution in the mitochondrial targeting sequence of manganese superoxide dismutase (Mn-SOD) represents a risk factor for severe ALD.	Alanine	65-72	superoxide dismutase 2	Homo sapiens	161-167
12447859-4	2002	Genotyping for the valine-alanine (Val-Ala) polymorphism of the Mn-SOD gene in 281 patients with advanced ALD (cirrhosis/fibrosis) and 218 drinkers without liver disease showed no differences in either the heterozygote (55% vs. 50%) or the homozygote (19% vs. 23%) frequency for the alanine allele.	valine-alanine	19-33	superoxide dismutase 2	Homo sapiens	64-70
12447859-4	2002	Genotyping for the valine-alanine (Val-Ala) polymorphism of the Mn-SOD gene in 281 patients with advanced ALD (cirrhosis/fibrosis) and 218 drinkers without liver disease showed no differences in either the heterozygote (55% vs. 50%) or the homozygote (19% vs. 23%) frequency for the alanine allele.	H-VAL-ALA-OH	35-42	superoxide dismutase 2	Homo sapiens	64-70
12447859-4	2002	Genotyping for the valine-alanine (Val-Ala) polymorphism of the Mn-SOD gene in 281 patients with advanced ALD (cirrhosis/fibrosis) and 218 drinkers without liver disease showed no differences in either the heterozygote (55% vs. 50%) or the homozygote (19% vs. 23%) frequency for the alanine allele.	Alanine	26-33	superoxide dismutase 2	Homo sapiens	64-70
12447859-6	2002	However, the carriers of the alanine Mn-SOD allele had titers of anti-MDA, anti-HER, and anti-OX-CL IgG comparable with heterozygotes and patients homozygous for the valine allele.	her	80-83	superoxide dismutase 2	Homo sapiens	37-43
12447859-6	2002	However, the carriers of the alanine Mn-SOD allele had titers of anti-MDA, anti-HER, and anti-OX-CL IgG comparable with heterozygotes and patients homozygous for the valine allele.	Valine	166-172	superoxide dismutase 2	Homo sapiens	37-43
12447859-8	2002	In conclusion, in our population Val-Ala polymorphism in Mn-SOD influences neither susceptibility to alcohol-induced liver fibrosis nor alcohol-induced oxidative stress.	H-VAL-ALA-OH	33-40	superoxide dismutase 2	Homo sapiens	57-63
12417255-6	2002	This pathway is sensitive to inhibitors of Ca(2+) uptake in the mitochondria (ruthenium red), Ca(2+) chelators (TMB-8, EGTA-AM), and antioxidants (PDTC, NAC, Mn-SOD).	8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate	112-117	superoxide dismutase 2	Homo sapiens	158-164
12126755-4	2002	SOD2, or Mn-SOD (EC 1.15.1.1), exists as a tetramer and is initially synthesized containing a leader peptide, which targets this manganese-containing enzyme exclusively to the mitochondrial spaces.	Manganese	129-138	superoxide dismutase 2	Homo sapiens	0-4
12361705-2	2002	Manganese superoxide dismutase (MnSOD) may regulate cell growth by changing the level of intracellular ROS.	Reactive Oxygen Species	103-106	superoxide dismutase 2	Homo sapiens	0-30
12361705-2	2002	Manganese superoxide dismutase (MnSOD) may regulate cell growth by changing the level of intracellular ROS.	Reactive Oxygen Species	103-106	superoxide dismutase 2	Homo sapiens	32-37
12448827-9	2002	In both cell lines, high glucose resulted in an increase of total SOD activity, as a consequence of the increase in Cu,Zn-SOD activity.	Glucose	25-32	superoxide dismutase 2	Homo sapiens	66-69
12160946-5	2002	We also showed that cytokines, e.g., tumor necrosis factor-alpha and interleukin-1beta, and reactive oxygen species are involved in the process of signal transduction for the Mn-SOD induction.	Reactive Oxygen Species	92-115	superoxide dismutase 2	Homo sapiens	175-181
12437453-2	2002	The manganese (Mn) superoxide dismutase (SOD) is a primary antioxidant enzyme that crucially contributes to the homeostasis of oxygen radicals within the mitochondria, and thus critically participates in the control of senescence and tumor generation.	Reactive Oxygen Species	127-142	superoxide dismutase 2	Homo sapiens	41-44
12207539-4	2002	Our experimental and computational data indicate that both reduced FeSOD and oxidized MnSOD do not bind hydroxide at high pH; rather, the active-site pK for these two species is attributed to deprotonation of a second-sphere tyrosine.	hydroxide ion	104-113	superoxide dismutase 2	Homo sapiens	86-91
12207539-4	2002	Our experimental and computational data indicate that both reduced FeSOD and oxidized MnSOD do not bind hydroxide at high pH; rather, the active-site pK for these two species is attributed to deprotonation of a second-sphere tyrosine.	Tyrosine	225-233	superoxide dismutase 2	Homo sapiens	86-91
12207539-6	2002	Intriguingly, in the Fe-substituted form of MnSOD this identical chemical event occurs at a significantly lower pH.	Iron	21-23	superoxide dismutase 2	Homo sapiens	44-49
12211050-2	2002	METHODS: In this present study, we examined the expression of manganese superoxide dismutase (Mn-SOD) and copper/zinc superoxide dismutase (Cu-Zn-SOD), which are essential enzymes that eliminate ROS, in squamous cell cancers (SCCs) of the lung (n = 12), larynx (n = 13), and oral cavity (n = 20).	Reactive Oxygen Species	195-198	superoxide dismutase 2	Homo sapiens	62-92
12211050-2	2002	METHODS: In this present study, we examined the expression of manganese superoxide dismutase (Mn-SOD) and copper/zinc superoxide dismutase (Cu-Zn-SOD), which are essential enzymes that eliminate ROS, in squamous cell cancers (SCCs) of the lung (n = 12), larynx (n = 13), and oral cavity (n = 20).	Reactive Oxygen Species	195-198	superoxide dismutase 2	Homo sapiens	94-100
12127599-2	2002	The manganese-containing form of this enzyme (MnSOD) is the major superoxide scavenger in mitochondria; a weak association between a functional genetic polymorphism (Ala-9Val) in the mitochondrial targeting sequence (MTS) of this enzyme and TD has been reported in a Japanese population.	Manganese	4-13	superoxide dismutase 2	Homo sapiens	46-51
12127599-2	2002	The manganese-containing form of this enzyme (MnSOD) is the major superoxide scavenger in mitochondria; a weak association between a functional genetic polymorphism (Ala-9Val) in the mitochondrial targeting sequence (MTS) of this enzyme and TD has been reported in a Japanese population.	Superoxides	66-76	superoxide dismutase 2	Homo sapiens	46-51
12127599-2	2002	The manganese-containing form of this enzyme (MnSOD) is the major superoxide scavenger in mitochondria; a weak association between a functional genetic polymorphism (Ala-9Val) in the mitochondrial targeting sequence (MTS) of this enzyme and TD has been reported in a Japanese population.	Alanine	166-169	superoxide dismutase 2	Homo sapiens	46-51
12127599-2	2002	The manganese-containing form of this enzyme (MnSOD) is the major superoxide scavenger in mitochondria; a weak association between a functional genetic polymorphism (Ala-9Val) in the mitochondrial targeting sequence (MTS) of this enzyme and TD has been reported in a Japanese population.	9val	170-174	superoxide dismutase 2	Homo sapiens	46-51
12126755-4	2002	SOD2, or Mn-SOD (EC 1.15.1.1), exists as a tetramer and is initially synthesized containing a leader peptide, which targets this manganese-containing enzyme exclusively to the mitochondrial spaces.	Manganese	129-138	superoxide dismutase 2	Homo sapiens	9-15
12144354-3	2002	By heating each sample, a shoulder at 1631 cm(-1) in the amide I band gradually appeared from 45 degrees C for Fe SOD and from 50 degrees C for Mn SOD but another shoulder at 1639 cm(-1) appeared from 50 degrees C for Cu/Zn SOD.	Amides	57-62	superoxide dismutase 2	Homo sapiens	144-150
12093828-1	2002	BACKGROUND: The present study was undertaken to investigate the cAMP-dependent regulation of copper-zinc superoxide dismutase (Cu,Zn-SOD) and manganese SOD (Mn-SOD) by ovarian steroids in human endometrial stromal cells (ESC).	Cyclic AMP	64-68	superoxide dismutase 2	Homo sapiens	142-155
12161520-5	2002	TNF alpha and TPA significantly increased Mn-SOD activities and Mn-SOD mRNA levels, and those effects were completely inhibited by MG132 and SN50.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	superoxide dismutase 2	Homo sapiens	42-48
12161520-5	2002	TNF alpha and TPA significantly increased Mn-SOD activities and Mn-SOD mRNA levels, and those effects were completely inhibited by MG132 and SN50.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	superoxide dismutase 2	Homo sapiens	64-70
12093828-1	2002	BACKGROUND: The present study was undertaken to investigate the cAMP-dependent regulation of copper-zinc superoxide dismutase (Cu,Zn-SOD) and manganese SOD (Mn-SOD) by ovarian steroids in human endometrial stromal cells (ESC).	Steroids	176-184	superoxide dismutase 2	Homo sapiens	142-155
12093828-1	2002	BACKGROUND: The present study was undertaken to investigate the cAMP-dependent regulation of copper-zinc superoxide dismutase (Cu,Zn-SOD) and manganese SOD (Mn-SOD) by ovarian steroids in human endometrial stromal cells (ESC).	Steroids	176-184	superoxide dismutase 2	Homo sapiens	157-163
12093828-1	2002	BACKGROUND: The present study was undertaken to investigate the cAMP-dependent regulation of copper-zinc superoxide dismutase (Cu,Zn-SOD) and manganese SOD (Mn-SOD) by ovarian steroids in human endometrial stromal cells (ESC).	Cyclic AMP	64-68	superoxide dismutase 2	Homo sapiens	157-163
12093828-6	2002	To study whether the increase in Mn-SOD by db-cAMP or E(2) + MPA was mediated by cAMP-dependent protein kinase A (PKA), ESC were incubated with protein kinase inhibitor (PKI) (10 microg/ml), an inhibitor of PKA, in the presence of db-cAMP or E(2) + MPA.	Bucladesine	43-50	superoxide dismutase 2	Homo sapiens	33-39
12093828-7	2002	The increase in Mn-SOD activity following db-cAMP or E(2) + MPA was completely inhibited by PKI.	Bucladesine	42-49	superoxide dismutase 2	Homo sapiens	16-22
12031898-0	2002	Induction of MnSOD gene by arachidonic acid is mediated by reactive oxygen species and p38 MAPK signaling pathway in human HepG2 hepatoma cells.	Arachidonic Acid	27-43	superoxide dismutase 2	Homo sapiens	13-18
12093828-8	2002	CONCLUSIONS: In the process of decidualization, E(2) + MPA increases Mn-SOD expression via a cAMP-dependent pathway.	Cyclic AMP	93-97	superoxide dismutase 2	Homo sapiens	69-75
12080470-6	2002	Indeed, the enzymatic activity of MnSOD is to transform the toxic O(2)(*)(-) in H(2)O(2).	o(2)	66-70	superoxide dismutase 2	Homo sapiens	34-39
12080470-6	2002	Indeed, the enzymatic activity of MnSOD is to transform the toxic O(2)(*)(-) in H(2)O(2).	Water	80-85	superoxide dismutase 2	Homo sapiens	34-39
11929863-0	2002	Activation of matrix metalloproteinase-2 by overexpression of manganese superoxide dismutase in human breast cancer MCF-7 cells involves reactive oxygen species.	Reactive Oxygen Species	137-160	superoxide dismutase 2	Homo sapiens	62-92
11929863-4	2002	We hypothesized that manganese superoxide dismutase (MnSOD) could mediate MMP-2 activity by changing the intracellular ROS level and that nitric oxide ((.	Reactive Oxygen Species	119-122	superoxide dismutase 2	Homo sapiens	21-51
11929863-4	2002	We hypothesized that manganese superoxide dismutase (MnSOD) could mediate MMP-2 activity by changing the intracellular ROS level and that nitric oxide ((.	Reactive Oxygen Species	119-122	superoxide dismutase 2	Homo sapiens	53-58
11929863-8	2002	Our data demonstrated that overexpression of MnSOD stimulated the activation of MMP-2 with a corresponding elevation of ROS.	Reactive Oxygen Species	120-123	superoxide dismutase 2	Homo sapiens	45-50
11929863-9	2002	A decrease in ROS by ebselen, a glutathione peroxidase mimetic, or by transduction of adenovirus containing human catalase or glutathione peroxidase cDNA abolished the effect of MnSOD on MMP-2 activation.	Reactive Oxygen Species	14-17	superoxide dismutase 2	Homo sapiens	178-183
11929863-9	2002	A decrease in ROS by ebselen, a glutathione peroxidase mimetic, or by transduction of adenovirus containing human catalase or glutathione peroxidase cDNA abolished the effect of MnSOD on MMP-2 activation.	ebselen	21-28	superoxide dismutase 2	Homo sapiens	178-183
11929863-18	2002	These results indicate that MnSOD induces MMP-2 activity by regulation of intracellular ROS and imply that signaling pathways involving (.	Reactive Oxygen Species	88-91	superoxide dismutase 2	Homo sapiens	28-33
12031898-0	2002	Induction of MnSOD gene by arachidonic acid is mediated by reactive oxygen species and p38 MAPK signaling pathway in human HepG2 hepatoma cells.	Reactive Oxygen Species	59-82	superoxide dismutase 2	Homo sapiens	13-18
12031898-5	2002	The AA-induced MnSOD expression required de novo transcription as demonstrated by cotreatment of HepG2 cells with AA and actinomycin D.	Dactinomycin	121-134	superoxide dismutase 2	Homo sapiens	15-20
12031898-7	2002	Further investigations into the mechanisms by which AA induced MnSOD expression showed that superoxide anions released from AA metabolism act as second messengers via a signal-controlling pathway involving protein kinase C and p38 mitogen activated protein kinase (MAPK).	Superoxides	92-109	superoxide dismutase 2	Homo sapiens	63-68
11888709-5	2002	The concentrations of urinary 8-OH-dG were significantly elevated in the presence of the MnSOD variant genotype (P=0.04) and in the case of GSTM1 null status (P=0.02) by multivariate regression.	8-ohdg	30-37	superoxide dismutase 2	Homo sapiens	89-94
12032830-9	2002	Therefore, MnSOD expression is induced by NF-kappaB in epithelial cancer cells in response to TNF-alpha, and is at least partially responsible for their resistance to TNF-alpha-induced apoptosis, presumably through the clearance of death-inducing ROS.	Reactive Oxygen Species	247-250	superoxide dismutase 2	Homo sapiens	11-16
12032862-5	2002	The results show that co-treatment with TAM and TNF-alpha increases the MnSOD promoter/enhancer driven luciferase activity, MnSOD mRNA and protein levels.	Tamoxifen	40-43	superoxide dismutase 2	Homo sapiens	72-77
12032862-5	2002	The results show that co-treatment with TAM and TNF-alpha increases the MnSOD promoter/enhancer driven luciferase activity, MnSOD mRNA and protein levels.	Tamoxifen	40-43	superoxide dismutase 2	Homo sapiens	124-129
12032862-10	2002	Modulation of the DNA binding activity in favor of the p50/p65 complex may enhance NF-kappaB mediated induction of MnSOD by TAM.	Tamoxifen	124-127	superoxide dismutase 2	Homo sapiens	115-120
12063011-4	2002	Within mitochondria manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	20-50
12063011-4	2002	Within mitochondria manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	52-57
11849743-1	2002	Manganese superoxide dismutase (MnSOD) activity is highly elevated in the biopsies of human asbestos-associated malignant mesothelioma.	Asbestos	92-100	superoxide dismutase 2	Homo sapiens	0-30
11849743-1	2002	Manganese superoxide dismutase (MnSOD) activity is highly elevated in the biopsies of human asbestos-associated malignant mesothelioma.	Asbestos	92-100	superoxide dismutase 2	Homo sapiens	32-37
12032862-0	2002	Tamoxifen enhancement of TNF-alpha induced MnSOD expression: modulation of NF-kappaB dimerization.	Tamoxifen	0-9	superoxide dismutase 2	Homo sapiens	43-48
12032862-4	2002	In this study we investigated TAM enhancement of MnSOD induction by TNF-alpha.	Tamoxifen	30-33	superoxide dismutase 2	Homo sapiens	49-54
11929218-1	2002	The highly homologous proteins of Fe-containing superoxide dismutase (FeSOD) and MnSOD from Escherichia coli nonetheless exert very different redox tuning on the active site metal ion [Vance; Miller J.	Metals	174-179	superoxide dismutase 2	Homo sapiens	81-86
11929218-7	2002	We now present density functional theory (DFT) calculations on Fe2+ and Fe3+ bound to models of both FeSOD and MnSOD.	ammonium ferrous sulfate	63-67	superoxide dismutase 2	Homo sapiens	111-116
11929218-7	2002	We now present density functional theory (DFT) calculations on Fe2+ and Fe3+ bound to models of both FeSOD and MnSOD.	ferric sulfate	72-76	superoxide dismutase 2	Homo sapiens	111-116
11929218-8	2002	The calculations support a very important role for the conserved second sphere Gln in MnSOD in specifically destabilizing coordinated H2O relative to coordinated OH-, and thus disfavouring the oxidized state of the metal ion.	Glutamine	79-82	superoxide dismutase 2	Homo sapiens	86-91
11929218-8	2002	The calculations support a very important role for the conserved second sphere Gln in MnSOD in specifically destabilizing coordinated H2O relative to coordinated OH-, and thus disfavouring the oxidized state of the metal ion.	Water	134-137	superoxide dismutase 2	Homo sapiens	86-91
11929218-8	2002	The calculations support a very important role for the conserved second sphere Gln in MnSOD in specifically destabilizing coordinated H2O relative to coordinated OH-, and thus disfavouring the oxidized state of the metal ion.	Metals	215-220	superoxide dismutase 2	Homo sapiens	86-91
12171441-5	2002	Although EGCG showed no effects on the Cu/Zn-SOD activity, the Mn-SOD activity in the cells was enhanced (p < 0.05) by the incubation with EGCG.	epigallocatechin gallate	142-146	superoxide dismutase 2	Homo sapiens	63-69
11879807-8	2002	Immunolocalization of the SOD1 and SOD2 proteins in paraffin-embedded tissue sections revealed a marked increase in the density of SOD immunopositive profiles (particularly glia) in the typical PSP brain, particularly within the white matter.	Paraffin	52-60	superoxide dismutase 2	Homo sapiens	35-39
11837748-0	2002	Increased expression of manganese superoxide dismutase is associated with that of nitrotyrosine in myopathies with rimmed vacuoles.	3-nitrotyrosine	82-95	superoxide dismutase 2	Homo sapiens	24-54
11878987-12	2002	Comparison with related enzymes (glyoxalase I and MnSOD) suggests that the change in the coordination environment on substrate binding may correspond to loss of the glutamate ligand.	Glutamic Acid	165-174	superoxide dismutase 2	Homo sapiens	50-55
12033431-5	2002	Peroxynitrite formed either extra- or intra-mitochondrially leads to oxidative damage, most notably at complexes I and II of the electron transport chain, ATPase, aconitase and Mn-superoxide dismutase.	Peroxynitrous Acid	0-13	superoxide dismutase 2	Homo sapiens	177-200
11836586-1	2002	Recently a T to C substitution in the mitochondrial targeting sequence of the manganese superoxide dismutase (MnSOD) gene was observed that changes the amino acid sequence of the protein from valine (V) to alanine (A) and is associated with a decreased defense capacity against oxidative stress.	Valine	192-198	superoxide dismutase 2	Homo sapiens	78-108
11836586-1	2002	Recently a T to C substitution in the mitochondrial targeting sequence of the manganese superoxide dismutase (MnSOD) gene was observed that changes the amino acid sequence of the protein from valine (V) to alanine (A) and is associated with a decreased defense capacity against oxidative stress.	Valine	192-198	superoxide dismutase 2	Homo sapiens	110-115
11836586-1	2002	Recently a T to C substitution in the mitochondrial targeting sequence of the manganese superoxide dismutase (MnSOD) gene was observed that changes the amino acid sequence of the protein from valine (V) to alanine (A) and is associated with a decreased defense capacity against oxidative stress.	Alanine	206-213	superoxide dismutase 2	Homo sapiens	78-108
11836586-1	2002	Recently a T to C substitution in the mitochondrial targeting sequence of the manganese superoxide dismutase (MnSOD) gene was observed that changes the amino acid sequence of the protein from valine (V) to alanine (A) and is associated with a decreased defense capacity against oxidative stress.	Alanine	206-213	superoxide dismutase 2	Homo sapiens	110-115
11801664-8	2002	Like MnSODs of other eukaryotic organisms, A. fumigatus MnSOD forms a homotetramer with the manganese ions coordinated by three histidines, one aspartic acid, and one water molecule.	Manganese	92-101	superoxide dismutase 2	Homo sapiens	5-10
11873523-5	2002	Mice injected with MnSOD-PL had significantly increased survival after irradiation at 3,500 cGy compared with control or LacZ-PL injected mice.	lacz-pl	121-128	superoxide dismutase 2	Homo sapiens	19-24
11837748-6	2002	Immunoreactivity for Mn-SOD was often colocalized with that of nitrotyrosine, cytochrome oxidase, tau, and lysosome-associated membrane proteins 2 (LAMP-2) in vacuolated fibers.	3-nitrotyrosine	63-76	superoxide dismutase 2	Homo sapiens	21-27
11837748-8	2002	The two SODs may have different roles for cell protection, and the expression of Mn-SOD is associated with nitric oxide-induced oxidative damage in myopathies with rimmed vacuoles.	Nitric Oxide	107-119	superoxide dismutase 2	Homo sapiens	81-87
12017280-5	2002	Activity staining of polyacryamide gel electrophoresis of MnSOD revealed the possible modification of the conformation and/or activity of this enzyme at an early stage of HL-60 cell death.	polyacryamide	21-34	superoxide dismutase 2	Homo sapiens	58-63
12017292-5	2002	Polyacrylamide gel electrophoresis and activity staining demonstrated that both MnSOD and CuZnSOD activities were significantly reduced at cytotoxic concentrations of all these compounds.	polyacrylamide	0-14	superoxide dismutase 2	Homo sapiens	80-85
12017292-6	2002	Incubation of an intracellular MnSOD-enriched fraction with apoptosis-inducing concentrations of sodium ascorbate, gallic acid or EGCG did not significantly reduce the MnSOD activity, suggesting that their actions might be cell-mediated.	Ascorbic Acid	97-113	superoxide dismutase 2	Homo sapiens	31-36
12017292-6	2002	Incubation of an intracellular MnSOD-enriched fraction with apoptosis-inducing concentrations of sodium ascorbate, gallic acid or EGCG did not significantly reduce the MnSOD activity, suggesting that their actions might be cell-mediated.	Gallic Acid	115-126	superoxide dismutase 2	Homo sapiens	31-36
12017292-6	2002	Incubation of an intracellular MnSOD-enriched fraction with apoptosis-inducing concentrations of sodium ascorbate, gallic acid or EGCG did not significantly reduce the MnSOD activity, suggesting that their actions might be cell-mediated.	epigallocatechin gallate	130-134	superoxide dismutase 2	Homo sapiens	31-36
12226550-2	2002	To defend against enhanced ROS, mammalian cells have a complex network of antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase.	Reactive Oxygen Species	27-30	superoxide dismutase 2	Homo sapiens	124-127
12269769-1	2002	The purpose of this study was to examine whether the increased sensitivity of cancer cells to adriamycin (ADM), which is known to produce superoxide radicals, was brought through suppressed manganese superoxide disumutase (MnSOD) expression in the presence of transforming growth factor beta1 (TGFbeta1).	Doxorubicin	94-104	superoxide dismutase 2	Homo sapiens	223-228
12269769-1	2002	The purpose of this study was to examine whether the increased sensitivity of cancer cells to adriamycin (ADM), which is known to produce superoxide radicals, was brought through suppressed manganese superoxide disumutase (MnSOD) expression in the presence of transforming growth factor beta1 (TGFbeta1).	Doxorubicin	106-109	superoxide dismutase 2	Homo sapiens	223-228
12269769-1	2002	The purpose of this study was to examine whether the increased sensitivity of cancer cells to adriamycin (ADM), which is known to produce superoxide radicals, was brought through suppressed manganese superoxide disumutase (MnSOD) expression in the presence of transforming growth factor beta1 (TGFbeta1).	Superoxides	138-148	superoxide dismutase 2	Homo sapiens	223-228
11744334-1	2001	Endogenous tyrosine nitration and inactivation of manganese superoxide dismutase (MnSOD) has previously been reported to occur during end-stage human renal allograft rejection.	Tyrosine	11-19	superoxide dismutase 2	Homo sapiens	50-80
11912930-1	2002	Measurement of catalysis by MnSOD using direct observation of the UV absorbance of superoxide allows determination of steady-state catalytic constants.	Superoxides	83-93	superoxide dismutase 2	Homo sapiens	28-33
11912930-3	2002	Studies show that kcat/Km for the decay of superoxide catalyzed by MnSOD proceeds at diffusion control.	Superoxides	43-53	superoxide dismutase 2	Homo sapiens	67-72
11912930-5	2002	The active site of MnSOD is dominated by a hydrogen bond network comprising the manganese-bound aqueous ligand, the side chains of four residues (Gln-143, Tyr-34, His-30, and Tyr-166 from an adjacent subunit), as well as other water molecules.	Hydrogen	43-51	superoxide dismutase 2	Homo sapiens	19-24
11912930-5	2002	The active site of MnSOD is dominated by a hydrogen bond network comprising the manganese-bound aqueous ligand, the side chains of four residues (Gln-143, Tyr-34, His-30, and Tyr-166 from an adjacent subunit), as well as other water molecules.	Manganese	80-89	superoxide dismutase 2	Homo sapiens	19-24
11912930-5	2002	The active site of MnSOD is dominated by a hydrogen bond network comprising the manganese-bound aqueous ligand, the side chains of four residues (Gln-143, Tyr-34, His-30, and Tyr-166 from an adjacent subunit), as well as other water molecules.	Glutamine	146-149	superoxide dismutase 2	Homo sapiens	19-24
11912930-5	2002	The active site of MnSOD is dominated by a hydrogen bond network comprising the manganese-bound aqueous ligand, the side chains of four residues (Gln-143, Tyr-34, His-30, and Tyr-166 from an adjacent subunit), as well as other water molecules.	Tyrosine	155-158	superoxide dismutase 2	Homo sapiens	19-24
11912930-5	2002	The active site of MnSOD is dominated by a hydrogen bond network comprising the manganese-bound aqueous ligand, the side chains of four residues (Gln-143, Tyr-34, His-30, and Tyr-166 from an adjacent subunit), as well as other water molecules.	Histidine	163-166	superoxide dismutase 2	Homo sapiens	19-24
11912930-5	2002	The active site of MnSOD is dominated by a hydrogen bond network comprising the manganese-bound aqueous ligand, the side chains of four residues (Gln-143, Tyr-34, His-30, and Tyr-166 from an adjacent subunit), as well as other water molecules.	Tyrosine	175-178	superoxide dismutase 2	Homo sapiens	19-24
11912930-5	2002	The active site of MnSOD is dominated by a hydrogen bond network comprising the manganese-bound aqueous ligand, the side chains of four residues (Gln-143, Tyr-34, His-30, and Tyr-166 from an adjacent subunit), as well as other water molecules.	Water	227-232	superoxide dismutase 2	Homo sapiens	19-24
11912930-8	2002	During catalysis, MnSOD is inhibited by a peroxide complex of the metal in the active site, different from the inhibition of FeSOD and Cu,ZnSOD by Fenton chemistry.	Peroxides	42-50	superoxide dismutase 2	Homo sapiens	18-23
11912930-8	2002	During catalysis, MnSOD is inhibited by a peroxide complex of the metal in the active site, different from the inhibition of FeSOD and Cu,ZnSOD by Fenton chemistry.	Metals	66-71	superoxide dismutase 2	Homo sapiens	18-23
11912930-9	2002	Site-specific mutagenesis of active-site residues alters the extent of product inhibition of MnSOD as well, indicating that this is not only a property of the metal.	Metals	159-164	superoxide dismutase 2	Homo sapiens	93-98
12469626-1	2002	AIM: Distribution of alleles of tetranucleotide microsatellite D6S392 located nearby the gene of Mn-dependent superoxide dismutase (SOD2) was studied in healthy donors (n = 143), patients with insulin-dependent (n = 166) and insulin-independent (n = 101) diabetes mellitus (IDDM and IIDM).	tetranucleotide	32-47	superoxide dismutase 2	Homo sapiens	132-136
11744334-1	2001	Endogenous tyrosine nitration and inactivation of manganese superoxide dismutase (MnSOD) has previously been reported to occur during end-stage human renal allograft rejection.	Tyrosine	11-19	superoxide dismutase 2	Homo sapiens	82-87
11734214-0	2001	Manganese superoxide dismutase induction by iron is impaired in Friedreich ataxia cells.	Iron	44-48	superoxide dismutase 2	Homo sapiens	0-30
11761717-6	2001	Together with the fact that nitric oxide (NO) plays a potential role in neuronal differentiation, and that large amounts of NO have cytotoxicity from the reaction of NO with superoxide anions, our data suggested that the expressions of both SOD1 and SOD2, as scavengers of superoxide anions, were maintained from an early developmental stage to prepare stage-specific nNOS expression for a potential differentiation role and to elude NO cytotoxicity.	Superoxides	174-191	superoxide dismutase 2	Homo sapiens	250-254
11761717-6	2001	Together with the fact that nitric oxide (NO) plays a potential role in neuronal differentiation, and that large amounts of NO have cytotoxicity from the reaction of NO with superoxide anions, our data suggested that the expressions of both SOD1 and SOD2, as scavengers of superoxide anions, were maintained from an early developmental stage to prepare stage-specific nNOS expression for a potential differentiation role and to elude NO cytotoxicity.	Superoxides	174-184	superoxide dismutase 2	Homo sapiens	250-254
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Superoxides	31-41	superoxide dismutase 2	Homo sapiens	206-236
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Superoxides	31-41	superoxide dismutase 2	Homo sapiens	238-243
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Acetylcysteine	140-159	superoxide dismutase 2	Homo sapiens	238-243
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Acetylcysteine	161-164	superoxide dismutase 2	Homo sapiens	206-236
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Acetylcysteine	161-164	superoxide dismutase 2	Homo sapiens	238-243
11729237-0	2001	Manganese superoxide dismutase attenuates Cisplatin-induced renal injury: importance of superoxide.	Cisplatin	42-51	superoxide dismutase 2	Homo sapiens	0-30
11729237-4	2001	To address the mechanism, it was hypothesized that overexpression of antioxidant enzymes, such as mitochondria-localized manganese superoxide dismutase (MnSOD) or mitochondria-targeted catalase (mito-Cat), would be cytoprotective in cisplatin-induced cell injury.	Cisplatin	233-242	superoxide dismutase 2	Homo sapiens	121-151
11729237-6	2001	Cells that overexpressed MnSOD exhibited significantly less cell rounding and detachment compared with both mito-Cat and vector controls after exposure to 20 microM cisplatin.	Cisplatin	165-174	superoxide dismutase 2	Homo sapiens	25-30
11729237-8	2001	In addition, elevated levels of MnSOD were strongly associated with increased clonogenic potential after cisplatin challenge.	Cisplatin	105-114	superoxide dismutase 2	Homo sapiens	32-37
11729237-9	2001	Thus, overexpression of MnSOD, and not catalase, protects against cisplatin-induced renal epithelial cell injury.	Cisplatin	66-75	superoxide dismutase 2	Homo sapiens	24-29
11734214-2	2001	Here, we show that normal upregulation of the stress defense protein manganese superoxide dismutase (MnSOD) fails to occur in FRDA fibroblasts exposed to iron.	Iron	154-158	superoxide dismutase 2	Homo sapiens	69-99
11641265-3	2001	VEGF-mediated induction of MnSOD mRNA was inhibited by pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenesulfonyl fluoride, but not with the nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibitor allopurinol.	diphenyleneiodonium	124-127	superoxide dismutase 2	Homo sapiens	27-32
11641265-3	2001	VEGF-mediated induction of MnSOD mRNA was inhibited by pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenesulfonyl fluoride, but not with the nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibitor allopurinol.	diphenyleneiodonium	103-122	superoxide dismutase 2	Homo sapiens	27-32
11641265-3	2001	VEGF-mediated induction of MnSOD mRNA was inhibited by pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenesulfonyl fluoride, but not with the nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibitor allopurinol.	4-(2-aminoethyl)benzenesulfonylfluoride	134-175	superoxide dismutase 2	Homo sapiens	27-32
11641265-3	2001	VEGF-mediated induction of MnSOD mRNA was inhibited by pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenesulfonyl fluoride, but not with the nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibitor allopurinol.	nitric	194-200	superoxide dismutase 2	Homo sapiens	27-32
11641265-3	2001	VEGF-mediated induction of MnSOD mRNA was inhibited by pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenesulfonyl fluoride, but not with the nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibitor allopurinol.	NG-Nitroarginine Methyl Ester	226-232	superoxide dismutase 2	Homo sapiens	27-32
11641265-3	2001	VEGF-mediated induction of MnSOD mRNA was inhibited by pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenesulfonyl fluoride, but not with the nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibitor allopurinol.	omega-N-Methylarginine	234-257	superoxide dismutase 2	Homo sapiens	27-32
11641265-3	2001	VEGF-mediated induction of MnSOD mRNA was inhibited by pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenesulfonyl fluoride, but not with the nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibitor allopurinol.	Allopurinol	293-304	superoxide dismutase 2	Homo sapiens	27-32
11529760-5	2001	The pH-dependent role of superoxide was probed using Mn-SOD and compared to guanosine and 8-methoxyguanosine photooxidation.	Superoxides	25-35	superoxide dismutase 2	Homo sapiens	53-59
11675473-5	2001	Incubation of ESC with actinomycin D, an RNA synthesis inhibitor, blocked TNFalpha-induced Mn-SOD mRNA expression, but cycloheximide, a protein synthesis inhibitor, had no effect.	Dactinomycin	23-36	superoxide dismutase 2	Homo sapiens	91-97
11553022-4	2001	The Mn-SOD mRNA levels were markedly increased after exposure to nitrogen gas for 5 min.	Nitrogen	65-73	superoxide dismutase 2	Homo sapiens	4-10
11553022-6	2001	Pretreatment with chelerythrine or GF109203x, inhibitors of PKC, attenuated the increase in Mn-SOD mRNA following hypoxia in a concentration-dependent manner.	chelerythrine	18-31	superoxide dismutase 2	Homo sapiens	92-98
11553022-6	2001	Pretreatment with chelerythrine or GF109203x, inhibitors of PKC, attenuated the increase in Mn-SOD mRNA following hypoxia in a concentration-dependent manner.	bisindolylmaleimide I	35-44	superoxide dismutase 2	Homo sapiens	92-98
11553022-8	2001	Incubation with phorbol 12-myristate 13-acetate, the PKC activator, enhanced the increase in Mn-SOD gene expression in response to transient hypoxia.	Tetradecanoylphorbol Acetate	16-47	superoxide dismutase 2	Homo sapiens	93-99
11696579-5	2001	Both the inhibition of eNOS and the changes in its post-translational modifications were reversed by antisense inhibition of glutamine:fructose-6-phosphate amidotransferase, the rate-limiting enzyme of the hexosamine pathway, or by blocking mitochondrial superoxide overproduction with uncoupling protein-1 (UCP-1) or manganese superoxide dismutase (MnSOD).	Glutamine	125-134	superoxide dismutase 2	Homo sapiens	318-348
11696579-5	2001	Both the inhibition of eNOS and the changes in its post-translational modifications were reversed by antisense inhibition of glutamine:fructose-6-phosphate amidotransferase, the rate-limiting enzyme of the hexosamine pathway, or by blocking mitochondrial superoxide overproduction with uncoupling protein-1 (UCP-1) or manganese superoxide dismutase (MnSOD).	Glutamine	125-134	superoxide dismutase 2	Homo sapiens	350-355
11696579-5	2001	Both the inhibition of eNOS and the changes in its post-translational modifications were reversed by antisense inhibition of glutamine:fructose-6-phosphate amidotransferase, the rate-limiting enzyme of the hexosamine pathway, or by blocking mitochondrial superoxide overproduction with uncoupling protein-1 (UCP-1) or manganese superoxide dismutase (MnSOD).	Hexosamines	206-216	superoxide dismutase 2	Homo sapiens	318-348
11696579-5	2001	Both the inhibition of eNOS and the changes in its post-translational modifications were reversed by antisense inhibition of glutamine:fructose-6-phosphate amidotransferase, the rate-limiting enzyme of the hexosamine pathway, or by blocking mitochondrial superoxide overproduction with uncoupling protein-1 (UCP-1) or manganese superoxide dismutase (MnSOD).	Hexosamines	206-216	superoxide dismutase 2	Homo sapiens	350-355
11672836-5	2001	MnSOD increased in hippocampus at 24, 48 and 72 h after ischemia, coincident with the marked reduction in the activity of glutathione-related enzymes.	Glutathione	122-133	superoxide dismutase 2	Homo sapiens	0-5
11580280-1	2001	Manganese superoxide dismutase (MnSOD) cycles between the Mn(II) and Mn(III) states during the catalyzed disproportionation of O(2)(*-), a catalysis that is limited at micromolar levels of superoxide by a peroxide-inhibited complex with the metal.	Superoxides	127-131	superoxide dismutase 2	Homo sapiens	0-30
11580280-1	2001	Manganese superoxide dismutase (MnSOD) cycles between the Mn(II) and Mn(III) states during the catalyzed disproportionation of O(2)(*-), a catalysis that is limited at micromolar levels of superoxide by a peroxide-inhibited complex with the metal.	Superoxides	127-131	superoxide dismutase 2	Homo sapiens	32-37
11580280-1	2001	Manganese superoxide dismutase (MnSOD) cycles between the Mn(II) and Mn(III) states during the catalyzed disproportionation of O(2)(*-), a catalysis that is limited at micromolar levels of superoxide by a peroxide-inhibited complex with the metal.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
11580280-1	2001	Manganese superoxide dismutase (MnSOD) cycles between the Mn(II) and Mn(III) states during the catalyzed disproportionation of O(2)(*-), a catalysis that is limited at micromolar levels of superoxide by a peroxide-inhibited complex with the metal.	Peroxides	12-20	superoxide dismutase 2	Homo sapiens	32-37
11580280-1	2001	Manganese superoxide dismutase (MnSOD) cycles between the Mn(II) and Mn(III) states during the catalyzed disproportionation of O(2)(*-), a catalysis that is limited at micromolar levels of superoxide by a peroxide-inhibited complex with the metal.	Metals	241-246	superoxide dismutase 2	Homo sapiens	0-30
11580280-1	2001	Manganese superoxide dismutase (MnSOD) cycles between the Mn(II) and Mn(III) states during the catalyzed disproportionation of O(2)(*-), a catalysis that is limited at micromolar levels of superoxide by a peroxide-inhibited complex with the metal.	Metals	241-246	superoxide dismutase 2	Homo sapiens	32-37
11580280-3	2001	Crystal structures of mutants of human MnSOD in which Trp161 was replaced with Ala or Phe showed significant conformational changes on adjacent residues near the active site, particularly Gln143 and Tyr34 which in wild-type MnSOD participate in a hydrogen bond network believed to support proton transfer during catalysis.	Hydrogen	247-255	superoxide dismutase 2	Homo sapiens	39-44
11580280-3	2001	Crystal structures of mutants of human MnSOD in which Trp161 was replaced with Ala or Phe showed significant conformational changes on adjacent residues near the active site, particularly Gln143 and Tyr34 which in wild-type MnSOD participate in a hydrogen bond network believed to support proton transfer during catalysis.	Hydrogen	247-255	superoxide dismutase 2	Homo sapiens	224-229
11580280-6	2001	Catalysis by W161A and W161F MnSOD was associated with a decrease of at least 100-fold in the catalytic rate of reduction of superoxide, which then promotes a competing pathway leading to product inhibition.	Superoxides	125-135	superoxide dismutase 2	Homo sapiens	29-34
11461912-5	2001	Both Cu,Zn-SOD and Mn-SOD inhibited the aerobic oxidation of NADPH by AS, but the amounts required were approximately 100-fold greater than those needed to inhibit the reduction of cytochrome c.	NADP	61-66	superoxide dismutase 2	Homo sapiens	19-25
11461912-5	2001	Both Cu,Zn-SOD and Mn-SOD inhibited the aerobic oxidation of NADPH by AS, but the amounts required were approximately 100-fold greater than those needed to inhibit the reduction of cytochrome c.	oxyhyponitrite	70-72	superoxide dismutase 2	Homo sapiens	19-25
11481695-5	2001	However, we identified a previously described polymorphism of the mitochondrial targeting sequence consisting of a C47T in exon 2 of SOD2, which results in an alanine to valine substitution.	Alanine	159-166	superoxide dismutase 2	Homo sapiens	133-137
11555836-2	2001	Manganese (Mn)(2+)-dependent superoxide dismutase (SOD-2) is primarily responsible for metabolism of superoxide produced in mitochondria by respiratory chain activity during aerobic metabolism of glucose and other substrates.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	51-56
11555836-2	2001	Manganese (Mn)(2+)-dependent superoxide dismutase (SOD-2) is primarily responsible for metabolism of superoxide produced in mitochondria by respiratory chain activity during aerobic metabolism of glucose and other substrates.	Superoxides	29-39	superoxide dismutase 2	Homo sapiens	51-56
11555836-2	2001	Manganese (Mn)(2+)-dependent superoxide dismutase (SOD-2) is primarily responsible for metabolism of superoxide produced in mitochondria by respiratory chain activity during aerobic metabolism of glucose and other substrates.	Glucose	196-203	superoxide dismutase 2	Homo sapiens	51-56
11555836-6	2001	In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad.	Glucose	60-67	superoxide dismutase 2	Homo sapiens	23-28
11555836-6	2001	In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad.	Glucose	60-67	superoxide dismutase 2	Homo sapiens	30-38
11555836-6	2001	In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad.	Glucose	60-67	superoxide dismutase 2	Homo sapiens	30-35
11555836-6	2001	In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad.	Glucose	60-67	superoxide dismutase 2	Homo sapiens	30-35
11555836-6	2001	In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad.	Glucose	222-229	superoxide dismutase 2	Homo sapiens	23-28
11555836-6	2001	In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad.	Glucose	222-229	superoxide dismutase 2	Homo sapiens	30-38
11555836-6	2001	In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad.	Glucose	222-229	superoxide dismutase 2	Homo sapiens	30-35
11555836-6	2001	In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad.	Glucose	222-229	superoxide dismutase 2	Homo sapiens	30-35
11555836-11	2001	These results support a role for increased cellular superoxide production derived from NAD(P)H oxidase activity in the stimulation of collagen accumulation induced in MC by high glucose and demonstrate that an increase in mitochondrial SOD-2 activity suppresses this response.	Glucose	178-185	superoxide dismutase 2	Homo sapiens	236-241
11560779-0	2001	TPA-activated transcription of the human MnSOD gene: role of transcription factors Sp-1 and Egr-1.	Tetradecanoylphorbol Acetate	0-3	superoxide dismutase 2	Homo sapiens	41-46
11560779-6	2001	We also found that the basal promoter is responsive to 12-O-tetradecanoylphorbol-13-acetate (TPA)-activated hMnSOD transcription in the human hepatocarcinoma cell line HepG2.	Tetradecanoylphorbol Acetate	55-91	superoxide dismutase 2	Homo sapiens	108-114
11560779-6	2001	We also found that the basal promoter is responsive to 12-O-tetradecanoylphorbol-13-acetate (TPA)-activated hMnSOD transcription in the human hepatocarcinoma cell line HepG2.	Tetradecanoylphorbol Acetate	93-96	superoxide dismutase 2	Homo sapiens	108-114
11560779-7	2001	The contributions of these binding sites and the roles of the transcription factors Egr-1, AP-2, and Sp1 in the activation of hMnSOD transcription by TPA were investigated by site-directed mutation analysis, Western blotting, and overexpression of transcription factors.	Tetradecanoylphorbol Acetate	150-153	superoxide dismutase 2	Homo sapiens	126-132
11560779-8	2001	The results showed that Sp1 plays a positive role for both basal and TPA-activated hMnSOD transcription, whereas overexpression of Egr-1 has a negative role in the basal promoter activity without any effect on TPA-mediated activation of hMnSOD transcription.	Tetradecanoylphorbol Acetate	69-72	superoxide dismutase 2	Homo sapiens	83-89
11551744-6	2001	This iron-induced oxidative stress is often accentuated by ascorbate and oxidized glutathione, although it is suppressed by the following antioxidants: S-nitrosoglutathione or nitric oxide, MnSOD mimics, manganese, U-78517F, Trolox, and deferoxamine.	Iron	5-9	superoxide dismutase 2	Homo sapiens	190-195
11592093-1	2001	Manganese superoxide dismutase (MnSOD) is an antioxidant enzyme capable of neutralizing superoxide anion molecules.	Superoxides	88-104	superoxide dismutase 2	Homo sapiens	0-30
11592093-1	2001	Manganese superoxide dismutase (MnSOD) is an antioxidant enzyme capable of neutralizing superoxide anion molecules.	Superoxides	88-104	superoxide dismutase 2	Homo sapiens	32-37
11536448-2	2001	We hypothesized that MnSOD increases in human lung in response to oxygen treatment, although this response could be restricted to certain cell types and depend on gestational age.	Oxygen	66-72	superoxide dismutase 2	Homo sapiens	21-26
11536448-9	2001	However, the inability to induce MnSOD in response to oxygen treatment may result in a poor outcome.	Oxygen	54-60	superoxide dismutase 2	Homo sapiens	33-38
20954153-3	2001	Activity can be measured as described in this unit by a number of indirect competitive inhibition assays based on the principle that the superoxide anion radical will reduce an inhibitory substrate [such as nitroblue tetrazolium (NBT) or cytochrome c] and SOD activity will reduce the rate of reduction in a competitive fashion.	Superoxides	137-161	superoxide dismutase 2	Homo sapiens	256-259
20954153-3	2001	Activity can be measured as described in this unit by a number of indirect competitive inhibition assays based on the principle that the superoxide anion radical will reduce an inhibitory substrate [such as nitroblue tetrazolium (NBT) or cytochrome c] and SOD activity will reduce the rate of reduction in a competitive fashion.	Nitroblue Tetrazolium	230-233	superoxide dismutase 2	Homo sapiens	256-259
11454680-2	2001	We found that overexpression of Mn-SOD reduced the levels of reactive oxygen species in the mitochondria and intracellular phospholipid peroxidation product (4-hydroxy-2-nonenal) and prevented cell death.	Reactive Oxygen Species	61-84	superoxide dismutase 2	Homo sapiens	32-38
11454680-2	2001	We found that overexpression of Mn-SOD reduced the levels of reactive oxygen species in the mitochondria and intracellular phospholipid peroxidation product (4-hydroxy-2-nonenal) and prevented cell death.	4-hydroxy-2-nonenal	158-177	superoxide dismutase 2	Homo sapiens	32-38
11454680-4	2001	The results suggested that Mn-SOD might play an important role in protecting cells against radiation-induced cell death by controlling the generation of mitochondrial reactive oxygen species and intracellular lipid peroxidation.	Reactive Oxygen Species	167-190	superoxide dismutase 2	Homo sapiens	27-33
11481695-5	2001	However, we identified a previously described polymorphism of the mitochondrial targeting sequence consisting of a C47T in exon 2 of SOD2, which results in an alanine to valine substitution.	Valine	170-176	superoxide dismutase 2	Homo sapiens	133-137
11491650-2	2001	The inhibition of tumor cell growth can be attributed to the increase in the steady-state levels of H2O2 as a result of the increased dismuting activity of MnSOD.	Hydrogen Peroxide	100-104	superoxide dismutase 2	Homo sapiens	156-161
11264281-4	2001	The mitochondrial electron transport chain inhibitors, antimycin A and myxothiazol, selectively blocked TNF-alpha-inducible expression of MnSOD but not that of IL-1beta or LPS, indicating different signaling pathways.	Antimycin A	55-66	superoxide dismutase 2	Homo sapiens	138-143
11264281-4	2001	The mitochondrial electron transport chain inhibitors, antimycin A and myxothiazol, selectively blocked TNF-alpha-inducible expression of MnSOD but not that of IL-1beta or LPS, indicating different signaling pathways.	myxothiazol	71-82	superoxide dismutase 2	Homo sapiens	138-143
11264281-5	2001	N-Acetylcysteine could reliably decrease inducible MnSOD expression by TNF-alpha, but not IL-1, linking reactive oxygen species (ROS) to the TNF-alpha signaling pathway.	Acetylcysteine	0-16	superoxide dismutase 2	Homo sapiens	51-56
11264281-5	2001	N-Acetylcysteine could reliably decrease inducible MnSOD expression by TNF-alpha, but not IL-1, linking reactive oxygen species (ROS) to the TNF-alpha signaling pathway.	Reactive Oxygen Species	104-127	superoxide dismutase 2	Homo sapiens	51-56
11264281-5	2001	N-Acetylcysteine could reliably decrease inducible MnSOD expression by TNF-alpha, but not IL-1, linking reactive oxygen species (ROS) to the TNF-alpha signaling pathway.	Reactive Oxygen Species	129-132	superoxide dismutase 2	Homo sapiens	51-56
11264281-7	2001	A specific cytoplasmic phospholipase A(2) inhibitor reduced stimulated MnSOD expression by TNF-alpha, but not by IL-1beta, further supporting the role of ROS.	Reactive Oxygen Species	154-157	superoxide dismutase 2	Homo sapiens	71-76
11499385-3	2001	The levels of the myogenic transcription factor, MyoD, and the muscle-specific marker, alpha-actin, were increased over time with 5-azacytidine treatment in the SOD-H cell line.	Azacitidine	130-143	superoxide dismutase 2	Homo sapiens	161-164
11491650-3	2001	Here we demonstrate that overexpression of MnSOD enhances the activity of the superoxide (O2*-)-sensitive enzyme aconitase, decreases the intracellular GSH/GSSG ratio, and dose-dependently inhibits pyruvate carboxylase activity.	Superoxides	78-88	superoxide dismutase 2	Homo sapiens	43-48
11491650-3	2001	Here we demonstrate that overexpression of MnSOD enhances the activity of the superoxide (O2*-)-sensitive enzyme aconitase, decreases the intracellular GSH/GSSG ratio, and dose-dependently inhibits pyruvate carboxylase activity.	Superoxides	90-92	superoxide dismutase 2	Homo sapiens	43-48
11491650-3	2001	Here we demonstrate that overexpression of MnSOD enhances the activity of the superoxide (O2*-)-sensitive enzyme aconitase, decreases the intracellular GSH/GSSG ratio, and dose-dependently inhibits pyruvate carboxylase activity.	Glutathione Disulfide	152-155	superoxide dismutase 2	Homo sapiens	43-48
11491650-3	2001	Here we demonstrate that overexpression of MnSOD enhances the activity of the superoxide (O2*-)-sensitive enzyme aconitase, decreases the intracellular GSH/GSSG ratio, and dose-dependently inhibits pyruvate carboxylase activity.	Glutathione Disulfide	156-160	superoxide dismutase 2	Homo sapiens	43-48
11491650-4	2001	Thus, alterations in the steady-state concentrations of mitochondrial O2*- and H2O2 as a result of MnSOD overexpression can alter the metabolic capacity of the cell leading to inhibition of cell growth.	Superoxides	70-73	superoxide dismutase 2	Homo sapiens	99-104
11491650-4	2001	Thus, alterations in the steady-state concentrations of mitochondrial O2*- and H2O2 as a result of MnSOD overexpression can alter the metabolic capacity of the cell leading to inhibition of cell growth.	Hydrogen Peroxide	79-83	superoxide dismutase 2	Homo sapiens	99-104
11491650-5	2001	Furthermore, we propose that MnSOD overexpression can modulate the activity of nitric oxide (*NO) by preventing its reaction with O2*-.	Nitric Oxide	79-91	superoxide dismutase 2	Homo sapiens	29-34
11491650-5	2001	Furthermore, we propose that MnSOD overexpression can modulate the activity of nitric oxide (*NO) by preventing its reaction with O2*-.	Superoxides	130-134	superoxide dismutase 2	Homo sapiens	29-34
11491650-6	2001	This hypothesis suggests that the redox environment of the mitochondria can be altered to favor the activity of *NO rather than peroxynitrite (ONOO-) and may explain the enhanced toxicity of *NO-generating compounds toward MnSOD-overexpressing cell lines.	Peroxynitrous Acid	128-141	superoxide dismutase 2	Homo sapiens	223-228
11491650-6	2001	This hypothesis suggests that the redox environment of the mitochondria can be altered to favor the activity of *NO rather than peroxynitrite (ONOO-) and may explain the enhanced toxicity of *NO-generating compounds toward MnSOD-overexpressing cell lines.	oxido nitrite	143-148	superoxide dismutase 2	Homo sapiens	223-228
11491657-1	2001	Cancer cells are in general low in the enzymatic activities of both manganese-containing (MnSOD) and copper- and zinc-containing superoxide dismutase.	Manganese	68-77	superoxide dismutase 2	Homo sapiens	90-95
11491657-5	2001	We have also shown that MnSOD overexpression causes the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) to have increased cytotoxicity.	Carmustine	72-108	superoxide dismutase 2	Homo sapiens	24-29
11491657-5	2001	We have also shown that MnSOD overexpression causes the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) to have increased cytotoxicity.	Carmustine	110-114	superoxide dismutase 2	Homo sapiens	24-29
11491657-6	2001	Our hypothesis for the mechanism of action of this combination is that overexpression of MnSOD leads to increased peroxide levels and that BCNU inhibits peroxide removal.	Peroxides	114-122	superoxide dismutase 2	Homo sapiens	89-94
11334889-4	2001	The presence of CuZn-SOD, Mn-SOD or Mn(II) enhanced the frequency of DNA damage induced by hydrogen peroxide (H2O2) and Cu(II), and altered the site specificity of the latter: H2O2 induced Cu(II)-dependent DNA damage with high frequency at the 5"-guanine of poly G sequences; when SODs were added, the frequency of cleavages at thymine and cytosine residues increased.	Hydrogen Peroxide	91-108	superoxide dismutase 2	Homo sapiens	26-32
23045062-3	2001	As described in this unit, this activity can be measured indirectly based on competition between SOD and an indicator molecule that reacts avidly with superoxide to produce a measurable change in absorption, thus it is possible to measure total SOD activity or that of CuZn-SOD and MnSOD.	Superoxides	151-161	superoxide dismutase 2	Homo sapiens	97-100
23045062-3	2001	As described in this unit, this activity can be measured indirectly based on competition between SOD and an indicator molecule that reacts avidly with superoxide to produce a measurable change in absorption, thus it is possible to measure total SOD activity or that of CuZn-SOD and MnSOD.	Superoxides	151-161	superoxide dismutase 2	Homo sapiens	245-248
23045062-3	2001	As described in this unit, this activity can be measured indirectly based on competition between SOD and an indicator molecule that reacts avidly with superoxide to produce a measurable change in absorption, thus it is possible to measure total SOD activity or that of CuZn-SOD and MnSOD.	Superoxides	151-161	superoxide dismutase 2	Homo sapiens	282-287
11313317-2	2001	A genetic dimorphism encodes for either alanine or valine in the mitochondrial targeting sequence of manganese superoxide dismutase and could modulate its mitochondrial import.	Alanine	40-47	superoxide dismutase 2	Homo sapiens	101-131
11313317-2	2001	A genetic dimorphism encodes for either alanine or valine in the mitochondrial targeting sequence of manganese superoxide dismutase and could modulate its mitochondrial import.	Valine	51-57	superoxide dismutase 2	Homo sapiens	101-131
11278550-1	2001	Manganese superoxide dismutase (Mn-SOD) is a primary antioxidant enzyme whose expression is essential for life in oxygen.	Oxygen	114-120	superoxide dismutase 2	Homo sapiens	32-38
11411799-8	2001	Free oxygen radicals released during preconditioning are likely to take part in the delayed protection through the production of peroxynitrite which activates PKC and through the increase of the activity of antioxidant enzymes such as Mn superoxide-dismutase.	free oxygen radicals	0-20	superoxide dismutase 2	Homo sapiens	235-258
11411799-8	2001	Free oxygen radicals released during preconditioning are likely to take part in the delayed protection through the production of peroxynitrite which activates PKC and through the increase of the activity of antioxidant enzymes such as Mn superoxide-dismutase.	Peroxynitrous Acid	129-142	superoxide dismutase 2	Homo sapiens	235-258
11370671-7	2001	When CuZn-SOD or Mn-SOD was added, the DNA damage was enhanced and its predominant cleavage sites were changed into thymine and cytosine residues.	Thymine	116-123	superoxide dismutase 2	Homo sapiens	17-23
11370671-7	2001	When CuZn-SOD or Mn-SOD was added, the DNA damage was enhanced and its predominant cleavage sites were changed into thymine and cytosine residues.	Cytosine	128-136	superoxide dismutase 2	Homo sapiens	17-23
11370671-8	2001	We consider that SOD may increase the frequency of mutations due to DNA damage induced by o-aminophenol and thus increase its carcinogenic potential.	2-aminophenol	90-103	superoxide dismutase 2	Homo sapiens	17-20
11323405-2	2001	Within mitochondria manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	20-50
11323405-2	2001	Within mitochondria manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species.	Reactive Oxygen Species	112-135	superoxide dismutase 2	Homo sapiens	52-57
11334889-4	2001	The presence of CuZn-SOD, Mn-SOD or Mn(II) enhanced the frequency of DNA damage induced by hydrogen peroxide (H2O2) and Cu(II), and altered the site specificity of the latter: H2O2 induced Cu(II)-dependent DNA damage with high frequency at the 5"-guanine of poly G sequences; when SODs were added, the frequency of cleavages at thymine and cytosine residues increased.	Hydrogen Peroxide	110-114	superoxide dismutase 2	Homo sapiens	26-32
11334889-4	2001	The presence of CuZn-SOD, Mn-SOD or Mn(II) enhanced the frequency of DNA damage induced by hydrogen peroxide (H2O2) and Cu(II), and altered the site specificity of the latter: H2O2 induced Cu(II)-dependent DNA damage with high frequency at the 5"-guanine of poly G sequences; when SODs were added, the frequency of cleavages at thymine and cytosine residues increased.	cu(ii)	120-126	superoxide dismutase 2	Homo sapiens	26-32
11334889-4	2001	The presence of CuZn-SOD, Mn-SOD or Mn(II) enhanced the frequency of DNA damage induced by hydrogen peroxide (H2O2) and Cu(II), and altered the site specificity of the latter: H2O2 induced Cu(II)-dependent DNA damage with high frequency at the 5"-guanine of poly G sequences; when SODs were added, the frequency of cleavages at thymine and cytosine residues increased.	Hydrogen Peroxide	176-180	superoxide dismutase 2	Homo sapiens	26-32
11334889-4	2001	The presence of CuZn-SOD, Mn-SOD or Mn(II) enhanced the frequency of DNA damage induced by hydrogen peroxide (H2O2) and Cu(II), and altered the site specificity of the latter: H2O2 induced Cu(II)-dependent DNA damage with high frequency at the 5"-guanine of poly G sequences; when SODs were added, the frequency of cleavages at thymine and cytosine residues increased.	cu(ii)	189-195	superoxide dismutase 2	Homo sapiens	26-32
11334889-4	2001	The presence of CuZn-SOD, Mn-SOD or Mn(II) enhanced the frequency of DNA damage induced by hydrogen peroxide (H2O2) and Cu(II), and altered the site specificity of the latter: H2O2 induced Cu(II)-dependent DNA damage with high frequency at the 5"-guanine of poly G sequences; when SODs were added, the frequency of cleavages at thymine and cytosine residues increased.	5"-guanine	244-254	superoxide dismutase 2	Homo sapiens	26-32
11334889-4	2001	The presence of CuZn-SOD, Mn-SOD or Mn(II) enhanced the frequency of DNA damage induced by hydrogen peroxide (H2O2) and Cu(II), and altered the site specificity of the latter: H2O2 induced Cu(II)-dependent DNA damage with high frequency at the 5"-guanine of poly G sequences; when SODs were added, the frequency of cleavages at thymine and cytosine residues increased.	Cytosine	340-348	superoxide dismutase 2	Homo sapiens	26-32
11369207-11	2001	Ki-Ras, on the other hand, stimulates the scavenging of ROS by activating posttranscriptionally the mitochondrial antioxidant enzyme, Mn-superoxide dismutase (Mn-SOD), via an ERK1/2-dependent pathway.	Reactive Oxygen Species	56-59	superoxide dismutase 2	Homo sapiens	134-157
11294629-4	2001	The 2.2 A resolution X-ray structure of H30A-MnSOD shows that removing the Tyr174-->His30 hydrogen bond from the acceptor side results in a significant displacement of the main-chain segment containing the Y174 residue, with local rearrangement of the protein.	Hydrogen	93-101	superoxide dismutase 2	Homo sapiens	45-50
11294629-5	2001	The 1.35 A resolution structure of Y174F-MnSOD shows that disruption of the same hydrogen bond from the donor side has much greater consequences, with reorientation of F174 having a domino effect on the neighboring residues, resulting in a major rearrangement of the dimer interface and flipping of the His30 ring.	Hydrogen	81-89	superoxide dismutase 2	Homo sapiens	41-46
11294629-7	2001	This observation supports assignment of the pH sensitivity of MnSOD to coordination of hydroxide ion at high pH rather than to ionization of the phenolic group of Y34.	hydroxide ion	87-96	superoxide dismutase 2	Homo sapiens	62-67
11369207-11	2001	Ki-Ras, on the other hand, stimulates the scavenging of ROS by activating posttranscriptionally the mitochondrial antioxidant enzyme, Mn-superoxide dismutase (Mn-SOD), via an ERK1/2-dependent pathway.	Reactive Oxygen Species	56-59	superoxide dismutase 2	Homo sapiens	159-165
11369207-12	2001	Glutamic acid substitution of the four lysine residues in the polybasic stretch at the COOH terminus of Ki-Ras completely abolishes the activation of Mn-SOD, although it does not inhibit ERK1/2-induced transcription.	Glutamic Acid	0-13	superoxide dismutase 2	Homo sapiens	150-156
11369207-12	2001	Glutamic acid substitution of the four lysine residues in the polybasic stretch at the COOH terminus of Ki-Ras completely abolishes the activation of Mn-SOD, although it does not inhibit ERK1/2-induced transcription.	Lysine	39-45	superoxide dismutase 2	Homo sapiens	150-156
11369207-13	2001	In contrast, an alanine substitution of the cysteine of the CAAX box has very little effect on Mn-SOD activity but eliminates ERK1/2- dependent transcription.	Alanine	16-23	superoxide dismutase 2	Homo sapiens	95-101
11306437-3	2001	After exposure to 95% O(2) for 10 d, 44 to 57% of cells overexpressing both MnSOD and CAT and 37 to 47% of cells overexpressing MnSOD alone were viable compared with 7 to 12% of empty vector or parental cells (P < 0.05).	o(2)	22-26	superoxide dismutase 2	Homo sapiens	76-81
11306437-6	2001	In addition, 54 to 72% of cells overexpressing both MnSOD and CAT survived in 1 mM paraquat compared with 58 to 73% with MnSOD alone and 27% with control cells.	Paraquat	83-91	superoxide dismutase 2	Homo sapiens	52-57
11179510-5	2001	The increase in MnSOD in the presence of Fe(3+)-NTA was greater under the condition of 20% O(2) than under the condition of 1% O(2).	fe(3+)-nta	41-51	superoxide dismutase 2	Homo sapiens	16-21
11289144-4	2001	Using reverse transcription-PCR, Western blot and immunofluorescence, and transactivation assays, we found that the manganese superoxide dismutase (MnSOD), an enzyme that converts O2*- in H2O2, is up-regulated by cRel through a kappaB site in intron 2.	o2*- in	180-187	superoxide dismutase 2	Homo sapiens	116-146
11289144-4	2001	Using reverse transcription-PCR, Western blot and immunofluorescence, and transactivation assays, we found that the manganese superoxide dismutase (MnSOD), an enzyme that converts O2*- in H2O2, is up-regulated by cRel through a kappaB site in intron 2.	o2*- in	180-187	superoxide dismutase 2	Homo sapiens	148-153
11289144-4	2001	Using reverse transcription-PCR, Western blot and immunofluorescence, and transactivation assays, we found that the manganese superoxide dismutase (MnSOD), an enzyme that converts O2*- in H2O2, is up-regulated by cRel through a kappaB site in intron 2.	Hydrogen Peroxide	188-192	superoxide dismutase 2	Homo sapiens	116-146
11289144-4	2001	Using reverse transcription-PCR, Western blot and immunofluorescence, and transactivation assays, we found that the manganese superoxide dismutase (MnSOD), an enzyme that converts O2*- in H2O2, is up-regulated by cRel through a kappaB site in intron 2.	Hydrogen Peroxide	188-192	superoxide dismutase 2	Homo sapiens	148-153
11289144-5	2001	Inhibition of MnSOD induction by antisense oligonucleotides and overexpression of MnSOD respectively reverts and mimics both the antiproliferative and antiapoptotic effects of cRel, suggesting that they both occur via the induction of this gene.	Oligonucleotides	43-59	superoxide dismutase 2	Homo sapiens	14-19
11289144-6	2001	On one hand, MnSOD could improve the efficiency of cRel-overexpressing cells in eliminating toxic O2*- produced on TNF-alpha treatment, explaining why they escape TNF-alpha-induced apoptosis.	o2*	98-101	superoxide dismutase 2	Homo sapiens	13-18
11328670-10	2001	Our laboratory has recently demonstrated that MnSOD is tyrosine nitrated and inactivated during human kidney allograft rejection and human pancreatic ductal adenocarcinoma.	Tyrosine	55-63	superoxide dismutase 2	Homo sapiens	46-51
11328670-11	2001	We have determined that peroxynitrite (ONOO- ) is the only known biological oxidant competent to inactivate enzymatic activity, to nitrate critical tyrosine residues, and to induce dityrosine formation in MnSOD.	Peroxynitrous Acid	24-37	superoxide dismutase 2	Homo sapiens	205-210
11328670-11	2001	We have determined that peroxynitrite (ONOO- ) is the only known biological oxidant competent to inactivate enzymatic activity, to nitrate critical tyrosine residues, and to induce dityrosine formation in MnSOD.	oxido nitrite	39-44	superoxide dismutase 2	Homo sapiens	205-210
11328670-11	2001	We have determined that peroxynitrite (ONOO- ) is the only known biological oxidant competent to inactivate enzymatic activity, to nitrate critical tyrosine residues, and to induce dityrosine formation in MnSOD.	dityrosine	181-191	superoxide dismutase 2	Homo sapiens	205-210
11328670-12	2001	Tyrosine nitration and inactivation of MnSOD would lead to increased levels of superoxide and concomitant increases in ONOO- within the mitochondria which, could lead to tyrosine nitration/oxidation of key mitochondrial proteins and ultimately mitochondrial dysfunction and cell death.	Superoxides	79-89	superoxide dismutase 2	Homo sapiens	39-44
11328670-12	2001	Tyrosine nitration and inactivation of MnSOD would lead to increased levels of superoxide and concomitant increases in ONOO- within the mitochondria which, could lead to tyrosine nitration/oxidation of key mitochondrial proteins and ultimately mitochondrial dysfunction and cell death.	onoo	119-123	superoxide dismutase 2	Homo sapiens	39-44
11328670-12	2001	Tyrosine nitration and inactivation of MnSOD would lead to increased levels of superoxide and concomitant increases in ONOO- within the mitochondria which, could lead to tyrosine nitration/oxidation of key mitochondrial proteins and ultimately mitochondrial dysfunction and cell death.	Tyrosine	170-178	superoxide dismutase 2	Homo sapiens	39-44
11179510-5	2001	The increase in MnSOD in the presence of Fe(3+)-NTA was greater under the condition of 20% O(2) than under the condition of 1% O(2).	Oxygen	127-131	superoxide dismutase 2	Homo sapiens	16-21
11179510-5	2001	The increase in MnSOD in the presence of Fe(3+)-NTA was greater under the condition of 20% O(2) than under the condition of 1% O(2).	Oxygen	91-95	superoxide dismutase 2	Homo sapiens	16-21
11159050-3	2001	In the current study, we investigated the role of reactive oxygen species (ROS) in the induction of TNF-alpha and MnSOD messenger RNAs (mRNAs) in human monocytes.	Reactive Oxygen Species	50-73	superoxide dismutase 2	Homo sapiens	114-119
11245424-5	2001	Complete sequencing of the nuclear MnSOD gene, which protects cells from the mitogenic and toxic effects of oxygen radicals, did not reveal any mutations.	Reactive Oxygen Species	108-123	superoxide dismutase 2	Homo sapiens	35-40
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	111-114	superoxide dismutase 2	Homo sapiens	68-73
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	111-114	superoxide dismutase 2	Homo sapiens	185-190
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	111-114	superoxide dismutase 2	Homo sapiens	185-190
11159050-3	2001	In the current study, we investigated the role of reactive oxygen species (ROS) in the induction of TNF-alpha and MnSOD messenger RNAs (mRNAs) in human monocytes.	Reactive Oxygen Species	75-78	superoxide dismutase 2	Homo sapiens	114-119
11159050-4	2001	Hypoxia (1% O2) inhibited the production of superoxide (O2-) and the induction of MnSOD, but not TNF-alpha, mRNA.	Superoxides	12-14	superoxide dismutase 2	Homo sapiens	82-87
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	31-34	superoxide dismutase 2	Homo sapiens	68-73
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	31-34	superoxide dismutase 2	Homo sapiens	185-190
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	31-34	superoxide dismutase 2	Homo sapiens	185-190
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	111-114	superoxide dismutase 2	Homo sapiens	68-73
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	111-114	superoxide dismutase 2	Homo sapiens	185-190
11159050-7	2001	These results suggest that (1) ROS is important in the induction of MnSOD, but not TNF-alpha, mRNA by LPS, (2) ROS from sources other than NADPH oxidase is involved in LPS induction of MnSOD mRNA, and (3) ROS-mediated LPS induction of MnSOD mRNA is independent of NF-kappaB activation.	Reactive Oxygen Species	111-114	superoxide dismutase 2	Homo sapiens	185-190
11243718-2	2001	Cyclosporine induced malondialdehyde formation and hydrogen peroxide production in mitochondria and attenuated the activity of MnSOD and glutathione peroxidase.	Cyclosporine	0-12	superoxide dismutase 2	Homo sapiens	127-132
11165870-6	2001	Isolated 4.6-fold overexpression of MnSOD activity in stably transfected fibroblasts led to specific resistance from UVA-mediated phototoxicity under selenium-deficient conditions.	Selenium	150-158	superoxide dismutase 2	Homo sapiens	36-41
11165872-9	2001	To further determine the specificity in MnSOD-induced gene regulation, MCF+SOD cells were stably transfected with an antisense MnSOD sequence whose expression was controlled by a tetracycline-inducible regulator.	Tetracycline	179-191	superoxide dismutase 2	Homo sapiens	40-45
11165872-9	2001	To further determine the specificity in MnSOD-induced gene regulation, MCF+SOD cells were stably transfected with an antisense MnSOD sequence whose expression was controlled by a tetracycline-inducible regulator.	Tetracycline	179-191	superoxide dismutase 2	Homo sapiens	127-132
11115408-1	2001	Manganese superoxide dismutase (MnSOD) serves a protective role under conditions of oxidative stress mediated by such diverse agents as adriamycin, radiation, chemical hypoxia and ischaemia and might act as a newly recognized type of tumour-suppressor.	Doxorubicin	136-146	superoxide dismutase 2	Homo sapiens	0-30
11115408-1	2001	Manganese superoxide dismutase (MnSOD) serves a protective role under conditions of oxidative stress mediated by such diverse agents as adriamycin, radiation, chemical hypoxia and ischaemia and might act as a newly recognized type of tumour-suppressor.	Doxorubicin	136-146	superoxide dismutase 2	Homo sapiens	32-37
11299047-11	2001	CONCLUSIONS: Ala(-9)Val substitution in the Mn-SOD gene was associated with DN in a Russian population	Alanine	13-16	superoxide dismutase 2	Homo sapiens	44-50
11299047-11	2001	CONCLUSIONS: Ala(-9)Val substitution in the Mn-SOD gene was associated with DN in a Russian population	Valine	20-23	superoxide dismutase 2	Homo sapiens	44-50
11785103-3	2001	Growth of resistance to DOX caused enhancement of antioxidant enzymes (Cu, Zn-SOD, Mn-SOD, catalase) elevation of Mn-SOD activity being predominant.	Doxorubicin	24-27	superoxide dismutase 2	Homo sapiens	83-89
11212499-4	2001	A transient increase in Mn-SOD activity was detected in cells arrested at the G1/S transition using two different techniques, suggesting that oxidative modulation of regulatory subunits by free radicals may modify cAMP binding sites during the cell cycle.	Cyclic AMP	214-218	superoxide dismutase 2	Homo sapiens	24-30
11785103-3	2001	Growth of resistance to DOX caused enhancement of antioxidant enzymes (Cu, Zn-SOD, Mn-SOD, catalase) elevation of Mn-SOD activity being predominant.	Doxorubicin	24-27	superoxide dismutase 2	Homo sapiens	114-120
11102640-4	2000	Malondialdehyde, a marker of lipid peroxidation, was three times higher than the control value and was accompanied by increased expression of superoxide dismutase 2 (Mn SOD).	Malondialdehyde	0-15	superoxide dismutase 2	Homo sapiens	166-172
11063906-0	2000	Mitochondrial or cytosolic catalase reverses the MnSOD-dependent inhibition of proliferation by enhancing respiratory chain activity, net ATP production, and decreasing the steady state levels of H(2)O(2).	Adenosine Triphosphate	138-141	superoxide dismutase 2	Homo sapiens	49-54
11090541-3	2000	Chemical signals released by a sublethal ischemic stress (such as NO, reactive oxygen species, and adenosine) trigger a complex cascade of signaling events that includes the activation of protein kinase C, Src protein tyrosine kinases, and nuclear factor kappaB and culminates in increased synthesis of inducible NO synthase, cyclooxygenase-2, aldose reductase, Mn superoxide dismutase, and probably other cardioprotective proteins.	Reactive Oxygen Species	70-93	superoxide dismutase 2	Homo sapiens	362-385
11090541-3	2000	Chemical signals released by a sublethal ischemic stress (such as NO, reactive oxygen species, and adenosine) trigger a complex cascade of signaling events that includes the activation of protein kinase C, Src protein tyrosine kinases, and nuclear factor kappaB and culminates in increased synthesis of inducible NO synthase, cyclooxygenase-2, aldose reductase, Mn superoxide dismutase, and probably other cardioprotective proteins.	Adenosine	99-108	superoxide dismutase 2	Homo sapiens	362-385
11063906-0	2000	Mitochondrial or cytosolic catalase reverses the MnSOD-dependent inhibition of proliferation by enhancing respiratory chain activity, net ATP production, and decreasing the steady state levels of H(2)O(2).	Water	196-201	superoxide dismutase 2	Homo sapiens	49-54
11063906-6	2000	In addition, mitochondrial or cytosolic catalase enhances respiration through complex I and II in both control and MnSOD overexpressing cell lines and reverses a MnSOD-dependent decrease in net ATP production.	Adenosine Triphosphate	194-197	superoxide dismutase 2	Homo sapiens	162-167
11053990-4	2000	The T/N ratio of Mn-SOD mRNA expression was less than 0.5 in 11 (32.4%) of 34 esophageal carcinoma cases without any preoperative treatments, while none of 11 cases who underwent preoperative chemotherapy showed a T/N ratio of <0.5 (p < 0.05).	Nitrogen	6-7	superoxide dismutase 2	Homo sapiens	17-23
10962437-9	2000	Our cell line experiments indicated that cells expressing high MnSOD levels were more resistant to apoptosis and showed lower proliferation when exposed to epirubicin in vitro.	Epirubicin	156-166	superoxide dismutase 2	Homo sapiens	63-68
11062559-4	2000	A single manganese ion is bound per germin monomer by ligands similar to those of manganese superoxide dismutase (MnSOD).	Manganese	9-18	superoxide dismutase 2	Homo sapiens	82-112
11062559-4	2000	A single manganese ion is bound per germin monomer by ligands similar to those of manganese superoxide dismutase (MnSOD).	Manganese	9-18	superoxide dismutase 2	Homo sapiens	114-119
10974411-6	2000	Interestingly, these cell lines showed cross-resistance to paclitaxel, cisplatin, and doxorubicin, suggesting that other factors such as HSP27 and Mn-SOD could be also involved in the mechanism of multidrug resistance in these cell lines.	Paclitaxel	59-69	superoxide dismutase 2	Homo sapiens	147-153
10974411-6	2000	Interestingly, these cell lines showed cross-resistance to paclitaxel, cisplatin, and doxorubicin, suggesting that other factors such as HSP27 and Mn-SOD could be also involved in the mechanism of multidrug resistance in these cell lines.	Doxorubicin	86-97	superoxide dismutase 2	Homo sapiens	147-153
10970696-0	2000	Suppression of manganese superoxide dismutase augments sensitivity to radiation, hyperthermia and doxorubicin in colon cancer cell lines by inducing apoptosis.	Doxorubicin	98-109	superoxide dismutase 2	Homo sapiens	15-45
10970696-3	2000	Suppression of Mn-SOD in HCT116 was accompanied by an increased sensitivity to radiation, hyperthermia and doxorubicin, as compared with findings in controls.	Doxorubicin	107-118	superoxide dismutase 2	Homo sapiens	15-21
10996156-0	2000	Methamphetamine toxicity is attenuated in mice that overexpress human manganese superoxide dismutase.	Methamphetamine	0-15	superoxide dismutase 2	Homo sapiens	70-100
11053990-4	2000	The T/N ratio of Mn-SOD mRNA expression was less than 0.5 in 11 (32.4%) of 34 esophageal carcinoma cases without any preoperative treatments, while none of 11 cases who underwent preoperative chemotherapy showed a T/N ratio of <0.5 (p < 0.05).	Nitrogen	26-27	superoxide dismutase 2	Homo sapiens	17-23
11053990-7	2000	Our results suggest that Mn-SOD mRNA was frequently reduced in esophageal carcinoma when compared to the normal mucosa and the reduced expression levels of Mn-SOD mRNA may lead to an accumulation of superoxide radicals in conjunction with the increased invasiveness of esophageal carcinoma.	Superoxides	199-209	superoxide dismutase 2	Homo sapiens	156-162
10996508-5	2000	Antioxidants and thiol reductants, such as N-acetylcysteine, and overexpression of manganese superoxide (MnSOD) can block or delay apoptosis.	manganese dioxide	83-103	superoxide dismutase 2	Homo sapiens	105-110
10924720-10	2000	The findings suggest that large changes in the SOD isoenzymes might occur in vascular diseases, significantly altering the susceptibility of the vascular wall to adverse effects of the superoxide radical.	Superoxides	185-195	superoxide dismutase 2	Homo sapiens	47-50
10924331-1	2000	Human MnSOD localizes to the mitochondria and plays a key protective role by detoxifying oxygen free radicals.	oxygen free radicals	89-109	superoxide dismutase 2	Homo sapiens	6-11
10962132-5	2000	Upregulation of Mn-SOD in the mitochondria in the course of the induction of i-NOS and, compared to the astrocytes, higher GSH levels in the microglial cells probably explain the resistance of the cultures against nitrosative stress.	Glutathione	123-126	superoxide dismutase 2	Homo sapiens	16-22
10962132-6	2000	Increased SOD-activities in the mitochondria could lower the superoxide concentration in this organelle and may prevent an oxidative and/or nitrosative damage via a decreased peroxynitrite formation.	Superoxides	61-71	superoxide dismutase 2	Homo sapiens	10-13
10962132-6	2000	Increased SOD-activities in the mitochondria could lower the superoxide concentration in this organelle and may prevent an oxidative and/or nitrosative damage via a decreased peroxynitrite formation.	Peroxynitrous Acid	175-188	superoxide dismutase 2	Homo sapiens	10-13
11001096-13	2000	We have directly observed the side chain of the active site Gln in Fe2+ SOD and Fe2+ (Mn)SOD by 15N NMR.	Glutamine	60-63	superoxide dismutase 2	Homo sapiens	89-92
10882843-2	2000	In the present study, we investigated the genetic association between a functional polymorphism (Ala-9Val) in the human manganese (Mn) SOD gene and schizophrenia or TD (192 schizophrenics: 39 with TD and 153 without TD; 141 controls).	ala-9val	97-105	superoxide dismutase 2	Homo sapiens	135-138
10882843-2	2000	In the present study, we investigated the genetic association between a functional polymorphism (Ala-9Val) in the human manganese (Mn) SOD gene and schizophrenia or TD (192 schizophrenics: 39 with TD and 153 without TD; 141 controls).	Manganese	120-129	superoxide dismutase 2	Homo sapiens	135-138
10882843-7	2000	In conjunction with previous findings of increased free radicals and decreased SOD activities in TD subjects, these results suggest that the -9Ala (high activity) MnSOD allele may play a role in protecting against susceptibility to TD in schizophrenics.	Free Radicals	51-64	superoxide dismutase 2	Homo sapiens	163-168
10919671-1	2000	Manganese-containing superoxide dismutase (MnSOD) is an essential primary antioxidant enzyme that converts superoxide radical to hydrogen peroxide and molecular oxygen within the mitochondrial matrix.	Superoxides	107-125	superoxide dismutase 2	Homo sapiens	0-41
10919671-1	2000	Manganese-containing superoxide dismutase (MnSOD) is an essential primary antioxidant enzyme that converts superoxide radical to hydrogen peroxide and molecular oxygen within the mitochondrial matrix.	Superoxides	107-125	superoxide dismutase 2	Homo sapiens	43-48
10919671-1	2000	Manganese-containing superoxide dismutase (MnSOD) is an essential primary antioxidant enzyme that converts superoxide radical to hydrogen peroxide and molecular oxygen within the mitochondrial matrix.	Hydrogen Peroxide	129-146	superoxide dismutase 2	Homo sapiens	0-41
10919671-1	2000	Manganese-containing superoxide dismutase (MnSOD) is an essential primary antioxidant enzyme that converts superoxide radical to hydrogen peroxide and molecular oxygen within the mitochondrial matrix.	Hydrogen Peroxide	129-146	superoxide dismutase 2	Homo sapiens	43-48
10919671-1	2000	Manganese-containing superoxide dismutase (MnSOD) is an essential primary antioxidant enzyme that converts superoxide radical to hydrogen peroxide and molecular oxygen within the mitochondrial matrix.	Oxygen	161-167	superoxide dismutase 2	Homo sapiens	0-41
10919671-1	2000	Manganese-containing superoxide dismutase (MnSOD) is an essential primary antioxidant enzyme that converts superoxide radical to hydrogen peroxide and molecular oxygen within the mitochondrial matrix.	Oxygen	161-167	superoxide dismutase 2	Homo sapiens	43-48
10919671-4	2000	According to the enzymatic reactions catalyzed by MnSOD and cytosolic GPX, change in the cellular redox status, especially change attributable to accumulation of hydrogen peroxide or other hydroperoxides, is a possible reason to explain the suppression of tumor growth observed in MnSOD-overexpressing cells.	Hydrogen Peroxide	162-179	superoxide dismutase 2	Homo sapiens	50-55
10919671-4	2000	According to the enzymatic reactions catalyzed by MnSOD and cytosolic GPX, change in the cellular redox status, especially change attributable to accumulation of hydrogen peroxide or other hydroperoxides, is a possible reason to explain the suppression of tumor growth observed in MnSOD-overexpressing cells.	Hydrogen Peroxide	162-179	superoxide dismutase 2	Homo sapiens	281-286
10919671-4	2000	According to the enzymatic reactions catalyzed by MnSOD and cytosolic GPX, change in the cellular redox status, especially change attributable to accumulation of hydrogen peroxide or other hydroperoxides, is a possible reason to explain the suppression of tumor growth observed in MnSOD-overexpressing cells.	Hydrogen Peroxide	189-203	superoxide dismutase 2	Homo sapiens	50-55
10919671-4	2000	According to the enzymatic reactions catalyzed by MnSOD and cytosolic GPX, change in the cellular redox status, especially change attributable to accumulation of hydrogen peroxide or other hydroperoxides, is a possible reason to explain the suppression of tumor growth observed in MnSOD-overexpressing cells.	Hydrogen Peroxide	189-203	superoxide dismutase 2	Homo sapiens	281-286
10919671-8	2000	These results suggest that hydrogen peroxide or other hydroperoxides appear to be key reactants in the tumor suppression by MnSOD overexpression, and growth inhibition correlates with the intracellular redox status.	Hydrogen Peroxide	27-44	superoxide dismutase 2	Homo sapiens	124-129
10919671-8	2000	These results suggest that hydrogen peroxide or other hydroperoxides appear to be key reactants in the tumor suppression by MnSOD overexpression, and growth inhibition correlates with the intracellular redox status.	Hydrogen Peroxide	54-68	superoxide dismutase 2	Homo sapiens	124-129
10919671-9	2000	This work suggests that manipulations that inhibit peroxide removal should enhance the tumor suppressive effect of MnSOD overexpression.	Peroxides	51-59	superoxide dismutase 2	Homo sapiens	115-120
11001096-8	2000	We have generated a mutant of MnSOD with the active site Gln in the location characteristic of Fe-specific SODs.	Glutamine	57-60	superoxide dismutase 2	Homo sapiens	30-35
11001096-8	2000	We have generated a mutant of MnSOD with the active site Gln in the location characteristic of Fe-specific SODs.	Iron	95-97	superoxide dismutase 2	Homo sapiens	30-35
11001096-9	2000	The active site is similar to that of MnSOD when Mn2+, Fe3+ or Fe2+ are bound, based on EPR and NMR spectroscopy.	Manganese(2+)	49-53	superoxide dismutase 2	Homo sapiens	38-43
11001096-9	2000	The active site is similar to that of MnSOD when Mn2+, Fe3+ or Fe2+ are bound, based on EPR and NMR spectroscopy.	ferric sulfate	55-59	superoxide dismutase 2	Homo sapiens	38-43
11001096-9	2000	The active site is similar to that of MnSOD when Mn2+, Fe3+ or Fe2+ are bound, based on EPR and NMR spectroscopy.	ammonium ferrous sulfate	63-67	superoxide dismutase 2	Homo sapiens	38-43
11001096-10	2000	However, the mutant"s Fe-supported activity is at least 7% that of FeSOD, in contrast to Fe(Mn)SOD, which has 0% of FeSOD"s activity.	Iron	22-24	superoxide dismutase 2	Homo sapiens	69-72
11001096-11	2000	Thus, moving the active site Gln converts Mn-specific SOD into a cambialistic SOD and the Gln proves to be important but not the sole determinant of metal-ion specificity.	Glutamine	29-32	superoxide dismutase 2	Homo sapiens	54-57
11001096-11	2000	Thus, moving the active site Gln converts Mn-specific SOD into a cambialistic SOD and the Gln proves to be important but not the sole determinant of metal-ion specificity.	Glutamine	29-32	superoxide dismutase 2	Homo sapiens	78-81
11001096-11	2000	Thus, moving the active site Gln converts Mn-specific SOD into a cambialistic SOD and the Gln proves to be important but not the sole determinant of metal-ion specificity.	Glutamine	90-93	superoxide dismutase 2	Homo sapiens	54-57
11001096-11	2000	Thus, moving the active site Gln converts Mn-specific SOD into a cambialistic SOD and the Gln proves to be important but not the sole determinant of metal-ion specificity.	Metals	149-154	superoxide dismutase 2	Homo sapiens	54-57
11001096-11	2000	Thus, moving the active site Gln converts Mn-specific SOD into a cambialistic SOD and the Gln proves to be important but not the sole determinant of metal-ion specificity.	Metals	149-154	superoxide dismutase 2	Homo sapiens	78-81
11001096-12	2000	Indeed, subtle differences in the spectra of Mn2+, Fe3+ and 1H in the presence of Fe2+ distinguish the G77Q, Q146A mut-(Mn)SOD from WT (Mn)SOD, and may prove to be correlated with metal ion activity.	Manganese(2+)	45-49	superoxide dismutase 2	Homo sapiens	123-126
11001096-12	2000	Indeed, subtle differences in the spectra of Mn2+, Fe3+ and 1H in the presence of Fe2+ distinguish the G77Q, Q146A mut-(Mn)SOD from WT (Mn)SOD, and may prove to be correlated with metal ion activity.	ferric sulfate	51-55	superoxide dismutase 2	Homo sapiens	123-126
11001096-13	2000	We have directly observed the side chain of the active site Gln in Fe2+ SOD and Fe2+ (Mn)SOD by 15N NMR.	15n	96-99	superoxide dismutase 2	Homo sapiens	72-75
11001096-12	2000	Indeed, subtle differences in the spectra of Mn2+, Fe3+ and 1H in the presence of Fe2+ distinguish the G77Q, Q146A mut-(Mn)SOD from WT (Mn)SOD, and may prove to be correlated with metal ion activity.	Hydrogen	60-62	superoxide dismutase 2	Homo sapiens	123-126
11001096-12	2000	Indeed, subtle differences in the spectra of Mn2+, Fe3+ and 1H in the presence of Fe2+ distinguish the G77Q, Q146A mut-(Mn)SOD from WT (Mn)SOD, and may prove to be correlated with metal ion activity.	Hydrogen	60-62	superoxide dismutase 2	Homo sapiens	139-142
11001096-12	2000	Indeed, subtle differences in the spectra of Mn2+, Fe3+ and 1H in the presence of Fe2+ distinguish the G77Q, Q146A mut-(Mn)SOD from WT (Mn)SOD, and may prove to be correlated with metal ion activity.	ammonium ferrous sulfate	82-86	superoxide dismutase 2	Homo sapiens	123-126
11001096-12	2000	Indeed, subtle differences in the spectra of Mn2+, Fe3+ and 1H in the presence of Fe2+ distinguish the G77Q, Q146A mut-(Mn)SOD from WT (Mn)SOD, and may prove to be correlated with metal ion activity.	ammonium ferrous sulfate	82-86	superoxide dismutase 2	Homo sapiens	139-142
11001096-13	2000	We have directly observed the side chain of the active site Gln in Fe2+ SOD and Fe2+ (Mn)SOD by 15N NMR.	15n	96-99	superoxide dismutase 2	Homo sapiens	89-92
11001096-12	2000	Indeed, subtle differences in the spectra of Mn2+, Fe3+ and 1H in the presence of Fe2+ distinguish the G77Q, Q146A mut-(Mn)SOD from WT (Mn)SOD, and may prove to be correlated with metal ion activity.	Metals	180-185	superoxide dismutase 2	Homo sapiens	123-126
11001096-13	2000	We have directly observed the side chain of the active site Gln in Fe2+ SOD and Fe2+ (Mn)SOD by 15N NMR.	Glutamine	60-63	superoxide dismutase 2	Homo sapiens	72-75
11001096-15	2000	Since a shorter distance from Gln to Fe and stronger interaction with Fe correlate with a lower Em in Fe(Mn)SOD, Gln has the effect of destabilizing additional electron density on the metal ion.	Glutamine	30-33	superoxide dismutase 2	Homo sapiens	108-111
11001096-15	2000	Since a shorter distance from Gln to Fe and stronger interaction with Fe correlate with a lower Em in Fe(Mn)SOD, Gln has the effect of destabilizing additional electron density on the metal ion.	Iron	37-39	superoxide dismutase 2	Homo sapiens	108-111
11001096-15	2000	Since a shorter distance from Gln to Fe and stronger interaction with Fe correlate with a lower Em in Fe(Mn)SOD, Gln has the effect of destabilizing additional electron density on the metal ion.	Iron	70-72	superoxide dismutase 2	Homo sapiens	108-111
11001096-15	2000	Since a shorter distance from Gln to Fe and stronger interaction with Fe correlate with a lower Em in Fe(Mn)SOD, Gln has the effect of destabilizing additional electron density on the metal ion.	Glutamine	113-116	superoxide dismutase 2	Homo sapiens	108-111
11001096-15	2000	Since a shorter distance from Gln to Fe and stronger interaction with Fe correlate with a lower Em in Fe(Mn)SOD, Gln has the effect of destabilizing additional electron density on the metal ion.	Metals	184-189	superoxide dismutase 2	Homo sapiens	108-111
10889449-0	2000	Oxygen free radicals mediate the induction of manganese superoxide dismutase gene expression by TNF-alpha.	oxygen free radicals	0-20	superoxide dismutase 2	Homo sapiens	46-76
10892348-9	2000	SODs, particularly MnSOD, play an important role in defending DNA from reactive oxygen species.	Reactive Oxygen Species	71-94	superoxide dismutase 2	Homo sapiens	19-24
10852710-0	2000	Multiple replacements of glutamine 143 in human manganese superoxide dismutase: effects on structure, stability, and catalysis.	Glutamine	25-34	superoxide dismutase 2	Homo sapiens	48-78
10852710-1	2000	Glutamine 143 in human manganese superoxide dismutase (MnSOD) forms a hydrogen bond with the manganese-bound solvent molecule and is investigated by replacement using site-specific mutagenesis.	Glutamine	0-9	superoxide dismutase 2	Homo sapiens	23-53
10852710-1	2000	Glutamine 143 in human manganese superoxide dismutase (MnSOD) forms a hydrogen bond with the manganese-bound solvent molecule and is investigated by replacement using site-specific mutagenesis.	Glutamine	0-9	superoxide dismutase 2	Homo sapiens	55-60
10852710-1	2000	Glutamine 143 in human manganese superoxide dismutase (MnSOD) forms a hydrogen bond with the manganese-bound solvent molecule and is investigated by replacement using site-specific mutagenesis.	Hydrogen	70-78	superoxide dismutase 2	Homo sapiens	23-53
10852710-1	2000	Glutamine 143 in human manganese superoxide dismutase (MnSOD) forms a hydrogen bond with the manganese-bound solvent molecule and is investigated by replacement using site-specific mutagenesis.	Hydrogen	70-78	superoxide dismutase 2	Homo sapiens	55-60
10852710-1	2000	Glutamine 143 in human manganese superoxide dismutase (MnSOD) forms a hydrogen bond with the manganese-bound solvent molecule and is investigated by replacement using site-specific mutagenesis.	Manganese	23-32	superoxide dismutase 2	Homo sapiens	55-60
10852710-3	2000	Two new water molecules in Q143A MnSOD were situated in positions nearly identical with the Oepsilon1 and Nepsilon2 of the replaced Gln 143 side chain and maintained a hydrogen-bonded network connecting the manganese-bound solvent molecule to other residues in the active site.	Water	8-13	superoxide dismutase 2	Homo sapiens	33-38
10852710-3	2000	Two new water molecules in Q143A MnSOD were situated in positions nearly identical with the Oepsilon1 and Nepsilon2 of the replaced Gln 143 side chain and maintained a hydrogen-bonded network connecting the manganese-bound solvent molecule to other residues in the active site.	Glutamine	132-135	superoxide dismutase 2	Homo sapiens	33-38
10852710-3	2000	Two new water molecules in Q143A MnSOD were situated in positions nearly identical with the Oepsilon1 and Nepsilon2 of the replaced Gln 143 side chain and maintained a hydrogen-bonded network connecting the manganese-bound solvent molecule to other residues in the active site.	Hydrogen	168-176	superoxide dismutase 2	Homo sapiens	33-38
10852710-3	2000	Two new water molecules in Q143A MnSOD were situated in positions nearly identical with the Oepsilon1 and Nepsilon2 of the replaced Gln 143 side chain and maintained a hydrogen-bonded network connecting the manganese-bound solvent molecule to other residues in the active site.	Manganese	207-216	superoxide dismutase 2	Homo sapiens	33-38
10852710-5	2000	The mutant Q143A MnSOD and other mutants at position 143 showed very low levels of product inhibition and favored Mn(II)SOD in the resting state, whereas the wild type showed strong product inhibition and favored Mn(III)SOD.	manganese(III) acetate dihydrate	213-220	superoxide dismutase 2	Homo sapiens	17-22
10851038-6	2000	The reaction is not sensitive to high concentrations of cyanide, which allows the separate determination of Cu,Zn- and Mn-SOD in mixtures.	Cyanides	56-63	superoxide dismutase 2	Homo sapiens	119-125
10889449-3	2000	In the presence of the oxygen free radical spin trapping reagent, 5,5-dimethyl pyrroline-N-oxide (DMPO), the induction of MnSOD gene expression by TNF-alpha was significantly reduced.	Oxygen	23-29	superoxide dismutase 2	Homo sapiens	122-127
10889449-3	2000	In the presence of the oxygen free radical spin trapping reagent, 5,5-dimethyl pyrroline-N-oxide (DMPO), the induction of MnSOD gene expression by TNF-alpha was significantly reduced.	5,5-dimethyl-pyrroline N-oxide	66-96	superoxide dismutase 2	Homo sapiens	122-127
10889449-3	2000	In the presence of the oxygen free radical spin trapping reagent, 5,5-dimethyl pyrroline-N-oxide (DMPO), the induction of MnSOD gene expression by TNF-alpha was significantly reduced.	5,5-dimethyl-pyrroline N-oxide	98-102	superoxide dismutase 2	Homo sapiens	122-127
10889449-5	2000	Taken together, these observations suggest that the induction of MnSOD expression by TNF-alpha is at least partially mediated by intracellular formation of oxygen free radicals, and that superoxide is most likely the initiating species involved in the mediation of MnSOD gene expression by TNF-alpha.	oxygen free radicals	156-176	superoxide dismutase 2	Homo sapiens	65-70
10889449-5	2000	Taken together, these observations suggest that the induction of MnSOD expression by TNF-alpha is at least partially mediated by intracellular formation of oxygen free radicals, and that superoxide is most likely the initiating species involved in the mediation of MnSOD gene expression by TNF-alpha.	Superoxides	187-197	superoxide dismutase 2	Homo sapiens	265-270
10653605-4	2000	In the current study, we determined the effects of PTK inhibitors, genistein and herbimycin A, on the induction of MnSOD and TNFalpha in human monocytes.	Genistein	67-76	superoxide dismutase 2	Homo sapiens	115-120
10762167-0	2000	Nitration of manganese superoxide dismutase in cerebrospinal fluids is a marker for peroxynitrite-mediated oxidative stress in neurodegenerative diseases.	Peroxynitrous Acid	84-97	superoxide dismutase 2	Homo sapiens	13-43
10762167-3	2000	Nitrated tyrosine residue-containing protein was observed in the cerebrospinal fluid and was concluded to be manganese superoxide dismutase (Mn-SOD).	Tyrosine	9-17	superoxide dismutase 2	Homo sapiens	109-139
10762167-3	2000	Nitrated tyrosine residue-containing protein was observed in the cerebrospinal fluid and was concluded to be manganese superoxide dismutase (Mn-SOD).	Tyrosine	9-17	superoxide dismutase 2	Homo sapiens	141-147
10702810-10	2000	During ATRA exposure, MnSOD was induced in the sensitive cell line, but not until after 72 h. Buthionine sulfoximine significantly increased the inhibitory effect of ATRA on colony formation in both cell lines, but only marginally enhanced the effect of ATRA on the induction of apoptosis.	Tretinoin	7-11	superoxide dismutase 2	Homo sapiens	22-27
10702810-10	2000	During ATRA exposure, MnSOD was induced in the sensitive cell line, but not until after 72 h. Buthionine sulfoximine significantly increased the inhibitory effect of ATRA on colony formation in both cell lines, but only marginally enhanced the effect of ATRA on the induction of apoptosis.	Buthionine Sulfoximine	94-116	superoxide dismutase 2	Homo sapiens	22-27
10702810-10	2000	During ATRA exposure, MnSOD was induced in the sensitive cell line, but not until after 72 h. Buthionine sulfoximine significantly increased the inhibitory effect of ATRA on colony formation in both cell lines, but only marginally enhanced the effect of ATRA on the induction of apoptosis.	Tretinoin	166-170	superoxide dismutase 2	Homo sapiens	22-27
10702810-10	2000	During ATRA exposure, MnSOD was induced in the sensitive cell line, but not until after 72 h. Buthionine sulfoximine significantly increased the inhibitory effect of ATRA on colony formation in both cell lines, but only marginally enhanced the effect of ATRA on the induction of apoptosis.	Tretinoin	166-170	superoxide dismutase 2	Homo sapiens	22-27
10653605-1	2000	A mutant Escherichia coli lipopolysaccharide (LPS) lacking myristoyl fatty acid markedly stimulates the activity of manganese superoxide dismutase (MnSOD) without inducing tumor necrosis factor alpha (TNFalpha) production by human monocytes (Tian et al., 1998, Am J Physiol 275:C740.	myristoyl fatty acid	59-79	superoxide dismutase 2	Homo sapiens	148-153
10749746-3	2000	We investigated the levels of manganese superoxide dismutase (Mn SOD), its inducibility, and its protective role against tumor necrosis factor-alpha and cytotoxic drugs (cisplatin, epirubicin, methotrexate, and vindesin) in human pleural mesothelioma (M14K) and pulmonary adenocarcinoma (A549) cells.	Cisplatin	170-179	superoxide dismutase 2	Homo sapiens	30-60
10749746-3	2000	We investigated the levels of manganese superoxide dismutase (Mn SOD), its inducibility, and its protective role against tumor necrosis factor-alpha and cytotoxic drugs (cisplatin, epirubicin, methotrexate, and vindesin) in human pleural mesothelioma (M14K) and pulmonary adenocarcinoma (A549) cells.	Epirubicin	181-191	superoxide dismutase 2	Homo sapiens	30-60
10759716-0	2000	Induction of mitochondrial manganese superoxide dismutase confers resistance to apoptosis in acute myeloblastic leukaemia cells exposed to etoposide.	Etoposide	139-148	superoxide dismutase 2	Homo sapiens	27-57
10759716-6	2000	Etoposide caused a potent induction of MnSOD, more than 400% at 12 h, in the ER but not in the ES subclone.	Etoposide	0-9	superoxide dismutase 2	Homo sapiens	39-44
10759716-8	2000	In conclusion, we suggest that MnSOD might have a special role in the protection of AML cells against etoposide-induced cell death.	Etoposide	102-111	superoxide dismutase 2	Homo sapiens	31-36
10653605-4	2000	In the current study, we determined the effects of PTK inhibitors, genistein and herbimycin A, on the induction of MnSOD and TNFalpha in human monocytes.	herbimycin	81-93	superoxide dismutase 2	Homo sapiens	115-120
10653605-7	2000	In addition, inhibition of NFkappaB activation by gliotoxin and pyrrodiline dithiocarbamate, inhibited LPS induction of TNFalpha and MnSOD mRNAs.	pyrrodiline dithiocarbamate	64-91	superoxide dismutase 2	Homo sapiens	133-138
10692109-1	2000	On the basis of our recent observation that copper, zinc-superoxide dismutase and manganese-superoxide dismutase change differently following a single exposure to ultraviolet-B irradiation in the human keratinocyte cell line HaCaT, we have examined the possible role of endogenous copper,zinc-superoxide dismutase or manganese-superoxide dismutase against ultraviolet-B-induced reactive-oxygen- species-mediated keratinocyte injury in vitro.	Copper	44-50	superoxide dismutase 2	Homo sapiens	317-347
10692109-2	2000	To evaluate the individual defensive roles of copper, zinc-superoxide dismutase and manganese-super-oxide dismutase, we treated HaCaT cells with diethyldithiocarbamate, a chelating agent of ionic copper that inactivates copper,zinc-superoxide dismutase activities, tumor necrosis factor alpha, which enhances manganese-superoxide dismutase levels, or transforming growth factor beta1, which inhibits manganese-superoxide dismutase levels.	Ditiocarb	145-167	superoxide dismutase 2	Homo sapiens	84-115
10692109-2	2000	To evaluate the individual defensive roles of copper, zinc-superoxide dismutase and manganese-super-oxide dismutase, we treated HaCaT cells with diethyldithiocarbamate, a chelating agent of ionic copper that inactivates copper,zinc-superoxide dismutase activities, tumor necrosis factor alpha, which enhances manganese-superoxide dismutase levels, or transforming growth factor beta1, which inhibits manganese-superoxide dismutase levels.	Ditiocarb	145-167	superoxide dismutase 2	Homo sapiens	309-339
10644478-1	2000	BACKGROUND: Manganese superoxide dismutase (MnSOD) catalyzes the scavenging of superoxide radicals in order to protect cells from the damage caused by reactive oxygen species.	Superoxides	22-32	superoxide dismutase 2	Homo sapiens	44-49
10774745-8	2000	Taken together, these results strongly suggest that increases in levels of metallothionein, glutathione S-transferase, Cu,Zn-SOD and Mn-SOD play important roles in protective mechanisms against toxicity of PQ or ROS in AML cells.	Paraquat	206-208	superoxide dismutase 2	Homo sapiens	133-139
10774745-8	2000	Taken together, these results strongly suggest that increases in levels of metallothionein, glutathione S-transferase, Cu,Zn-SOD and Mn-SOD play important roles in protective mechanisms against toxicity of PQ or ROS in AML cells.	Reactive Oxygen Species	212-215	superoxide dismutase 2	Homo sapiens	133-139
10644478-1	2000	BACKGROUND: Manganese superoxide dismutase (MnSOD) catalyzes the scavenging of superoxide radicals in order to protect cells from the damage caused by reactive oxygen species.	Reactive Oxygen Species	151-174	superoxide dismutase 2	Homo sapiens	12-42
10644478-1	2000	BACKGROUND: Manganese superoxide dismutase (MnSOD) catalyzes the scavenging of superoxide radicals in order to protect cells from the damage caused by reactive oxygen species.	Reactive Oxygen Species	151-174	superoxide dismutase 2	Homo sapiens	44-49
11281288-8	2000	MnSOD mRNA levels were markedly increased after 24 h of exposure to ChOx, suggesting associated induction of mitochondrial protection repair or turnover.	chox	68-72	superoxide dismutase 2	Homo sapiens	0-5
10601319-0	1999	Transcriptional activation of the human manganese superoxide dismutase gene mediated by tetradecanoylphorbol acetate.	Tetradecanoylphorbol Acetate	88-116	superoxide dismutase 2	Homo sapiens	40-70
10601319-1	1999	Transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA induced by a phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), was examined to identify the responsive transcriptional regulator.	Tetradecanoylphorbol Acetate	108-144	superoxide dismutase 2	Homo sapiens	68-73
10656287-6	2000	Moreover, analyses of oxidative stress markers showed that treatment with BA, ACLA, and DOX lead to a decrease in reduced glutathione and antioxidant enzymes (glutathione peroxidase [GPx], glutathione reductase [GRase], CuZn superoxide dismutase [SOD], and catalase [CAT]).	Butyric Acid	74-76	superoxide dismutase 2	Homo sapiens	247-250
10656287-6	2000	Moreover, analyses of oxidative stress markers showed that treatment with BA, ACLA, and DOX lead to a decrease in reduced glutathione and antioxidant enzymes (glutathione peroxidase [GPx], glutathione reductase [GRase], CuZn superoxide dismutase [SOD], and catalase [CAT]).	Aclarubicin	78-82	superoxide dismutase 2	Homo sapiens	247-250
10656287-6	2000	Moreover, analyses of oxidative stress markers showed that treatment with BA, ACLA, and DOX lead to a decrease in reduced glutathione and antioxidant enzymes (glutathione peroxidase [GPx], glutathione reductase [GRase], CuZn superoxide dismutase [SOD], and catalase [CAT]).	Doxorubicin	88-91	superoxide dismutase 2	Homo sapiens	247-250
10656287-7	2000	In addition, DOX increased thiobarbituric acid reactants (TBARs), and MnSOD activity was decreased by BA and DOX.	Doxorubicin	109-112	superoxide dismutase 2	Homo sapiens	70-75
11521054-3	2000	In the current study, we demonstrated that E5531, while having no effect on TNF-alpha and MnSOD mRNAs by itself, markedly inhibited LPS- and lipid A-, but not TNF-alpha-, induced increases in TNF-alpha and MnSOD mRNAs in human monocytes.	Lipid A	141-148	superoxide dismutase 2	Homo sapiens	206-211
10963624-6	2000	A number of molecular epidemiologic studies have been conducted to evaluate associations between polymorphic genes involved in steroid hormone metabolism (i.e., CYP17, COMT, CYP1A1, CYP19, GST, and MnSOD) that may account for a proportion of enzymatic variability, and results are discussed in this review.	Steroids	127-142	superoxide dismutase 2	Homo sapiens	198-203
10601319-1	1999	Transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA induced by a phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), was examined to identify the responsive transcriptional regulator.	Tetradecanoylphorbol Acetate	146-149	superoxide dismutase 2	Homo sapiens	36-66
10601319-1	1999	Transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA induced by a phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), was examined to identify the responsive transcriptional regulator.	Tetradecanoylphorbol Acetate	146-149	superoxide dismutase 2	Homo sapiens	68-73
10601319-1	1999	Transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA induced by a phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), was examined to identify the responsive transcriptional regulator.	Phorbol Esters	93-106	superoxide dismutase 2	Homo sapiens	36-66
10601319-4	1999	The region between -1292 and -1202 contains a cAMP-responsive element-like sequence, TGACGTCT, which we identified as the manganese superoxide dismutase TPA-responsive element, MSTRE.	Cyclic AMP	46-50	superoxide dismutase 2	Homo sapiens	122-152
10601319-4	1999	The region between -1292 and -1202 contains a cAMP-responsive element-like sequence, TGACGTCT, which we identified as the manganese superoxide dismutase TPA-responsive element, MSTRE.	Tetradecanoylphorbol Acetate	153-156	superoxide dismutase 2	Homo sapiens	122-152
10601319-1	1999	Transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA induced by a phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), was examined to identify the responsive transcriptional regulator.	Phorbol Esters	93-106	superoxide dismutase 2	Homo sapiens	68-73
10601319-8	1999	These results led us to conclude that the human MnSOD gene having the promoter construct used in this study is induced by TPA via activation of a CREB-1/ATF-1-like factor and not via either NF-kappaB or AP-1.	Tetradecanoylphorbol Acetate	122-125	superoxide dismutase 2	Homo sapiens	48-53
10601319-1	1999	Transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA induced by a phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), was examined to identify the responsive transcriptional regulator.	Tetradecanoylphorbol Acetate	108-144	superoxide dismutase 2	Homo sapiens	36-66
10626823-1	1999	Two polymorphic variants of manganese superoxide dismutase (MnSOD), with either Ile or Thr at amino acid 58, (Ile58MnSOD or Thr58MnSOD), have been found in the human population.	thr58mnsod	124-134	superoxide dismutase 2	Homo sapiens	60-65
10626823-1	1999	Two polymorphic variants of manganese superoxide dismutase (MnSOD), with either Ile or Thr at amino acid 58, (Ile58MnSOD or Thr58MnSOD), have been found in the human population.	Isoleucine	80-83	superoxide dismutase 2	Homo sapiens	28-58
10626823-7	1999	However, far more Thrs58MnSOD protein was required to obtain the same amount of MnSOD activity, making the Thr58MnSOD far less effective.	thr58mnsod	107-117	superoxide dismutase 2	Homo sapiens	24-29
10626823-1	1999	Two polymorphic variants of manganese superoxide dismutase (MnSOD), with either Ile or Thr at amino acid 58, (Ile58MnSOD or Thr58MnSOD), have been found in the human population.	Isoleucine	80-83	superoxide dismutase 2	Homo sapiens	60-65
10626823-1	1999	Two polymorphic variants of manganese superoxide dismutase (MnSOD), with either Ile or Thr at amino acid 58, (Ile58MnSOD or Thr58MnSOD), have been found in the human population.	Threonine	87-90	superoxide dismutase 2	Homo sapiens	28-58
10626823-1	1999	Two polymorphic variants of manganese superoxide dismutase (MnSOD), with either Ile or Thr at amino acid 58, (Ile58MnSOD or Thr58MnSOD), have been found in the human population.	Threonine	87-90	superoxide dismutase 2	Homo sapiens	60-65
10694037-6	1999	This was supported by the absence of changes in plants treated with Cd in the Mn-SOD activity, responsible for O2*- removal in the peroxisomal matrix.	Cadmium	68-70	superoxide dismutase 2	Homo sapiens	78-84
10626823-1	1999	Two polymorphic variants of manganese superoxide dismutase (MnSOD), with either Ile or Thr at amino acid 58, (Ile58MnSOD or Thr58MnSOD), have been found in the human population.	thr58mnsod	124-134	superoxide dismutase 2	Homo sapiens	28-58
10694037-6	1999	This was supported by the absence of changes in plants treated with Cd in the Mn-SOD activity, responsible for O2*- removal in the peroxisomal matrix.	Oxygen	111-115	superoxide dismutase 2	Homo sapiens	78-84
10644010-5	1999	Our results show a 20-50% increase in both SOD activities when cells were exposed to TNF or to an oxidative stress produced by Paraquat (a generator of superoxide anion radicals), both in terms of enzymes activity (zymogram) and protein levels (Western blotting and ELISA).	Paraquat	127-135	superoxide dismutase 2	Homo sapiens	43-46
10644010-5	1999	Our results show a 20-50% increase in both SOD activities when cells were exposed to TNF or to an oxidative stress produced by Paraquat (a generator of superoxide anion radicals), both in terms of enzymes activity (zymogram) and protein levels (Western blotting and ELISA).	Superoxides	152-177	superoxide dismutase 2	Homo sapiens	43-46
10644010-8	1999	In contrast, the addition of a SOD mimetic (MnTMPyP) completely inhibited Paraquat-stimulated ICAM-1 expression in melanoma cells and significantly decreased it in HUVEC (50%).	Paraquat	74-82	superoxide dismutase 2	Homo sapiens	31-34
10521117-7	1999	RESULT(S): In the follicular stage, Mn-SOD immunoreactivity was detected in granulosa and theca interna cells of steroid-producing follicles, that is, preantral, nondominant, dominant, and atretic follicles, whereas Cu,Zn-SOD was detected in theca interna cells of these follicles and in granulosa cells of dominant follicles.	Steroids	113-120	superoxide dismutase 2	Homo sapiens	36-42
10529750-1	1999	An alanin-9valin (Ala-9Val) polymorphism in the mitochondrial targeting sequence of manganese-containing superoxide dismutase (Mn-SOD) has recently been described.	alanin-9valin	3-16	superoxide dismutase 2	Homo sapiens	84-125
10529750-1	1999	An alanin-9valin (Ala-9Val) polymorphism in the mitochondrial targeting sequence of manganese-containing superoxide dismutase (Mn-SOD) has recently been described.	alanin-9valin	3-16	superoxide dismutase 2	Homo sapiens	127-133
10529750-1	1999	An alanin-9valin (Ala-9Val) polymorphism in the mitochondrial targeting sequence of manganese-containing superoxide dismutase (Mn-SOD) has recently been described.	ala-9val	18-26	superoxide dismutase 2	Homo sapiens	84-125
10529750-1	1999	An alanin-9valin (Ala-9Val) polymorphism in the mitochondrial targeting sequence of manganese-containing superoxide dismutase (Mn-SOD) has recently been described.	ala-9val	18-26	superoxide dismutase 2	Homo sapiens	127-133
10529750-7	1999	The results suggest that mutations influencing the cellular allocation of Mn-SOD may be a risk factor in MND, especially in females, and that MND may be a disease of misdistribution of the superoxide dismutase enzymes.	Superoxides	189-199	superoxide dismutase 2	Homo sapiens	74-80
10521117-9	1999	In the early degenerating corpus luteum, both Mn-SOD and Cu,Zn-SOD were positive in steroid-producing luteinized theca cells.	Steroids	84-91	superoxide dismutase 2	Homo sapiens	46-52
10765000-1	1999	To investigate whether the two free-radical scavengers, Cu, Zn- and Mn-superoxide dismutase (SOD), are changed in leukocytes of diabetic patients, and the alteration of these enzymes correlates with the diabetic state, we measured the activity and concentration of these enzymes in leukocytes from diabetic patients.	Free Radicals	31-43	superoxide dismutase 2	Homo sapiens	93-96
10509755-5	1999	Manganese (Mn) SOD activity was increased when HepG2 cells were treated for 1 day with 0.50 or 0.75 mM clofibric acid.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	15-18
10509755-5	1999	Manganese (Mn) SOD activity was increased when HepG2 cells were treated for 1 day with 0.50 or 0.75 mM clofibric acid.	Clofibric Acid	103-117	superoxide dismutase 2	Homo sapiens	15-18
10509755-7	1999	For a 5-day treatment, total SOD and MnSOD activities as well as the enzyme apoprotein and MnSOD mRNA levels increased whatever the clofibric acid concentration used.	Clofibric Acid	132-146	superoxide dismutase 2	Homo sapiens	91-96
10512624-0	1999	Role of tryptophan 161 in catalysis by human manganese superoxide dismutase.	Tryptophan	8-18	superoxide dismutase 2	Homo sapiens	45-75
10512624-1	1999	Tryptophan 161 is a highly conserved residue that forms a hydrophobic side of the active site cavity of manganese superoxide dismutase (MnSOD), with its indole ring adjacent to and about 5 A from the manganese.	Tryptophan	0-10	superoxide dismutase 2	Homo sapiens	104-134
10512624-1	1999	Tryptophan 161 is a highly conserved residue that forms a hydrophobic side of the active site cavity of manganese superoxide dismutase (MnSOD), with its indole ring adjacent to and about 5 A from the manganese.	Tryptophan	0-10	superoxide dismutase 2	Homo sapiens	136-141
10512624-1	1999	Tryptophan 161 is a highly conserved residue that forms a hydrophobic side of the active site cavity of manganese superoxide dismutase (MnSOD), with its indole ring adjacent to and about 5 A from the manganese.	Manganese	104-113	superoxide dismutase 2	Homo sapiens	136-141
10512624-2	1999	We have made a mutant containing the conservative replacement Trp 161 --> Phe in human MnSOD (W161F MnSOD), determined its crystal structure, and measured the catalysis of the resulting mutant using pulse radiolysis to produce O(2)(*)(-).	Tryptophan	62-65	superoxide dismutase 2	Homo sapiens	90-95
10512624-2	1999	We have made a mutant containing the conservative replacement Trp 161 --> Phe in human MnSOD (W161F MnSOD), determined its crystal structure, and measured the catalysis of the resulting mutant using pulse radiolysis to produce O(2)(*)(-).	Tryptophan	62-65	superoxide dismutase 2	Homo sapiens	103-108
10512624-2	1999	We have made a mutant containing the conservative replacement Trp 161 --> Phe in human MnSOD (W161F MnSOD), determined its crystal structure, and measured the catalysis of the resulting mutant using pulse radiolysis to produce O(2)(*)(-).	Phenylalanine	77-80	superoxide dismutase 2	Homo sapiens	90-95
10512624-2	1999	We have made a mutant containing the conservative replacement Trp 161 --> Phe in human MnSOD (W161F MnSOD), determined its crystal structure, and measured the catalysis of the resulting mutant using pulse radiolysis to produce O(2)(*)(-).	Phenylalanine	77-80	superoxide dismutase 2	Homo sapiens	103-108
10512624-2	1999	We have made a mutant containing the conservative replacement Trp 161 --> Phe in human MnSOD (W161F MnSOD), determined its crystal structure, and measured the catalysis of the resulting mutant using pulse radiolysis to produce O(2)(*)(-).	Superoxides	230-234	superoxide dismutase 2	Homo sapiens	90-95
10512624-3	1999	In the structure of W161F MnSOD the phenyl side chain of Phe 161 superimposes on the indole ring of Trp 161 in the wild type.	Phenylalanine	57-60	superoxide dismutase 2	Homo sapiens	26-31
10512624-3	1999	In the structure of W161F MnSOD the phenyl side chain of Phe 161 superimposes on the indole ring of Trp 161 in the wild type.	indole	85-91	superoxide dismutase 2	Homo sapiens	26-31
10512624-3	1999	In the structure of W161F MnSOD the phenyl side chain of Phe 161 superimposes on the indole ring of Trp 161 in the wild type.	Tryptophan	100-103	superoxide dismutase 2	Homo sapiens	26-31
10512624-5	1999	The tryptophan in MnSOD is not essential for the half-cycle of catalytic activity involving reduction of the manganese; the mutant W161F MnSOD had k(cat)/K(m) at 2.5 x 10(8) M(-)(1) s(-)(1), reduced only 3-fold compared with wild type.	Tryptophan	4-14	superoxide dismutase 2	Homo sapiens	18-23
10512624-5	1999	The tryptophan in MnSOD is not essential for the half-cycle of catalytic activity involving reduction of the manganese; the mutant W161F MnSOD had k(cat)/K(m) at 2.5 x 10(8) M(-)(1) s(-)(1), reduced only 3-fold compared with wild type.	Tryptophan	4-14	superoxide dismutase 2	Homo sapiens	137-142
10512624-5	1999	The tryptophan in MnSOD is not essential for the half-cycle of catalytic activity involving reduction of the manganese; the mutant W161F MnSOD had k(cat)/K(m) at 2.5 x 10(8) M(-)(1) s(-)(1), reduced only 3-fold compared with wild type.	Manganese	109-118	superoxide dismutase 2	Homo sapiens	137-142
10511315-0	1999	Nitric oxide enhances the manganese superoxide dismutase-dependent suppression of proliferation in HT-1080 fibrosarcoma cells.	Nitric Oxide	0-12	superoxide dismutase 2	Homo sapiens	26-56
10511315-1	1999	The overexpression of manganese superoxide dismutase (MnSOD), an enzyme that catalyzes the removal of superoxide (O2*-) from the mitochondria, has been shown to be closely associated with tumor regression in vivo and loss of the malignant phenotype in vitro.	Superoxides	32-42	superoxide dismutase 2	Homo sapiens	54-59
10511315-1	1999	The overexpression of manganese superoxide dismutase (MnSOD), an enzyme that catalyzes the removal of superoxide (O2*-) from the mitochondria, has been shown to be closely associated with tumor regression in vivo and loss of the malignant phenotype in vitro.	o2*-	114-118	superoxide dismutase 2	Homo sapiens	22-52
10511315-1	1999	The overexpression of manganese superoxide dismutase (MnSOD), an enzyme that catalyzes the removal of superoxide (O2*-) from the mitochondria, has been shown to be closely associated with tumor regression in vivo and loss of the malignant phenotype in vitro.	o2*-	114-118	superoxide dismutase 2	Homo sapiens	54-59
10511315-4	1999	Incubating cells in 3% oxygen can prevent the inhibition of cellular proliferation mediated by MnSOD, suggesting that oxygen is a prerequisite component of the MnSOD-dependent proliferative inhibition.	Oxygen	23-29	superoxide dismutase 2	Homo sapiens	95-100
10511315-4	1999	Incubating cells in 3% oxygen can prevent the inhibition of cellular proliferation mediated by MnSOD, suggesting that oxygen is a prerequisite component of the MnSOD-dependent proliferative inhibition.	Oxygen	23-29	superoxide dismutase 2	Homo sapiens	160-165
10511315-4	1999	Incubating cells in 3% oxygen can prevent the inhibition of cellular proliferation mediated by MnSOD, suggesting that oxygen is a prerequisite component of the MnSOD-dependent proliferative inhibition.	Oxygen	118-124	superoxide dismutase 2	Homo sapiens	95-100
10511315-4	1999	Incubating cells in 3% oxygen can prevent the inhibition of cellular proliferation mediated by MnSOD, suggesting that oxygen is a prerequisite component of the MnSOD-dependent proliferative inhibition.	Oxygen	118-124	superoxide dismutase 2	Homo sapiens	160-165
10511315-5	1999	Confocal laser microscopy was used in combination with the oxidant-sensitive fluorescent dyes dihydrorhodamine-123, dihydroethidium, and 2",7"-dichlorodihydrofluorescein diacetate to determine the oxidizing capacity of the MnSOD-overexpressing cells.	2',7'-dichlorodihydrofluorescein diacetate	137-179	superoxide dismutase 2	Homo sapiens	223-228
10511315-9	1999	In this study, we have shown that MnSOD overexpression enhances the cytostatic action of the NO* donors, sodium nitroprusside, 3-morpholinosydnonomine, and (Z)-1-[2-aminethyl)-N-(2-ammonioethyl)amino]diazen-1-+ ++ium-1,2-diolate in a dose-dependent manner.	Nitroprusside	105-125	superoxide dismutase 2	Homo sapiens	34-39
10511315-9	1999	In this study, we have shown that MnSOD overexpression enhances the cytostatic action of the NO* donors, sodium nitroprusside, 3-morpholinosydnonomine, and (Z)-1-[2-aminethyl)-N-(2-ammonioethyl)amino]diazen-1-+ ++ium-1,2-diolate in a dose-dependent manner.	3-morpholinosydnonomine	127-150	superoxide dismutase 2	Homo sapiens	34-39
10511315-9	1999	In this study, we have shown that MnSOD overexpression enhances the cytostatic action of the NO* donors, sodium nitroprusside, 3-morpholinosydnonomine, and (Z)-1-[2-aminethyl)-N-(2-ammonioethyl)amino]diazen-1-+ ++ium-1,2-diolate in a dose-dependent manner.	(z)-1-[2-aminethyl)-n-(2-ammonioethyl)amino]diazen-1-+ ++ium-1,2-diolate	156-228	superoxide dismutase 2	Homo sapiens	34-39
10480957-1	1999	OBJECTIVES: to assess the efficacy of recombinant human manganese superoxide dismutase (rhMnSOD) in prevention of early and late skeletal muscle ischaemia-reperfusion injury mediated by superoxide (O2-).	Superoxides	198-200	superoxide dismutase 2	Homo sapiens	56-86
10498818-3	1999	Among the ROS scavenging enzymes superoxide dismutase (Cu/Zn- and Mn-isoform), glutathione peroxidase and catalase only mitochondrial Mn-SOD was found to be upregulated in the course of i-NOS induction (Western blots).	Reactive Oxygen Species	10-13	superoxide dismutase 2	Homo sapiens	134-140
10488113-0	1999	Interrupting the hydrogen bond network at the active site of human manganese superoxide dismutase.	Hydrogen	17-25	superoxide dismutase 2	Homo sapiens	67-97
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Histidine	0-9	superoxide dismutase 2	Homo sapiens	22-52
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Histidine	0-9	superoxide dismutase 2	Homo sapiens	54-59
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Hydrogen	150-158	superoxide dismutase 2	Homo sapiens	22-52
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Hydrogen	150-158	superoxide dismutase 2	Homo sapiens	54-59
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Tyrosine	213-216	superoxide dismutase 2	Homo sapiens	22-52
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Tyrosine	213-216	superoxide dismutase 2	Homo sapiens	54-59
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Tyrosine	226-229	superoxide dismutase 2	Homo sapiens	22-52
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Tyrosine	226-229	superoxide dismutase 2	Homo sapiens	54-59
10488113-1	1999	Histidine 30 in human manganese superoxide dismutase (MnSOD) is located at a site partially exposed to solvent with its side chain participating in a hydrogen-bonded network that includes the active-site residues Tyr(166) and Tyr(34) and extends to the manganese-bound solvent molecule.	Manganese	22-31	superoxide dismutase 2	Homo sapiens	54-59
10488113-2	1999	We have replaced His(30) with a series of amino acids and Tyr(166) with Phe in human MnSOD.	Histidine	17-20	superoxide dismutase 2	Homo sapiens	85-90
10488113-3	1999	The crystal structure of the mutant of MnSOD containing Asn(30) superimposed closely with the wild type, but the side chain of Asn(30) did not participate in the hydrogen-bonded network in the active site.	Asparagine	56-59	superoxide dismutase 2	Homo sapiens	39-44
10455106-1	1999	The reduction with excess H(2)O(2) of human Mn(III) superoxide dismutase (SOD) and the active-site mutant Y34F Mn(III)SOD was measured by scanning stopped-flow spectrophotometry and revealed the presence of an intermediate in the reduction of the manganese.	Water	26-31	superoxide dismutase 2	Homo sapiens	74-77
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	Nitric Oxide	166-178	superoxide dismutase 2	Homo sapiens	57-87
10455106-1	1999	The reduction with excess H(2)O(2) of human Mn(III) superoxide dismutase (SOD) and the active-site mutant Y34F Mn(III)SOD was measured by scanning stopped-flow spectrophotometry and revealed the presence of an intermediate in the reduction of the manganese.	Manganese	247-256	superoxide dismutase 2	Homo sapiens	74-77
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	Nitric Oxide	166-178	superoxide dismutase 2	Homo sapiens	89-95
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	Peroxynitrous Acid	202-215	superoxide dismutase 2	Homo sapiens	57-87
10455106-5	1999	The visible spectrum of the product-inhibited complex resembles that of the azide-Mn-SOD complex, suggesting that the inhibited complex has expanded geometry about the metal to octahedral.	Metals	168-173	superoxide dismutase 2	Homo sapiens	82-88
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	Peroxynitrous Acid	202-215	superoxide dismutase 2	Homo sapiens	89-95
10455106-6	1999	This study shows that the inhibited complex responsible for the zero-order phase in the catalysis by Mn-SOD of superoxide dismutation can be reached through both the forward (O-(2)) and reverse (H(2)O(2)) reactions, supporting a mechanism in which the zero-order phase results from product inhibition.	Superoxides	111-121	superoxide dismutase 2	Homo sapiens	101-107
10425186-4	1999	In addition, processing efficiency of Val-type SOD2 leader peptide in the presence of mitochondria was siginificantly lower than that of the Ala-type by 11 +/- 4%, suggesting that this lower processing efficiency was in part an underlying mechanism of the association between the SOD2-VV genotype and nonfamilial IDC.	Alanine	141-144	superoxide dismutase 2	Homo sapiens	47-51
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	onoo(-)	217-224	superoxide dismutase 2	Homo sapiens	57-87
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	onoo(-)	217-224	superoxide dismutase 2	Homo sapiens	89-95
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	dihydrorhodamine-1,2,3	256-278	superoxide dismutase 2	Homo sapiens	57-87
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	dihydrorhodamine-1,2,3	256-278	superoxide dismutase 2	Homo sapiens	89-95
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	dhr	280-283	superoxide dismutase 2	Homo sapiens	57-87
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	dhr	280-283	superoxide dismutase 2	Homo sapiens	89-95
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	rhodamine-1,2,3	263-278	superoxide dismutase 2	Homo sapiens	57-87
10452962-1	1999	Isolated copper/zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) together with hydrogen peroxide (H(2)O(2)) caused rapid breakdown of nitric oxide (NO) and production of peroxynitrite (ONOO(-)) indicated by the oxidation of dihydrorhodamine-1,2,3 (DHR) to rhodamine-1,2,3.	rhodamine-1,2,3	263-278	superoxide dismutase 2	Homo sapiens	89-95
10452962-3	1999	In the presence of phenol, the reaction of SOD, H(2)O(2) and NO caused nitration of phenol, which is known to be a footprint of ONOO(-) formation.	Phenol	19-25	superoxide dismutase 2	Homo sapiens	43-46
10452962-3	1999	In the presence of phenol, the reaction of SOD, H(2)O(2) and NO caused nitration of phenol, which is known to be a footprint of ONOO(-) formation.	Phenol	84-90	superoxide dismutase 2	Homo sapiens	43-46
10452962-3	1999	In the presence of phenol, the reaction of SOD, H(2)O(2) and NO caused nitration of phenol, which is known to be a footprint of ONOO(-) formation.	onoo	128-132	superoxide dismutase 2	Homo sapiens	43-46
10452962-9	1999	The production of ONOO(-) by SOD may be of significant importance pathologically under conditions of elevated H(2)O(2) and NO levels, and might contribute to cell death in inflammatory and neurodegenerative diseases, as well as in macrophage-mediated host defence.	onoo	18-22	superoxide dismutase 2	Homo sapiens	29-32
10452962-9	1999	The production of ONOO(-) by SOD may be of significant importance pathologically under conditions of elevated H(2)O(2) and NO levels, and might contribute to cell death in inflammatory and neurodegenerative diseases, as well as in macrophage-mediated host defence.	Hydrogen Peroxide	110-118	superoxide dismutase 2	Homo sapiens	29-32
10428046-0	1999	Induction of the manganese superoxide dismutase gene by sphingomyelinase and ceramide.	Ceramides	77-85	superoxide dismutase 2	Homo sapiens	17-47
10463060-6	1999	A region located in intron 2 displayed a significant increase in cytosine methylation in both transformed cell lines that expressed low levels of MnSOD mRNA compared with their normal cell counterparts.	Cytosine	65-73	superoxide dismutase 2	Homo sapiens	146-151
10463060-8	1999	The association between increased cytosine methylation of the SOD2 intron 2 region and decreased MnSOD expression in transformed cells compared with their normal counterparts suggests that an epigenetic mechanism contributes to the differential SOD2 gene expression between these normal and SV40-transformed cells.	Cytosine	34-42	superoxide dismutase 2	Homo sapiens	62-66
10463060-8	1999	The association between increased cytosine methylation of the SOD2 intron 2 region and decreased MnSOD expression in transformed cells compared with their normal counterparts suggests that an epigenetic mechanism contributes to the differential SOD2 gene expression between these normal and SV40-transformed cells.	Cytosine	34-42	superoxide dismutase 2	Homo sapiens	97-102
10463060-8	1999	The association between increased cytosine methylation of the SOD2 intron 2 region and decreased MnSOD expression in transformed cells compared with their normal counterparts suggests that an epigenetic mechanism contributes to the differential SOD2 gene expression between these normal and SV40-transformed cells.	Cytosine	34-42	superoxide dismutase 2	Homo sapiens	245-249
10428065-8	1999	It is interesting that manganese superoxide dismutase protein levels and levels of intracellular total glutathione increased in neurons exposed to this fatty acid for 24 h, consistent with a compensatory response to increased oxidative stress.	Fatty Acids	152-162	superoxide dismutase 2	Homo sapiens	23-53
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Ceramides	40-48	superoxide dismutase 2	Homo sapiens	201-231
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Ceramides	40-48	superoxide dismutase 2	Homo sapiens	233-238
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Sphingomyelins	85-98	superoxide dismutase 2	Homo sapiens	201-231
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Sphingomyelins	85-98	superoxide dismutase 2	Homo sapiens	233-238
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Ceramides	161-169	superoxide dismutase 2	Homo sapiens	201-231
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Ceramides	161-169	superoxide dismutase 2	Homo sapiens	233-238
10428046-4	1999	A similar effect on the expression of MnSOD was observed with the addition of cell-permeable ceramide analogues (C2 and C6).	Ceramides	93-101	superoxide dismutase 2	Homo sapiens	38-43
10428046-6	1999	Nuclear run-on analysis showed that SMase and ceramide increased the rate of transcription of the MnSOD gene.	Ceramides	46-54	superoxide dismutase 2	Homo sapiens	98-103
10428046-8	1999	Markedly higher expression of mRNA, protein, and activity of MnSOD in skin fibroblasts from patients with Farber disease, a human disorder with pathognomonic accumulation of ceramide due to a deficiency of ceramidase, than in normal skin fibroblasts indicate that ceramide may act as a physiological inducer of MnSOD gene expression.	Ceramides	174-182	superoxide dismutase 2	Homo sapiens	61-66
10428046-8	1999	Markedly higher expression of mRNA, protein, and activity of MnSOD in skin fibroblasts from patients with Farber disease, a human disorder with pathognomonic accumulation of ceramide due to a deficiency of ceramidase, than in normal skin fibroblasts indicate that ceramide may act as a physiological inducer of MnSOD gene expression.	Ceramides	264-272	superoxide dismutase 2	Homo sapiens	61-66
10428046-9	1999	However, stimulation of ceramide-mediated DNA fragmentation by antisense knockdown of MnSOD suggests that induction of MnSOD by ceramide is a protective response of the cell.	Ceramides	24-32	superoxide dismutase 2	Homo sapiens	86-91
10428046-9	1999	However, stimulation of ceramide-mediated DNA fragmentation by antisense knockdown of MnSOD suggests that induction of MnSOD by ceramide is a protective response of the cell.	Ceramides	24-32	superoxide dismutase 2	Homo sapiens	119-124
10428046-9	1999	However, stimulation of ceramide-mediated DNA fragmentation by antisense knockdown of MnSOD suggests that induction of MnSOD by ceramide is a protective response of the cell.	Ceramides	128-136	superoxide dismutase 2	Homo sapiens	86-91
10428046-9	1999	However, stimulation of ceramide-mediated DNA fragmentation by antisense knockdown of MnSOD suggests that induction of MnSOD by ceramide is a protective response of the cell.	Ceramides	128-136	superoxide dismutase 2	Homo sapiens	119-124
10328827-1	1999	MnCl2 induced manganese-containing superoxide dismutase (MnSOD) expression (mRNA, immunoreactive protein, and enzyme activity) in human breast cancer Hs578T cells.	manganese chloride	0-5	superoxide dismutase 2	Homo sapiens	14-55
10334867-4	1999	Both WT-MnSOD (IC50 = 65 microM, 15 microM MnSOD) and Y34F-MnSOD (IC50 = 55 microM, 15 microM Y34F) displayed similar dose-dependent sensitivity to ONOO--mediated inactivation.	onoo	148-152	superoxide dismutase 2	Homo sapiens	5-13
10334867-4	1999	Both WT-MnSOD (IC50 = 65 microM, 15 microM MnSOD) and Y34F-MnSOD (IC50 = 55 microM, 15 microM Y34F) displayed similar dose-dependent sensitivity to ONOO--mediated inactivation.	onoo	148-152	superoxide dismutase 2	Homo sapiens	8-13
10334867-6	1999	Collectively, these results suggest that complete inactivation of MnSOD by ONOO- can occur independent of the active site tyrosine residue and includes not only nitration of critical tyrosine residues but also tyrosine oxidation and subsequent formation of dityrosine.	onoo	75-79	superoxide dismutase 2	Homo sapiens	66-71
10334867-6	1999	Collectively, these results suggest that complete inactivation of MnSOD by ONOO- can occur independent of the active site tyrosine residue and includes not only nitration of critical tyrosine residues but also tyrosine oxidation and subsequent formation of dityrosine.	Tyrosine	122-130	superoxide dismutase 2	Homo sapiens	66-71
10334867-6	1999	Collectively, these results suggest that complete inactivation of MnSOD by ONOO- can occur independent of the active site tyrosine residue and includes not only nitration of critical tyrosine residues but also tyrosine oxidation and subsequent formation of dityrosine.	Tyrosine	183-191	superoxide dismutase 2	Homo sapiens	66-71
10334867-6	1999	Collectively, these results suggest that complete inactivation of MnSOD by ONOO- can occur independent of the active site tyrosine residue and includes not only nitration of critical tyrosine residues but also tyrosine oxidation and subsequent formation of dityrosine.	Tyrosine	183-191	superoxide dismutase 2	Homo sapiens	66-71
10334867-6	1999	Collectively, these results suggest that complete inactivation of MnSOD by ONOO- can occur independent of the active site tyrosine residue and includes not only nitration of critical tyrosine residues but also tyrosine oxidation and subsequent formation of dityrosine.	dityrosine	257-267	superoxide dismutase 2	Homo sapiens	66-71
10401622-3	1999	Correlation of biochemical studies with cell cycle studies suggested that heteroploidy observed in the nonadapted MnSOD-overexpressing cell line may be due to increased intracellular peroxides with resultant disruption of the microtubule network, while a decreased mitotic rate was associated with decreased ATP levels in mitosis.	Peroxides	183-192	superoxide dismutase 2	Homo sapiens	114-119
10401622-3	1999	Correlation of biochemical studies with cell cycle studies suggested that heteroploidy observed in the nonadapted MnSOD-overexpressing cell line may be due to increased intracellular peroxides with resultant disruption of the microtubule network, while a decreased mitotic rate was associated with decreased ATP levels in mitosis.	Adenosine Triphosphate	308-311	superoxide dismutase 2	Homo sapiens	114-119
10352126-6	1999	Manganese superoxide dismutase (MnSOD) content was also increased 49% overall in the cells grown in the absence of supplemental copper.	Copper	128-134	superoxide dismutase 2	Homo sapiens	32-37
10352126-8	1999	These findings indicate that in cells grown under conditions of copper deprivation that suppress cytochrome-c oxidase activity, oxidative stress in mitochondria is increased sufficiently to induce MnSOD, potentiate protein oxidation, and possibly cause the oxidative inactivation of complex I.	Copper	64-70	superoxide dismutase 2	Homo sapiens	197-202
10424621-0	1999	Peroxynitrite modulates manganese-containing superoxide dismutase gene expression in lung epithelial cells.	Peroxynitrous Acid	0-13	superoxide dismutase 2	Homo sapiens	24-65
10334867-0	1999	Tyrosine modifications and inactivation of active site manganese superoxide dismutase mutant (Y34F) by peroxynitrite.	Peroxynitrous Acid	103-116	superoxide dismutase 2	Homo sapiens	55-85
10334867-1	1999	Recent studies from this laboratory have demonstrated that human manganese superoxide dismutase (MnSOD) is a target for tyrosine nitration in several chronic inflammatory diseases including chronic organ rejection, arthritis, and tumorigenesis.	Tyrosine	120-128	superoxide dismutase 2	Homo sapiens	65-95
10334867-1	1999	Recent studies from this laboratory have demonstrated that human manganese superoxide dismutase (MnSOD) is a target for tyrosine nitration in several chronic inflammatory diseases including chronic organ rejection, arthritis, and tumorigenesis.	Tyrosine	120-128	superoxide dismutase 2	Homo sapiens	97-102
10334867-2	1999	Furthermore, we demonstrated that peroxynitrite (ONOO-) is the only known biological oxidant competent to inactivate enzymatic activity, nitrate critical tyrosine residues, and induce dityrosine formation in MnSOD.	Peroxynitrous Acid	34-47	superoxide dismutase 2	Homo sapiens	208-213
10334867-2	1999	Furthermore, we demonstrated that peroxynitrite (ONOO-) is the only known biological oxidant competent to inactivate enzymatic activity, nitrate critical tyrosine residues, and induce dityrosine formation in MnSOD.	oxido nitrite	49-54	superoxide dismutase 2	Homo sapiens	208-213
10334867-2	1999	Furthermore, we demonstrated that peroxynitrite (ONOO-) is the only known biological oxidant competent to inactivate enzymatic activity, nitrate critical tyrosine residues, and induce dityrosine formation in MnSOD.	dityrosine	184-194	superoxide dismutase 2	Homo sapiens	208-213
10328827-1	1999	MnCl2 induced manganese-containing superoxide dismutase (MnSOD) expression (mRNA, immunoreactive protein, and enzyme activity) in human breast cancer Hs578T cells.	manganese chloride	0-5	superoxide dismutase 2	Homo sapiens	57-62
10328827-3	1999	Northern blotting demonstrated that tiron or DG affected at the mRNA level, while pyruvate affected Mn-induced MnSOD expression at both the mRNA and protein levels.	Pyruvic Acid	82-90	superoxide dismutase 2	Homo sapiens	111-116
9920876-1	1999	Mitochondrial manganese superoxide dismutase (Mn-SOD) is the primary cellular defense against damaging superoxide radicals generated by aerobic metabolism and as a consequence of inflammatory disease.	Superoxides	24-34	superoxide dismutase 2	Homo sapiens	46-52
10222400-2	1999	Altered amounts of copper-zinc (CuZnSOD) and manganese (MnSOD) superoxide dismutases have been implicated in multistage carcinogesis of both rodents and humans.	Copper	19-25	superoxide dismutase 2	Homo sapiens	56-61
10391096-3	1999	The Mn-SOD activity was increased by treatments with 5-fluorouracil (5-FU), peplomycin and 137Cs, reaching plateau levels at 12 h after treatment and then decreasing gradually.	Fluorouracil	53-67	superoxide dismutase 2	Homo sapiens	4-10
10391096-3	1999	The Mn-SOD activity was increased by treatments with 5-fluorouracil (5-FU), peplomycin and 137Cs, reaching plateau levels at 12 h after treatment and then decreasing gradually.	Fluorouracil	69-73	superoxide dismutase 2	Homo sapiens	4-10
10391096-3	1999	The Mn-SOD activity was increased by treatments with 5-fluorouracil (5-FU), peplomycin and 137Cs, reaching plateau levels at 12 h after treatment and then decreasing gradually.	Peplomycin	76-86	superoxide dismutase 2	Homo sapiens	4-10
11670965-1	1999	Mn(II) complexes of C-substituted macrocyclic 1,4,7,10,13-pentaazacyclopentadecane ligands have been shown to be excellent functional mimics (Synzymes) of the native enzyme manganese superoxide dismutase (Mn SOD).	Manganese(2+)	0-6	superoxide dismutase 2	Homo sapiens	173-203
11670965-1	1999	Mn(II) complexes of C-substituted macrocyclic 1,4,7,10,13-pentaazacyclopentadecane ligands have been shown to be excellent functional mimics (Synzymes) of the native enzyme manganese superoxide dismutase (Mn SOD).	Manganese(2+)	0-6	superoxide dismutase 2	Homo sapiens	205-211
11670965-1	1999	Mn(II) complexes of C-substituted macrocyclic 1,4,7,10,13-pentaazacyclopentadecane ligands have been shown to be excellent functional mimics (Synzymes) of the native enzyme manganese superoxide dismutase (Mn SOD).	1,4,7,10,13-Pentaazacyclopentadecane	46-82	superoxide dismutase 2	Homo sapiens	173-203
11670965-1	1999	Mn(II) complexes of C-substituted macrocyclic 1,4,7,10,13-pentaazacyclopentadecane ligands have been shown to be excellent functional mimics (Synzymes) of the native enzyme manganese superoxide dismutase (Mn SOD).	1,4,7,10,13-Pentaazacyclopentadecane	46-82	superoxide dismutase 2	Homo sapiens	205-211
11670965-5	1999	The DeltaE between the lowest energy folded ligand structure about Mn(II) and its corresponding Mn(III) structure correlates with catalytic activity; i.e., for a large series of complexes an excellent correlation is obtained for both the inner-sphere and outer-sphere rate constants for oxidation of Mn(II)-the rate-determining step in the catalytic cycle for these SOD mimics.	Manganese(2+)	67-73	superoxide dismutase 2	Homo sapiens	366-369
11670965-5	1999	The DeltaE between the lowest energy folded ligand structure about Mn(II) and its corresponding Mn(III) structure correlates with catalytic activity; i.e., for a large series of complexes an excellent correlation is obtained for both the inner-sphere and outer-sphere rate constants for oxidation of Mn(II)-the rate-determining step in the catalytic cycle for these SOD mimics.	manganese(III) acetate dihydrate	96-103	superoxide dismutase 2	Homo sapiens	366-369
11670965-5	1999	The DeltaE between the lowest energy folded ligand structure about Mn(II) and its corresponding Mn(III) structure correlates with catalytic activity; i.e., for a large series of complexes an excellent correlation is obtained for both the inner-sphere and outer-sphere rate constants for oxidation of Mn(II)-the rate-determining step in the catalytic cycle for these SOD mimics.	Manganese(2+)	300-306	superoxide dismutase 2	Homo sapiens	366-369
11225732-8	1999	The use of mitochondrial superoxide dismutase (MnSOD), which degrades superoxides arising from ischemia/reperfusion injury, is one example of this approach.	Superoxides	70-81	superoxide dismutase 2	Homo sapiens	11-45
11225732-8	1999	The use of mitochondrial superoxide dismutase (MnSOD), which degrades superoxides arising from ischemia/reperfusion injury, is one example of this approach.	Superoxides	70-81	superoxide dismutase 2	Homo sapiens	47-52
11225732-9	1999	MnSOD serves as a "garbage disposal" for potentially toxic ROS prior to cellular injury and the activation of signal transduction cascades important in whole-organ pathology and inflammation.	Reactive Oxygen Species	59-62	superoxide dismutase 2	Homo sapiens	0-5
9920876-7	1999	Dimethyl sulfate in vivo footprinting identified 10 putative constitutive protein-DNA binding sites in the proximal Mn-SOD promoter as well as two stimulus-specific enhanced guanine residues possibly due to alterations in chromatin structure.	dimethyl sulfate	0-16	superoxide dismutase 2	Homo sapiens	116-122
9973207-7	1999	Using a RFLP that distinguishes a valine (V) to alanine (A) change in the -9 position in the signal sequence of the protein for MnSOD, we characterized MnSOD genotypes in relation to breast cancer risk.	Valine	34-40	superoxide dismutase 2	Homo sapiens	128-133
9925760-3	1999	It was found that superoxide produced by hyperoxic culture conditions (95% O2 atm) or the redox cycling agent paraquat caused a lesion of the import/processing of precursor hMn-SOD in the baculovirus model.	Superoxides	18-28	superoxide dismutase 2	Homo sapiens	173-180
9925760-3	1999	It was found that superoxide produced by hyperoxic culture conditions (95% O2 atm) or the redox cycling agent paraquat caused a lesion of the import/processing of precursor hMn-SOD in the baculovirus model.	Paraquat	110-118	superoxide dismutase 2	Homo sapiens	173-180
9925760-4	1999	The oxidation of key sulfhydryl groups as a component of the mitochondrial processing lesion was implicated by the observation that the sulfhydryl reducing agent dithiothreitol was completely effective in preventing the block of hMn-SOD processing induced by paraquat.	Dithiothreitol	162-176	superoxide dismutase 2	Homo sapiens	229-236
9925760-5	1999	Interestingly, the peripheral benzodiazepine receptor (PBzR) agonists PK11194, Ro5-4864, and protoporphyrin IX were all found to enhance mitochondrial processing of the hMn-SOD precursor protein, suggesting a role for the PBzR in the regulation of mitochondrial import of proteins.	protoporphyrin IX	93-110	superoxide dismutase 2	Homo sapiens	169-176
9819222-12	1998	In the presence of a specific competitor oligoribonucleotide that inhibits MnSOD RNA protein-binding activity, translation of MnSOD RNA containing the 3" UTR was decreased by 65%.	Oligoribonucleotides	41-60	superoxide dismutase 2	Homo sapiens	75-80
10644056-0	1999	Overexpression of the human manganese superoxide dismutase (MnSOD) transgene in subclones of murine hematopoietic progenitor cell line 32D cl 3 decreases irradiation-induced apoptosis but does not alter G2/M or G1/S phase cell cycle arrest.	cl 3	139-143	superoxide dismutase 2	Homo sapiens	28-58
10644056-0	1999	Overexpression of the human manganese superoxide dismutase (MnSOD) transgene in subclones of murine hematopoietic progenitor cell line 32D cl 3 decreases irradiation-induced apoptosis but does not alter G2/M or G1/S phase cell cycle arrest.	cl 3	139-143	superoxide dismutase 2	Homo sapiens	60-65
9852137-8	1998	The PKC agonists thymeleatoxin (0.5 microM) and 12-deoxyphorbol 13-phenylacetate 20-acetate (dPPA; 10 nM) potently induced MnSOD gene expression.	12-deoxyphorbolphenylacetate-20-acetate	48-91	superoxide dismutase 2	Homo sapiens	123-128
9852137-8	1998	The PKC agonists thymeleatoxin (0.5 microM) and 12-deoxyphorbol 13-phenylacetate 20-acetate (dPPA; 10 nM) potently induced MnSOD gene expression.	12-deoxyphorbolphenylacetate-20-acetate	93-97	superoxide dismutase 2	Homo sapiens	123-128
9852137-10	1998	Down-regulation of PKC by prolonged treatment with phorbol 12-myristate 13-acetate (PMA) also inhibited induction of MnSOD by anticancer drugs, indicating an important role of PKC in MnSOD signaling by these agents.	Tetradecanoylphorbol Acetate	51-82	superoxide dismutase 2	Homo sapiens	117-122
9852137-10	1998	Down-regulation of PKC by prolonged treatment with phorbol 12-myristate 13-acetate (PMA) also inhibited induction of MnSOD by anticancer drugs, indicating an important role of PKC in MnSOD signaling by these agents.	Tetradecanoylphorbol Acetate	51-82	superoxide dismutase 2	Homo sapiens	183-188
9852137-10	1998	Down-regulation of PKC by prolonged treatment with phorbol 12-myristate 13-acetate (PMA) also inhibited induction of MnSOD by anticancer drugs, indicating an important role of PKC in MnSOD signaling by these agents.	Tetradecanoylphorbol Acetate	84-87	superoxide dismutase 2	Homo sapiens	117-122
9852137-10	1998	Down-regulation of PKC by prolonged treatment with phorbol 12-myristate 13-acetate (PMA) also inhibited induction of MnSOD by anticancer drugs, indicating an important role of PKC in MnSOD signaling by these agents.	Tetradecanoylphorbol Acetate	84-87	superoxide dismutase 2	Homo sapiens	183-188
9837861-5	1998	When transiently expressing, MnSOD inhibited AP-1 but increased NF-kappaB transactivation, which can be abolished by sodium pyruvate, a hydrogen peroxide scavenger.	SODIUM PYRUVATE	117-132	superoxide dismutase 2	Homo sapiens	29-34
9837861-5	1998	When transiently expressing, MnSOD inhibited AP-1 but increased NF-kappaB transactivation, which can be abolished by sodium pyruvate, a hydrogen peroxide scavenger.	Hydrogen Peroxide	136-153	superoxide dismutase 2	Homo sapiens	29-34
9837861-8	1998	Since TPA induces differentiation in human breast cancer cells and up-regulates MnSOD gene in HeLa cells, MnSOD expression and AP-1 and NF-kappaB activity were measured under TPA treatment.	Tetradecanoylphorbol Acetate	6-9	superoxide dismutase 2	Homo sapiens	80-85
9837861-9	1998	The results showed that TPA induced endogenous MnSOD expression and inhibited both AP-1 and NF-kappaB.	Tetradecanoylphorbol Acetate	24-27	superoxide dismutase 2	Homo sapiens	47-52
9886257-1	1999	In response to the attack of reactive oxygen species, the skin has developed a complex antioxidant defense system including among others the manganese-superoxide dismutase (MnSOD).	Reactive Oxygen Species	29-52	superoxide dismutase 2	Homo sapiens	141-171
9886257-1	1999	In response to the attack of reactive oxygen species, the skin has developed a complex antioxidant defense system including among others the manganese-superoxide dismutase (MnSOD).	Reactive Oxygen Species	29-52	superoxide dismutase 2	Homo sapiens	173-178
9886257-2	1999	MnSOD dismutates the superoxide anion (O2*-) derived from the reduction of molecular oxygen to hydrogen peroxide (H2O2), which is detoxified by glutathione peroxidase to water and molecular oxygen.	Superoxides	21-37	superoxide dismutase 2	Homo sapiens	0-5
9886257-2	1999	MnSOD dismutates the superoxide anion (O2*-) derived from the reduction of molecular oxygen to hydrogen peroxide (H2O2), which is detoxified by glutathione peroxidase to water and molecular oxygen.	o2*-	39-43	superoxide dismutase 2	Homo sapiens	0-5
9886257-2	1999	MnSOD dismutates the superoxide anion (O2*-) derived from the reduction of molecular oxygen to hydrogen peroxide (H2O2), which is detoxified by glutathione peroxidase to water and molecular oxygen.	Oxygen	85-91	superoxide dismutase 2	Homo sapiens	0-5
9886257-2	1999	MnSOD dismutates the superoxide anion (O2*-) derived from the reduction of molecular oxygen to hydrogen peroxide (H2O2), which is detoxified by glutathione peroxidase to water and molecular oxygen.	Hydrogen Peroxide	95-112	superoxide dismutase 2	Homo sapiens	0-5
9886257-2	1999	MnSOD dismutates the superoxide anion (O2*-) derived from the reduction of molecular oxygen to hydrogen peroxide (H2O2), which is detoxified by glutathione peroxidase to water and molecular oxygen.	Hydrogen Peroxide	114-118	superoxide dismutase 2	Homo sapiens	0-5
9886257-2	1999	MnSOD dismutates the superoxide anion (O2*-) derived from the reduction of molecular oxygen to hydrogen peroxide (H2O2), which is detoxified by glutathione peroxidase to water and molecular oxygen.	Water	170-175	superoxide dismutase 2	Homo sapiens	0-5
9886257-2	1999	MnSOD dismutates the superoxide anion (O2*-) derived from the reduction of molecular oxygen to hydrogen peroxide (H2O2), which is detoxified by glutathione peroxidase to water and molecular oxygen.	Oxygen	190-196	superoxide dismutase 2	Homo sapiens	0-5
12110940-3	1999	After 5 h induction with 1 mmol/L IPTG 800 mol/L Mn(2+) human Mn-SOD was highly expressed in E.coli BL21(DE3).	Isopropyl Thiogalactoside	34-38	superoxide dismutase 2	Homo sapiens	62-68
9852137-3	1998	Here we report that paclitaxel can induce MnSOD gene expression in human lung adenocarcinoma cell line A549 in a time- and dose-dependent manner.	Paclitaxel	20-30	superoxide dismutase 2	Homo sapiens	42-47
9852137-4	1998	Additional anticancer drugs, vinblastine and vincristine, also induced MnSOD gene expression.	Vinblastine	29-40	superoxide dismutase 2	Homo sapiens	71-76
9852137-4	1998	Additional anticancer drugs, vinblastine and vincristine, also induced MnSOD gene expression.	Vincristine	45-56	superoxide dismutase 2	Homo sapiens	71-76
9852137-8	1998	The PKC agonists thymeleatoxin (0.5 microM) and 12-deoxyphorbol 13-phenylacetate 20-acetate (dPPA; 10 nM) potently induced MnSOD gene expression.	thymeleatoxin	17-30	superoxide dismutase 2	Homo sapiens	123-128
9853553-7	1998	Upregulation of MnSOD in cancer tissue most likely serves as a protective mechanism against anti-cancer therapies known to produce superoxide radicals as a key component of their tumor-killing activity.	Superoxides	131-150	superoxide dismutase 2	Homo sapiens	16-21
9819222-12	1998	In the presence of a specific competitor oligoribonucleotide that inhibits MnSOD RNA protein-binding activity, translation of MnSOD RNA containing the 3" UTR was decreased by 65%.	Oligoribonucleotides	41-60	superoxide dismutase 2	Homo sapiens	126-131
9893946-3	1998	The induction of both CO-I and F0F1-ATPase 6 was abolished by the NOS inhibitor N-monomethyl-L-arginine (NMMA) or by the enzymatic scavenger superoxide dismutase/catalase (SOD/CAT).	omega-N-Methylarginine	105-109	superoxide dismutase 2	Homo sapiens	172-175
9893946-11	1998	The enzymatic activities of catalase and Mn-SOD (mitochondrial) showed a significant increase after LPS/INF gamma treatment, which was abolished by NMMA.	omega-N-Methylarginine	148-152	superoxide dismutase 2	Homo sapiens	41-47
9848095-4	1998	We found that MPTP toxicity was significantly attenuated in the MnSOD transgenic mice which overexpress the human manganese superoxide dismutase gene, with these mice showing threefold greater dopamine levels than controls following MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	14-18	superoxide dismutase 2	Homo sapiens	114-144
9773743-11	1998	The apparently paradoxical increase in MnSOD expression may be an adaptive response to increased superoxide generation.	Superoxides	97-107	superoxide dismutase 2	Homo sapiens	39-44
9848095-4	1998	We found that MPTP toxicity was significantly attenuated in the MnSOD transgenic mice which overexpress the human manganese superoxide dismutase gene, with these mice showing threefold greater dopamine levels than controls following MPTP.	Dopamine	193-201	superoxide dismutase 2	Homo sapiens	114-144
9848095-4	1998	We found that MPTP toxicity was significantly attenuated in the MnSOD transgenic mice which overexpress the human manganese superoxide dismutase gene, with these mice showing threefold greater dopamine levels than controls following MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	233-237	superoxide dismutase 2	Homo sapiens	114-144
9700139-2	1998	In this study we investigated the immunoreactivity of two important superoxide radical scavenging intracellular antioxidant enzymes, manganese superoxide dismutase (MnSOD) and copperzinc superoxide dismutase (CuZnSOD), in pulmonary sarcoidosis and extrinsic allergic alveolitis.	Superoxides	68-86	superoxide dismutase 2	Homo sapiens	133-163
9741582-0	1998	Peroxynitrite modulates MnSOD gene expression in lung epithelial cells.	Peroxynitrous Acid	0-13	superoxide dismutase 2	Homo sapiens	24-29
9741582-3	1998	These experiments tested whether ONOO regulated MnSOD gene expression in human lung epithelial (A549) cells.	onoo	33-37	superoxide dismutase 2	Homo sapiens	48-53
9741582-4	1998	3-morpholinosydnonimine HCI (SIN-1) (10 or 1000 microM) increased MnSOD mRNA, but did not change hypoxanthine guanine phosphoribosyl transferase (HPRT) mRNA.	3-morpholinosydnonimine hci	0-27	superoxide dismutase 2	Homo sapiens	66-71
9741582-5	1998	Authentic peroxynitrite (ONOO ) (100-500 microM) also increased MnSOD mRNA but did not change constitutive HPRT mRNA expression.	Peroxynitrous Acid	10-23	superoxide dismutase 2	Homo sapiens	64-69
9741582-5	1998	Authentic peroxynitrite (ONOO ) (100-500 microM) also increased MnSOD mRNA but did not change constitutive HPRT mRNA expression.	onoo	25-29	superoxide dismutase 2	Homo sapiens	64-69
9741582-7	1998	MnSOD gene induction due to ONOO- was inhibited effectively by L-cysteine (10 mM) and partially inhibited by N-acetyl cysteine (50 mM) or pyrrole dithiocarbamate (10 mM).	onoo	28-32	superoxide dismutase 2	Homo sapiens	0-5
9741582-7	1998	MnSOD gene induction due to ONOO- was inhibited effectively by L-cysteine (10 mM) and partially inhibited by N-acetyl cysteine (50 mM) or pyrrole dithiocarbamate (10 mM).	Cysteine	63-73	superoxide dismutase 2	Homo sapiens	0-5
9741582-7	1998	MnSOD gene induction due to ONOO- was inhibited effectively by L-cysteine (10 mM) and partially inhibited by N-acetyl cysteine (50 mM) or pyrrole dithiocarbamate (10 mM).	Acetylcysteine	109-126	superoxide dismutase 2	Homo sapiens	0-5
9741582-7	1998	MnSOD gene induction due to ONOO- was inhibited effectively by L-cysteine (10 mM) and partially inhibited by N-acetyl cysteine (50 mM) or pyrrole dithiocarbamate (10 mM).	pyrrole dithiocarbamate	138-161	superoxide dismutase 2	Homo sapiens	0-5
9741582-10	1998	Increased steady state [O2.-] in the presence of .NO yields ONOO , and ONOO has direct, stimulatory effects on MnSOD transcript expression.	Superoxides	24-26	superoxide dismutase 2	Homo sapiens	111-116
9741582-10	1998	Increased steady state [O2.-] in the presence of .NO yields ONOO , and ONOO has direct, stimulatory effects on MnSOD transcript expression.	onoo	71-75	superoxide dismutase 2	Homo sapiens	111-116
9700139-2	1998	In this study we investigated the immunoreactivity of two important superoxide radical scavenging intracellular antioxidant enzymes, manganese superoxide dismutase (MnSOD) and copperzinc superoxide dismutase (CuZnSOD), in pulmonary sarcoidosis and extrinsic allergic alveolitis.	Superoxides	68-86	superoxide dismutase 2	Homo sapiens	165-170
9728339-1	1998	Manganese superoxide dismutase (MnSOD) is the mitochondrial enzyme that disposes of superoxide generated by respiratory chain activity.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
9685724-2	1998	The enzymatic activity of a homogenate of Sf21 cells, infected with baculovirus carrying wild-type Mn-SOD and grown in the conventional medium, was indistinguishable from that of control cells, but was augmented by supplementation with Mn2+.	Manganese(2+)	236-240	superoxide dismutase 2	Homo sapiens	99-105
9685724-5	1998	While both Mn2+ and Fe3+ stimulated Mn-SOD accumulation within mitochondria, the active form was produced in the presence of submillimolar Mn2+ only.	Manganese(2+)	11-15	superoxide dismutase 2	Homo sapiens	36-42
9685724-5	1998	While both Mn2+ and Fe3+ stimulated Mn-SOD accumulation within mitochondria, the active form was produced in the presence of submillimolar Mn2+ only.	ferric sulfate	20-24	superoxide dismutase 2	Homo sapiens	36-42
9685724-6	1998	Amino acid substitutions at a signal peptide-cleavage site, His-Ser-Leu4 to Pro-Met-Va14, in the mature Mn-SOD prevented the processing of the precursor protein, and thus resulted in the accumulation of the precursor protein within mitochondria, as judged on immunostaining with an anti-Mn-SOD antibody.	Histidine	60-63	superoxide dismutase 2	Homo sapiens	104-110
9685724-6	1998	Amino acid substitutions at a signal peptide-cleavage site, His-Ser-Leu4 to Pro-Met-Va14, in the mature Mn-SOD prevented the processing of the precursor protein, and thus resulted in the accumulation of the precursor protein within mitochondria, as judged on immunostaining with an anti-Mn-SOD antibody.	Histidine	60-63	superoxide dismutase 2	Homo sapiens	287-293
9685724-6	1998	Amino acid substitutions at a signal peptide-cleavage site, His-Ser-Leu4 to Pro-Met-Va14, in the mature Mn-SOD prevented the processing of the precursor protein, and thus resulted in the accumulation of the precursor protein within mitochondria, as judged on immunostaining with an anti-Mn-SOD antibody.	Serine	64-67	superoxide dismutase 2	Homo sapiens	104-110
9685724-6	1998	Amino acid substitutions at a signal peptide-cleavage site, His-Ser-Leu4 to Pro-Met-Va14, in the mature Mn-SOD prevented the processing of the precursor protein, and thus resulted in the accumulation of the precursor protein within mitochondria, as judged on immunostaining with an anti-Mn-SOD antibody.	Serine	64-67	superoxide dismutase 2	Homo sapiens	287-293
9685724-6	1998	Amino acid substitutions at a signal peptide-cleavage site, His-Ser-Leu4 to Pro-Met-Va14, in the mature Mn-SOD prevented the processing of the precursor protein, and thus resulted in the accumulation of the precursor protein within mitochondria, as judged on immunostaining with an anti-Mn-SOD antibody.	pro-met-va14	76-88	superoxide dismutase 2	Homo sapiens	104-110
9685724-6	1998	Amino acid substitutions at a signal peptide-cleavage site, His-Ser-Leu4 to Pro-Met-Va14, in the mature Mn-SOD prevented the processing of the precursor protein, and thus resulted in the accumulation of the precursor protein within mitochondria, as judged on immunostaining with an anti-Mn-SOD antibody.	pro-met-va14	76-88	superoxide dismutase 2	Homo sapiens	287-293
9728339-2	1998	Of all electrons passing down the mitochondrial respiratory chain, 1-2% are diverted to form superoxide; thus production of hydrogen peroxide occurs at a constant rate due to MnSOD activity.	Superoxides	93-103	superoxide dismutase 2	Homo sapiens	175-180
9728339-2	1998	Of all electrons passing down the mitochondrial respiratory chain, 1-2% are diverted to form superoxide; thus production of hydrogen peroxide occurs at a constant rate due to MnSOD activity.	Hydrogen Peroxide	124-141	superoxide dismutase 2	Homo sapiens	175-180
9648725-9	1998	Two other indices of LDL oxidation, formation of conjugated dienes and increased LDL electrophoretic mobility, were similarly reduced by SOD transduction.	dienes	60-66	superoxide dismutase 2	Homo sapiens	137-140
9582091-6	1998	Both clones overexpressing MnSOD activity showed increased reactive oxygen species levels under basal cell culture conditions.	Reactive Oxygen Species	59-82	superoxide dismutase 2	Homo sapiens	27-32
9603906-0	1998	Inactivation of human manganese-superoxide dismutase by peroxynitrite is caused by exclusive nitration of tyrosine 34 to 3-nitrotyrosine.	Peroxynitrous Acid	56-69	superoxide dismutase 2	Homo sapiens	22-52
9603906-0	1998	Inactivation of human manganese-superoxide dismutase by peroxynitrite is caused by exclusive nitration of tyrosine 34 to 3-nitrotyrosine.	Tyrosine	106-114	superoxide dismutase 2	Homo sapiens	22-52
9603906-0	1998	Inactivation of human manganese-superoxide dismutase by peroxynitrite is caused by exclusive nitration of tyrosine 34 to 3-nitrotyrosine.	3-nitrotyrosine	121-136	superoxide dismutase 2	Homo sapiens	22-52
9603906-3	1998	This study proposes that nitration of a specific tyrosine residue is responsible for inactivation of recombinant human mitochondrial manganese-superoxide dismutase (Mn-SOD) by peroxynitrite.	Tyrosine	49-57	superoxide dismutase 2	Homo sapiens	133-163
9603906-3	1998	This study proposes that nitration of a specific tyrosine residue is responsible for inactivation of recombinant human mitochondrial manganese-superoxide dismutase (Mn-SOD) by peroxynitrite.	Tyrosine	49-57	superoxide dismutase 2	Homo sapiens	165-171
9603906-3	1998	This study proposes that nitration of a specific tyrosine residue is responsible for inactivation of recombinant human mitochondrial manganese-superoxide dismutase (Mn-SOD) by peroxynitrite.	Peroxynitrous Acid	176-189	superoxide dismutase 2	Homo sapiens	133-163
9603906-3	1998	This study proposes that nitration of a specific tyrosine residue is responsible for inactivation of recombinant human mitochondrial manganese-superoxide dismutase (Mn-SOD) by peroxynitrite.	Peroxynitrous Acid	176-189	superoxide dismutase 2	Homo sapiens	165-171
9603906-4	1998	Mass spectroscopic analysis of the peroxynitrite-inactivated Mn-SOD showed an increased molecular mass because of a single nitro group substituted onto a tyrosine residue.	Peroxynitrous Acid	35-48	superoxide dismutase 2	Homo sapiens	61-67
9603906-4	1998	Mass spectroscopic analysis of the peroxynitrite-inactivated Mn-SOD showed an increased molecular mass because of a single nitro group substituted onto a tyrosine residue.	nitro	123-128	superoxide dismutase 2	Homo sapiens	61-67
9603906-4	1998	Mass spectroscopic analysis of the peroxynitrite-inactivated Mn-SOD showed an increased molecular mass because of a single nitro group substituted onto a tyrosine residue.	Tyrosine	154-162	superoxide dismutase 2	Homo sapiens	61-67
9603906-5	1998	Single peptides that had different elution positions between samples from the native and peroxynitrite-inactivated Mn-SOD on reverse-phase high performance liquid chromatography were isolated after successive digestion of the samples by staphylococcal serine protease and lysylendopeptidase and subjected to amino acid sequence and molecular mass analyses.	Peroxynitrous Acid	89-102	superoxide dismutase 2	Homo sapiens	115-121
9603906-7	1998	This residue is located near manganese and in a substrate O-2 gateway in Mn-SOD.	Manganese	29-38	superoxide dismutase 2	Homo sapiens	73-79
9655186-9	1998	LiCl completely arrested or prevented growth of BL21 E. coli transformed with the sod2 gene.	Lithium Chloride	0-4	superoxide dismutase 2	Homo sapiens	82-86
9590133-2	1998	We have previously shown that endogenous tumor necrosis factor (enTNF) acts as an intracellular resistance factor to inhibit the cytotoxic effect of heat by scavenging oxygen-free radicals via the induction of manganous superoxide dismutase (MnSOD).	oxygen-free radicals	168-188	superoxide dismutase 2	Homo sapiens	210-240
9590133-2	1998	We have previously shown that endogenous tumor necrosis factor (enTNF) acts as an intracellular resistance factor to inhibit the cytotoxic effect of heat by scavenging oxygen-free radicals via the induction of manganous superoxide dismutase (MnSOD).	oxygen-free radicals	168-188	superoxide dismutase 2	Homo sapiens	242-247
9590133-5	1998	After treatment of these cells for 15 hr with adriamycin (ADM), the expression of enTNF was decreased by 43%, and MnSOD activity was suppressed by 55%.	Doxorubicin	46-56	superoxide dismutase 2	Homo sapiens	114-119
9590133-5	1998	After treatment of these cells for 15 hr with adriamycin (ADM), the expression of enTNF was decreased by 43%, and MnSOD activity was suppressed by 55%.	Doxorubicin	58-61	superoxide dismutase 2	Homo sapiens	114-119
9660302-12	1998	Both TNF and ethanol increased HepG2 cell MnSOD activity in short-term (72 hr) cultures with ethanol.	Ethanol	13-20	superoxide dismutase 2	Homo sapiens	42-47
9660302-12	1998	Both TNF and ethanol increased HepG2 cell MnSOD activity in short-term (72 hr) cultures with ethanol.	Ethanol	93-100	superoxide dismutase 2	Homo sapiens	42-47
9582369-5	1998	Besides TNF, phorbol ester-, okadaic acid-, ceramide-, and lipopolysaccharide-induced activation of NF-kappaB was blocked by Mn-SOD, indicating a common pathway of activation.	Phorbol Esters	13-26	superoxide dismutase 2	Homo sapiens	125-131
9582369-5	1998	Besides TNF, phorbol ester-, okadaic acid-, ceramide-, and lipopolysaccharide-induced activation of NF-kappaB was blocked by Mn-SOD, indicating a common pathway of activation.	Okadaic Acid	29-41	superoxide dismutase 2	Homo sapiens	125-131
9582369-5	1998	Besides TNF, phorbol ester-, okadaic acid-, ceramide-, and lipopolysaccharide-induced activation of NF-kappaB was blocked by Mn-SOD, indicating a common pathway of activation.	Ceramides	44-52	superoxide dismutase 2	Homo sapiens	125-131
9582369-9	1998	Suppression of apoptosis induced by okadaic acid, H2O2, and taxol was also inhibited by Mn-SOD but not that induced by vincristine, vinblastine, or daunomycin.	Okadaic Acid	36-48	superoxide dismutase 2	Homo sapiens	88-94
9582369-9	1998	Suppression of apoptosis induced by okadaic acid, H2O2, and taxol was also inhibited by Mn-SOD but not that induced by vincristine, vinblastine, or daunomycin.	Hydrogen Peroxide	50-54	superoxide dismutase 2	Homo sapiens	88-94
9582369-9	1998	Suppression of apoptosis induced by okadaic acid, H2O2, and taxol was also inhibited by Mn-SOD but not that induced by vincristine, vinblastine, or daunomycin.	Paclitaxel	60-65	superoxide dismutase 2	Homo sapiens	88-94
9537988-0	1998	Probing the active site of human manganese superoxide dismutase: the role of glutamine 143.	Glutamine	77-86	superoxide dismutase 2	Homo sapiens	33-63
9679710-1	1998	Endogenous tumour necrosis factor (enTNF) acts as a resistant factor against cytotoxicity of heat by induction of manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	reactive oxygen free radicals	173-202	superoxide dismutase 2	Homo sapiens	114-144
9679710-1	1998	Endogenous tumour necrosis factor (enTNF) acts as a resistant factor against cytotoxicity of heat by induction of manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	reactive oxygen free radicals	173-202	superoxide dismutase 2	Homo sapiens	146-151
9626579-3	1998	Cell defense against ROS includes overexpression of Mn-superoxide dismutase (SOD), an inducible mitochondrial enzyme.	Reactive Oxygen Species	21-24	superoxide dismutase 2	Homo sapiens	52-75
9626579-3	1998	Cell defense against ROS includes overexpression of Mn-superoxide dismutase (SOD), an inducible mitochondrial enzyme.	Reactive Oxygen Species	21-24	superoxide dismutase 2	Homo sapiens	77-80
9588192-9	1998	There was no significant correlation between total SOD activities and pentosidine levels in the plasma of hemodialysis patients, but, among the three SOD isozymes, the plasma EC-SOD levels correlated with the levels of pentosidine in hemodialysis patients (r2 = 0.286, P < 0.05).	pentosidine	219-230	superoxide dismutase 2	Homo sapiens	150-153
9588192-10	1998	As decreased GPx and increased SOD activities result in the increased H2O2 generation, which accelerates the glycoxidation of protein, these data suggest a link of altered redox regulation by antioxidant enzymes to increased glycoxidation reaction in the uremic plasma.	Hydrogen Peroxide	70-74	superoxide dismutase 2	Homo sapiens	31-34
9537987-0	1998	Crystal structure of Y34F mutant human mitochondrial manganese superoxide dismutase and the functional role of tyrosine 34.	Tyrosine	111-119	superoxide dismutase 2	Homo sapiens	53-83
9537987-2	1998	We have prepared the mutant containing the replacement Tyr 34 --> Phe (Y34F) in human manganese superoxide dismutase (hMnSOD) and crystallized it in two different crystal forms, orthorhombic and hexagonal.	Tyrosine	55-58	superoxide dismutase 2	Homo sapiens	89-119
9537987-2	1998	We have prepared the mutant containing the replacement Tyr 34 --> Phe (Y34F) in human manganese superoxide dismutase (hMnSOD) and crystallized it in two different crystal forms, orthorhombic and hexagonal.	Tyrosine	55-58	superoxide dismutase 2	Homo sapiens	121-127
9537987-2	1998	We have prepared the mutant containing the replacement Tyr 34 --> Phe (Y34F) in human manganese superoxide dismutase (hMnSOD) and crystallized it in two different crystal forms, orthorhombic and hexagonal.	Phenylalanine	69-72	superoxide dismutase 2	Homo sapiens	89-119
9537988-1	1998	Structural and biochemical characterization of the nonliganding residue glutamine 143 near the manganese of human Mn superoxide dismutase (hMnSOD), a homotetramer of 22 kDa, reveals a functional role for this residue.	Glutamine	72-81	superoxide dismutase 2	Homo sapiens	114-137
9537987-2	1998	We have prepared the mutant containing the replacement Tyr 34 --> Phe (Y34F) in human manganese superoxide dismutase (hMnSOD) and crystallized it in two different crystal forms, orthorhombic and hexagonal.	Phenylalanine	69-72	superoxide dismutase 2	Homo sapiens	121-127
9537987-4	1998	Both crystal forms give structures that are closely superimposable with that of wild-type hMnSOD, with the phenyl rings of Tyr 34 in the wild type and Phe 34 in the mutant very similar in orientation.	Tyrosine	123-126	superoxide dismutase 2	Homo sapiens	90-96
9537988-1	1998	Structural and biochemical characterization of the nonliganding residue glutamine 143 near the manganese of human Mn superoxide dismutase (hMnSOD), a homotetramer of 22 kDa, reveals a functional role for this residue.	Glutamine	72-81	superoxide dismutase 2	Homo sapiens	139-145
9537987-4	1998	Both crystal forms give structures that are closely superimposable with that of wild-type hMnSOD, with the phenyl rings of Tyr 34 in the wild type and Phe 34 in the mutant very similar in orientation.	Phenylalanine	151-154	superoxide dismutase 2	Homo sapiens	90-96
9537987-7	1998	The functional role of the side chain hydroxyl of Tyr 34 can be evaluated by comparison of the Y34F mutant with the wild-type hMnSOD.	Tyrosine	50-53	superoxide dismutase 2	Homo sapiens	126-132
9537988-1	1998	Structural and biochemical characterization of the nonliganding residue glutamine 143 near the manganese of human Mn superoxide dismutase (hMnSOD), a homotetramer of 22 kDa, reveals a functional role for this residue.	Manganese	95-104	superoxide dismutase 2	Homo sapiens	114-137
9537988-1	1998	Structural and biochemical characterization of the nonliganding residue glutamine 143 near the manganese of human Mn superoxide dismutase (hMnSOD), a homotetramer of 22 kDa, reveals a functional role for this residue.	Manganese	95-104	superoxide dismutase 2	Homo sapiens	139-145
9537988-3	1998	We have prepared the site-specific mutant of hMnSOD with the conservative replacement of Gln 143 --> Asn (Q143N).	Glutamine	89-92	superoxide dismutase 2	Homo sapiens	45-51
9537988-3	1998	We have prepared the site-specific mutant of hMnSOD with the conservative replacement of Gln 143 --> Asn (Q143N).	Asparagine	104-107	superoxide dismutase 2	Homo sapiens	45-51
9537988-10	1998	Also, unlike the wild-type Mn(III)SOD, which is electron paramagnetic resonance (EPR) silent, Q143N MnSOD has a complex EPR spectrum with many resonances in the region below 2250 G. We conclude that the Gln 143 --> Asn mutation has increased the reduction potential of manganese to stabilize Mn(II), indicating that Gln 143 has a substantial role in maintaining a reduction potential favorable for the oxidation and reduction cycles in the catalytic disproportionation of superoxide.	Glutamine	203-206	superoxide dismutase 2	Homo sapiens	100-105
9525927-6	1998	Overexpression of manganese superoxide dismutase reduced the levels of intracellular reactive oxygen species and calcium, restored mitochondrial transmembrane potential, and prevented cell death.	Reactive Oxygen Species	85-108	superoxide dismutase 2	Homo sapiens	18-48
9537988-10	1998	Also, unlike the wild-type Mn(III)SOD, which is electron paramagnetic resonance (EPR) silent, Q143N MnSOD has a complex EPR spectrum with many resonances in the region below 2250 G. We conclude that the Gln 143 --> Asn mutation has increased the reduction potential of manganese to stabilize Mn(II), indicating that Gln 143 has a substantial role in maintaining a reduction potential favorable for the oxidation and reduction cycles in the catalytic disproportionation of superoxide.	Asparagine	218-221	superoxide dismutase 2	Homo sapiens	100-105
9525927-6	1998	Overexpression of manganese superoxide dismutase reduced the levels of intracellular reactive oxygen species and calcium, restored mitochondrial transmembrane potential, and prevented cell death.	Calcium	113-120	superoxide dismutase 2	Homo sapiens	18-48
9537988-10	1998	Also, unlike the wild-type Mn(III)SOD, which is electron paramagnetic resonance (EPR) silent, Q143N MnSOD has a complex EPR spectrum with many resonances in the region below 2250 G. We conclude that the Gln 143 --> Asn mutation has increased the reduction potential of manganese to stabilize Mn(II), indicating that Gln 143 has a substantial role in maintaining a reduction potential favorable for the oxidation and reduction cycles in the catalytic disproportionation of superoxide.	Manganese	272-281	superoxide dismutase 2	Homo sapiens	100-105
9537988-10	1998	Also, unlike the wild-type Mn(III)SOD, which is electron paramagnetic resonance (EPR) silent, Q143N MnSOD has a complex EPR spectrum with many resonances in the region below 2250 G. We conclude that the Gln 143 --> Asn mutation has increased the reduction potential of manganese to stabilize Mn(II), indicating that Gln 143 has a substantial role in maintaining a reduction potential favorable for the oxidation and reduction cycles in the catalytic disproportionation of superoxide.	Manganese(2+)	295-301	superoxide dismutase 2	Homo sapiens	100-105
9537988-10	1998	Also, unlike the wild-type Mn(III)SOD, which is electron paramagnetic resonance (EPR) silent, Q143N MnSOD has a complex EPR spectrum with many resonances in the region below 2250 G. We conclude that the Gln 143 --> Asn mutation has increased the reduction potential of manganese to stabilize Mn(II), indicating that Gln 143 has a substantial role in maintaining a reduction potential favorable for the oxidation and reduction cycles in the catalytic disproportionation of superoxide.	Glutamine	319-322	superoxide dismutase 2	Homo sapiens	100-105
9537988-10	1998	Also, unlike the wild-type Mn(III)SOD, which is electron paramagnetic resonance (EPR) silent, Q143N MnSOD has a complex EPR spectrum with many resonances in the region below 2250 G. We conclude that the Gln 143 --> Asn mutation has increased the reduction potential of manganese to stabilize Mn(II), indicating that Gln 143 has a substantial role in maintaining a reduction potential favorable for the oxidation and reduction cycles in the catalytic disproportionation of superoxide.	Superoxides	475-485	superoxide dismutase 2	Homo sapiens	100-105
9537988-11	1998	A solvent hydrogen isotope effect near 2 for kcat in catalysis by Q143N hMnSOD indicates rate-contributing proton transfers to form product hydroperoxide anion or hydrogen peroxide.	Hydrogen	10-18	superoxide dismutase 2	Homo sapiens	72-78
9537988-11	1998	A solvent hydrogen isotope effect near 2 for kcat in catalysis by Q143N hMnSOD indicates rate-contributing proton transfers to form product hydroperoxide anion or hydrogen peroxide.	hydroperoxide anion	140-159	superoxide dismutase 2	Homo sapiens	72-78
9537988-11	1998	A solvent hydrogen isotope effect near 2 for kcat in catalysis by Q143N hMnSOD indicates rate-contributing proton transfers to form product hydroperoxide anion or hydrogen peroxide.	Hydrogen Peroxide	163-180	superoxide dismutase 2	Homo sapiens	72-78
9569045-10	1998	In addition to the high MnSOD activity, hydrogen peroxide scavenging antioxidant enzymes, glutathione and GST can partly explain the high hydrogen peroxide and epirubicin resistance of these cells in vitro.	Hydrogen Peroxide	138-155	superoxide dismutase 2	Homo sapiens	24-29
9569045-10	1998	In addition to the high MnSOD activity, hydrogen peroxide scavenging antioxidant enzymes, glutathione and GST can partly explain the high hydrogen peroxide and epirubicin resistance of these cells in vitro.	Epirubicin	160-170	superoxide dismutase 2	Homo sapiens	24-29
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	Hydrogen Peroxide	85-89	superoxide dismutase 2	Homo sapiens	195-200
9649709-1	1998	In recent studies, decreased expression of Mn SOD, an intramitochondrial enzyme responsible for the dismutation of anion superoxide, has been reported in multiple, malignant cell types, whereas its gene has been proposed as a tumour suppressor gene in melanoma.	anion superoxide	115-131	superoxide dismutase 2	Homo sapiens	43-49
9535218-2	1998	We found that induction of apoptosis in Mphi by oxLDL, C2-ceramide, tumor necrosis factor alpha (TNF-alpha), and hydrogen peroxide (H2O2) was associated with enhanced expression of manganese superoxide dismutase (MnSOD) and p53.	Hydrogen Peroxide	113-130	superoxide dismutase 2	Homo sapiens	181-211
9535218-2	1998	We found that induction of apoptosis in Mphi by oxLDL, C2-ceramide, tumor necrosis factor alpha (TNF-alpha), and hydrogen peroxide (H2O2) was associated with enhanced expression of manganese superoxide dismutase (MnSOD) and p53.	Hydrogen Peroxide	132-136	superoxide dismutase 2	Homo sapiens	181-211
9535218-2	1998	We found that induction of apoptosis in Mphi by oxLDL, C2-ceramide, tumor necrosis factor alpha (TNF-alpha), and hydrogen peroxide (H2O2) was associated with enhanced expression of manganese superoxide dismutase (MnSOD) and p53.	Hydrogen Peroxide	132-136	superoxide dismutase 2	Homo sapiens	213-218
9535218-3	1998	Treatment of cells with p53 or MnSOD antisense oligonucleotides prior to stimulation with oxLDL, C2-ceramide, TNF-alpha, or H2O2 caused an inhibition of the expression of the respective protein together with a marked reduction of apoptosis.	Oligonucleotides	47-63	superoxide dismutase 2	Homo sapiens	31-36
9535218-3	1998	Treatment of cells with p53 or MnSOD antisense oligonucleotides prior to stimulation with oxLDL, C2-ceramide, TNF-alpha, or H2O2 caused an inhibition of the expression of the respective protein together with a marked reduction of apoptosis.	N-acetylsphingosine	97-108	superoxide dismutase 2	Homo sapiens	31-36
9535218-3	1998	Treatment of cells with p53 or MnSOD antisense oligonucleotides prior to stimulation with oxLDL, C2-ceramide, TNF-alpha, or H2O2 caused an inhibition of the expression of the respective protein together with a marked reduction of apoptosis.	Hydrogen Peroxide	124-128	superoxide dismutase 2	Homo sapiens	31-36
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	Acetylcysteine	12-28	superoxide dismutase 2	Homo sapiens	195-200
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	N-acetylsphingosine	58-69	superoxide dismutase 2	Homo sapiens	195-200
9518260-10	1998	Subsequent thiol redox modulation studies showed that only the normal fibroblast cultures showed a potentiation of TNF-alpha-mediated MnSOD upregulation following GSH depletion.	Glutathione	163-166	superoxide dismutase 2	Homo sapiens	134-139
9651816-10	1998	Although the addition of 12-o-tetradecanoylphorbol-13-acetate (TPA) singly to the incubation medium had no effect on either Mn-, or Cu,Zn-SOD activity, it significantly augmented the IFN-gamma-dependent induction of Mn-SOD activity by anti-Fas antibody or by TNF-alpha.	Tetradecanoylphorbol Acetate	25-61	superoxide dismutase 2	Homo sapiens	216-222
9651816-10	1998	Although the addition of 12-o-tetradecanoylphorbol-13-acetate (TPA) singly to the incubation medium had no effect on either Mn-, or Cu,Zn-SOD activity, it significantly augmented the IFN-gamma-dependent induction of Mn-SOD activity by anti-Fas antibody or by TNF-alpha.	Tetradecanoylphorbol Acetate	63-66	superoxide dismutase 2	Homo sapiens	216-222
9559871-2	1998	The antioxidant enzymes manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), and glutathione peroxidase (GPx), are key intracellular antioxidants in the metabolism of ROS.	Reactive Oxygen Species	198-201	superoxide dismutase 2	Homo sapiens	24-54
9559871-2	1998	The antioxidant enzymes manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), and glutathione peroxidase (GPx), are key intracellular antioxidants in the metabolism of ROS.	Reactive Oxygen Species	198-201	superoxide dismutase 2	Homo sapiens	56-61
9559871-6	1998	The results suggested that MnSOD may play a central role in protecting cells against reactive oxygen species injury during ionizing radiation exposure among MnSOD, CuZnSOD, and GPx.	Reactive Oxygen Species	85-108	superoxide dismutase 2	Homo sapiens	27-32
9518260-8	1998	Proliferative growth levels of mitochondrial (Mn)SOD activities showed an activity spectrum ranging from lowest activity in AIDS-KS cells, to intermediate levels in matched, nonlesional cells from the AIDS-KS donors, to highest activities in HIV normal fibroblasts.	Potassium	129-131	superoxide dismutase 2	Homo sapiens	49-52
9518260-8	1998	Proliferative growth levels of mitochondrial (Mn)SOD activities showed an activity spectrum ranging from lowest activity in AIDS-KS cells, to intermediate levels in matched, nonlesional cells from the AIDS-KS donors, to highest activities in HIV normal fibroblasts.	Potassium	206-208	superoxide dismutase 2	Homo sapiens	49-52
9518260-9	1998	In contrast, following TNF-alpha challenge, the AIDS-KS and KS donor nonlesional cells showed a 11.89- and 5.86-fold respective increase in MnSOD activity, while the normal fibroblasts demonstrated a 1.35-fold decrease.	Potassium	53-55	superoxide dismutase 2	Homo sapiens	140-145
9651816-11	1998	The protein kinase C inhibitor, 1-(5-isoquinoline-sulfonyl)-2-methyl piperazine dihydrochloride (H-7), significantly inhibited the TPA-dependent increase in Mn-SOD activity.	1-(5-isoquinoline-sulfonyl)-2-methyl piperazine dihydrochloride	32-95	superoxide dismutase 2	Homo sapiens	157-163
9651816-11	1998	The protein kinase C inhibitor, 1-(5-isoquinoline-sulfonyl)-2-methyl piperazine dihydrochloride (H-7), significantly inhibited the TPA-dependent increase in Mn-SOD activity.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	97-100	superoxide dismutase 2	Homo sapiens	157-163
9651816-11	1998	The protein kinase C inhibitor, 1-(5-isoquinoline-sulfonyl)-2-methyl piperazine dihydrochloride (H-7), significantly inhibited the TPA-dependent increase in Mn-SOD activity.	Tetradecanoylphorbol Acetate	131-134	superoxide dismutase 2	Homo sapiens	157-163
9518260-11	1998	In addition, provision of the GSH precursor, N-acetylcysteine during TNF-alpha challenge only diminished MnSOD activity and mitochondrial compartmentalization in the AIDS-KS cells, a finding that likely reflects the lower levels of reduced thiols in this cellular population.	Glutathione	30-33	superoxide dismutase 2	Homo sapiens	105-110
9518260-11	1998	In addition, provision of the GSH precursor, N-acetylcysteine during TNF-alpha challenge only diminished MnSOD activity and mitochondrial compartmentalization in the AIDS-KS cells, a finding that likely reflects the lower levels of reduced thiols in this cellular population.	Acetylcysteine	45-61	superoxide dismutase 2	Homo sapiens	105-110
12174293-3	1998	Manganese superoxide dismutase (MnSOD) is a mitochondrial antioxidant enzyme involved in scavenging O(2)(-).	Superoxides	100-104	superoxide dismutase 2	Homo sapiens	32-37
9425011-4	1998	In cultured pheochromocytoma PC6 cells, overexpression of mitochondria-localized MnSOD prevented apoptosis induced by Fe2+, amyloid beta-peptide (Abeta), and nitric oxide-generating agents.	ammonium ferrous sulfate	118-122	superoxide dismutase 2	Homo sapiens	81-86
9425011-4	1998	In cultured pheochromocytoma PC6 cells, overexpression of mitochondria-localized MnSOD prevented apoptosis induced by Fe2+, amyloid beta-peptide (Abeta), and nitric oxide-generating agents.	Nitric Oxide	158-170	superoxide dismutase 2	Homo sapiens	81-86
9425011-5	1998	Accumulations of peroxynitrite, nitrated proteins, and the membrane lipid peroxidation product 4-hydroxynonenal (HNE) after exposure to the apoptotic insults were markedly attenuated in cells expressing MnSOD.	Peroxynitrous Acid	17-30	superoxide dismutase 2	Homo sapiens	203-208
9425011-5	1998	Accumulations of peroxynitrite, nitrated proteins, and the membrane lipid peroxidation product 4-hydroxynonenal (HNE) after exposure to the apoptotic insults were markedly attenuated in cells expressing MnSOD.	4-hydroxy-2-nonenal	95-111	superoxide dismutase 2	Homo sapiens	203-208
9425011-6	1998	Glutathione peroxidase activity levels were increased in cells overexpressing MnSOD, suggesting a compensatory response to increased H2O2 levels.	Hydrogen Peroxide	133-137	superoxide dismutase 2	Homo sapiens	78-83
9519816-3	1998	However, the sensitivity of HeLa cells against methylmercury was decreased by overexpression of Mn-SOD, an enzyme localized in matrix of mitochondria and which decomposes superoxide anions.	Superoxides	171-188	superoxide dismutase 2	Homo sapiens	96-102
9633023-6	1998	N-terminal sequencing was performed on the prominent band at approximately 23 kDa, showing it to be manganese superoxide dismutase (MnSOD), a mitochondrial enzyme responsible for protection against oxygen free radical-associated cellular damage.	oxygen free radical	198-217	superoxide dismutase 2	Homo sapiens	100-130
9633023-6	1998	N-terminal sequencing was performed on the prominent band at approximately 23 kDa, showing it to be manganese superoxide dismutase (MnSOD), a mitochondrial enzyme responsible for protection against oxygen free radical-associated cellular damage.	oxygen free radical	198-217	superoxide dismutase 2	Homo sapiens	132-137
9638637-0	1998	Induction of manganese superoxide dismutase gene expression in bronchoepithelial cells after rockwool exposure.	rockwool	93-101	superoxide dismutase 2	Homo sapiens	13-43
9638637-8	1998	However, at > 25 micrograms/cm2 MnSOD mRNA levels in silica- and crocidolite- but not in rockwool-exposed cells decreased.	Silicon Dioxide	56-62	superoxide dismutase 2	Homo sapiens	35-40
9638637-11	1998	Because oxidants (H2O2) and crocidolite fibers were shown to reduce SOD activity, lack of active MnSOD protein may be caused by inactivation on a post-translational level.	Hydrogen Peroxide	18-22	superoxide dismutase 2	Homo sapiens	68-71
9638637-13	1998	In conclusion, rockwool was demonstrated to induce MnSOD gene expression, perhaps because of its pro-oxidative effect in bronchoepithelial cells.	rockwool	15-23	superoxide dismutase 2	Homo sapiens	51-56
12174293-5	1998	The eukaryotic expressing vector, pHbetaAPr-3p-neo, containing sense and antisense human MnSOD cDNA have been introduced into Chinese hamster ovary (CHO) cells respectively by gene transfection method and the MnSOD overexpressing cell lines have been used in this study.	phbetaapr-3p-neo	34-50	superoxide dismutase 2	Homo sapiens	89-94
12174293-5	1998	The eukaryotic expressing vector, pHbetaAPr-3p-neo, containing sense and antisense human MnSOD cDNA have been introduced into Chinese hamster ovary (CHO) cells respectively by gene transfection method and the MnSOD overexpressing cell lines have been used in this study.	phbetaapr-3p-neo	34-50	superoxide dismutase 2	Homo sapiens	209-214
9434740-3	1997	We investigated the contribution of the individual transcription factors by using antioxidants and metal chelators to modulate MnSOD transcriptional activation in response to phorbol esters or hydrogen peroxide.	Metals	99-104	superoxide dismutase 2	Homo sapiens	127-132
9434740-3	1997	We investigated the contribution of the individual transcription factors by using antioxidants and metal chelators to modulate MnSOD transcriptional activation in response to phorbol esters or hydrogen peroxide.	Phorbol Esters	175-189	superoxide dismutase 2	Homo sapiens	127-132
9434740-5	1997	The metal chelator and antioxidant pyrrolidine dithiocarbamate (PDTC) at 60 or 100 microM induced the MnSOD transcript in HeLa cells while diminishing expression of the NF kappa B-responsive transcript I kappa B-alpha.	pyrrolidine dithiocarbamic acid	64-68	superoxide dismutase 2	Homo sapiens	102-107
9434740-3	1997	We investigated the contribution of the individual transcription factors by using antioxidants and metal chelators to modulate MnSOD transcriptional activation in response to phorbol esters or hydrogen peroxide.	Hydrogen Peroxide	193-210	superoxide dismutase 2	Homo sapiens	127-132
9434740-6	1997	Induction of the MnSOD mRNA by phorbol-12-myristate-13-acetate (PMA) was only slightly diminished in the presence of PDTC, which in contrast virtually eliminated induction of the NF kappa B-dependent transcript I kappa B-alpha by PMA.	Tetradecanoylphorbol Acetate	31-62	superoxide dismutase 2	Homo sapiens	17-22
9434740-6	1997	Induction of the MnSOD mRNA by phorbol-12-myristate-13-acetate (PMA) was only slightly diminished in the presence of PDTC, which in contrast virtually eliminated induction of the NF kappa B-dependent transcript I kappa B-alpha by PMA.	Tetradecanoylphorbol Acetate	64-67	superoxide dismutase 2	Homo sapiens	17-22
9434740-5	1997	The metal chelator and antioxidant pyrrolidine dithiocarbamate (PDTC) at 60 or 100 microM induced the MnSOD transcript in HeLa cells while diminishing expression of the NF kappa B-responsive transcript I kappa B-alpha.	Metals	4-9	superoxide dismutase 2	Homo sapiens	102-107
9434740-6	1997	Induction of the MnSOD mRNA by phorbol-12-myristate-13-acetate (PMA) was only slightly diminished in the presence of PDTC, which in contrast virtually eliminated induction of the NF kappa B-dependent transcript I kappa B-alpha by PMA.	pyrrolidine dithiocarbamic acid	117-121	superoxide dismutase 2	Homo sapiens	17-22
9434740-5	1997	The metal chelator and antioxidant pyrrolidine dithiocarbamate (PDTC) at 60 or 100 microM induced the MnSOD transcript in HeLa cells while diminishing expression of the NF kappa B-responsive transcript I kappa B-alpha.	pyrrolidine dithiocarbamic acid	35-62	superoxide dismutase 2	Homo sapiens	102-107
9434740-7	1997	MnSOD RNA induction by H2O2 was only approximately 1.5-fold, compared to a ca.	Hydrogen Peroxide	23-27	superoxide dismutase 2	Homo sapiens	0-5
9434740-10	1997	In vitro DNA binding studies confirmed strong AP-1 activation under conditions where NF kappa B is blocked but the MnSOD transcript is strongly induced (e.g., PMA treatment in the presence of PDTC).	Tetradecanoylphorbol Acetate	159-162	superoxide dismutase 2	Homo sapiens	115-120
9409558-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that dismutates potentially toxic superoxide radical into hydrogen peroxide and dioxygen.	Superoxides	99-117	superoxide dismutase 2	Homo sapiens	0-30
9409558-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that dismutates potentially toxic superoxide radical into hydrogen peroxide and dioxygen.	Superoxides	99-117	superoxide dismutase 2	Homo sapiens	32-37
9409558-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that dismutates potentially toxic superoxide radical into hydrogen peroxide and dioxygen.	Hydrogen Peroxide	123-140	superoxide dismutase 2	Homo sapiens	0-30
9409558-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that dismutates potentially toxic superoxide radical into hydrogen peroxide and dioxygen.	Hydrogen Peroxide	123-140	superoxide dismutase 2	Homo sapiens	32-37
9409558-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that dismutates potentially toxic superoxide radical into hydrogen peroxide and dioxygen.	Oxygen	145-153	superoxide dismutase 2	Homo sapiens	0-30
9409558-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that dismutates potentially toxic superoxide radical into hydrogen peroxide and dioxygen.	Oxygen	145-153	superoxide dismutase 2	Homo sapiens	32-37
9409558-6	1997	Elevation of MnSOD mRNA by TRX was inhibited by actinomycin D, but not cycloheximide, occurring both in cell lines and primary human lung microvascular endothelial cells.	Dactinomycin	48-61	superoxide dismutase 2	Homo sapiens	13-18
9409558-8	1997	Thiol oxidation by diamide or alkylation by chlorodinitrobenzene inhibited MnSOD induction, further indicating a requirement for reduced TRX.	Sulfhydryl Compounds	0-5	superoxide dismutase 2	Homo sapiens	75-80
9409558-8	1997	Thiol oxidation by diamide or alkylation by chlorodinitrobenzene inhibited MnSOD induction, further indicating a requirement for reduced TRX.	Diamide	19-26	superoxide dismutase 2	Homo sapiens	75-80
9409558-8	1997	Thiol oxidation by diamide or alkylation by chlorodinitrobenzene inhibited MnSOD induction, further indicating a requirement for reduced TRX.	Dinitrochlorobenzene	44-64	superoxide dismutase 2	Homo sapiens	75-80
9427324-4	1997	The NO donor sodium nitroprusside dose-dependently increased Mn-SOD-like immunoreactivity in NIL-pretreated BV-2 cells.	Nitroprusside	13-33	superoxide dismutase 2	Homo sapiens	61-67
9371723-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that scavenges superoxide (O2-) ions.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
9371723-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that scavenges superoxide (O2-) ions.	Superoxides	92-94	superoxide dismutase 2	Homo sapiens	0-30
9371723-1	1997	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that scavenges superoxide (O2-) ions.	Superoxides	92-94	superoxide dismutase 2	Homo sapiens	32-37
9409551-5	1997	In HHL rabbits, MnSOD activity and GSH concentration were significantly increased in atherosclerotic intima compared to the media of the aorta, but significantly decreased (P<0.01) in larger plaques compared with smaller ones, resulting in a significant inverse correlation of MnSOD activity (r=-0.67, P<0.001) and GSH concentration (r=-0.57, P<0.01) with plaque size.	Glutathione	321-324	superoxide dismutase 2	Homo sapiens	16-21
9498574-5	1997	Pretreatment with tumor necrosis factor (TNF) or phorbol ester (TPA), which increases the Mn-SOD level, prevented the apoptosis.	Phorbol Esters	49-62	superoxide dismutase 2	Homo sapiens	90-96
9498574-5	1997	Pretreatment with tumor necrosis factor (TNF) or phorbol ester (TPA), which increases the Mn-SOD level, prevented the apoptosis.	Tetradecanoylphorbol Acetate	64-67	superoxide dismutase 2	Homo sapiens	90-96
9394806-1	1997	Endogenous tumor necrosis factor (enTNF) acts as a resistance factor against cytotoxicity caused by heat by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	reactive oxygen free radicals	176-205	superoxide dismutase 2	Homo sapiens	117-147
9394806-1	1997	Endogenous tumor necrosis factor (enTNF) acts as a resistance factor against cytotoxicity caused by heat by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	reactive oxygen free radicals	176-205	superoxide dismutase 2	Homo sapiens	149-154
9335256-5	1997	Levels of manganese superoxide dismutase (Mn-SOD) in neurons were increased following exposure of cultures to TNFalpha and ceramide in control cultures, but not in cultures cotreated with kappaB decoy DNA.	Ceramides	123-131	superoxide dismutase 2	Homo sapiens	10-40
9372618-5	1997	Interestingly, genistein, a soy isoflavone and a tyrosine kinase inhibitor, was able to inhibit the induction of Mn-SOD activity and mRNA expression by TNF-alpha.	Genistein	15-24	superoxide dismutase 2	Homo sapiens	113-119
9372618-5	1997	Interestingly, genistein, a soy isoflavone and a tyrosine kinase inhibitor, was able to inhibit the induction of Mn-SOD activity and mRNA expression by TNF-alpha.	Isoflavones	32-42	superoxide dismutase 2	Homo sapiens	113-119
9371904-3	1997	We used a novel polymorphic mutation at -9 position of the signal peptide of the Mn SOD precursor protein, which caused valine to alanine substitution.	Valine	120-126	superoxide dismutase 2	Homo sapiens	81-87
9371904-3	1997	We used a novel polymorphic mutation at -9 position of the signal peptide of the Mn SOD precursor protein, which caused valine to alanine substitution.	Alanine	130-137	superoxide dismutase 2	Homo sapiens	81-87
9335256-5	1997	Levels of manganese superoxide dismutase (Mn-SOD) in neurons were increased following exposure of cultures to TNFalpha and ceramide in control cultures, but not in cultures cotreated with kappaB decoy DNA.	Ceramides	123-131	superoxide dismutase 2	Homo sapiens	42-48
9288180-1	1997	BACKGROUND: Antioxidant enzymes (AEs), which catalyze the conversion of reactive oxygen species (ROS) to water, include catalase (CAT), manganese-containing superoxide dismutase (MnSOD), and copper and zinc-containing superoxide dismutase (CuZnSOD).	Water	105-110	superoxide dismutase 2	Homo sapiens	179-184
9223372-4	1997	This expression system was used to study the effects of paraquat and menadione, two intracellular superoxide generators, on processing of precursor hMn-SOD by insect mitochondria.	Paraquat	56-64	superoxide dismutase 2	Homo sapiens	148-155
9288180-1	1997	BACKGROUND: Antioxidant enzymes (AEs), which catalyze the conversion of reactive oxygen species (ROS) to water, include catalase (CAT), manganese-containing superoxide dismutase (MnSOD), and copper and zinc-containing superoxide dismutase (CuZnSOD).	aes	33-36	superoxide dismutase 2	Homo sapiens	136-177
9288180-1	1997	BACKGROUND: Antioxidant enzymes (AEs), which catalyze the conversion of reactive oxygen species (ROS) to water, include catalase (CAT), manganese-containing superoxide dismutase (MnSOD), and copper and zinc-containing superoxide dismutase (CuZnSOD).	aes	33-36	superoxide dismutase 2	Homo sapiens	179-184
9288180-1	1997	BACKGROUND: Antioxidant enzymes (AEs), which catalyze the conversion of reactive oxygen species (ROS) to water, include catalase (CAT), manganese-containing superoxide dismutase (MnSOD), and copper and zinc-containing superoxide dismutase (CuZnSOD).	Reactive Oxygen Species	72-95	superoxide dismutase 2	Homo sapiens	179-184
9288180-1	1997	BACKGROUND: Antioxidant enzymes (AEs), which catalyze the conversion of reactive oxygen species (ROS) to water, include catalase (CAT), manganese-containing superoxide dismutase (MnSOD), and copper and zinc-containing superoxide dismutase (CuZnSOD).	Reactive Oxygen Species	97-100	superoxide dismutase 2	Homo sapiens	179-184
9271329-9	1997	The increased activity of antioxidant enzymes in the resistant cell lines (in particular MnSOD) strongly suggests that reactive oxygen species are, in large part, responsible for the toxicity of TPZ under aerobic conditions, and is consistent with aerobic and hypoxic drug cytotoxicity resulting from different mechanisms.	Reactive Oxygen Species	119-142	superoxide dismutase 2	Homo sapiens	89-94
9271329-9	1997	The increased activity of antioxidant enzymes in the resistant cell lines (in particular MnSOD) strongly suggests that reactive oxygen species are, in large part, responsible for the toxicity of TPZ under aerobic conditions, and is consistent with aerobic and hypoxic drug cytotoxicity resulting from different mechanisms.	Tirapazamine	195-198	superoxide dismutase 2	Homo sapiens	89-94
9223372-4	1997	This expression system was used to study the effects of paraquat and menadione, two intracellular superoxide generators, on processing of precursor hMn-SOD by insect mitochondria.	Vitamin K 3	69-78	superoxide dismutase 2	Homo sapiens	148-155
9223372-4	1997	This expression system was used to study the effects of paraquat and menadione, two intracellular superoxide generators, on processing of precursor hMn-SOD by insect mitochondria.	Superoxides	98-108	superoxide dismutase 2	Homo sapiens	148-155
9223372-5	1997	Paraquat was found to potently inhibit mitochondrial processing of hMn-SOD, leading to the accumulation of precursor hMn-SOD and a decrease in measurable Mn-SOD activity.	Paraquat	0-8	superoxide dismutase 2	Homo sapiens	67-74
9223372-5	1997	Paraquat was found to potently inhibit mitochondrial processing of hMn-SOD, leading to the accumulation of precursor hMn-SOD and a decrease in measurable Mn-SOD activity.	Paraquat	0-8	superoxide dismutase 2	Homo sapiens	117-124
9223372-5	1997	Paraquat was found to potently inhibit mitochondrial processing of hMn-SOD, leading to the accumulation of precursor hMn-SOD and a decrease in measurable Mn-SOD activity.	Paraquat	0-8	superoxide dismutase 2	Homo sapiens	68-74
9109515-2	1997	The 24-h treatment with S-nitroso-N-acetylpenicillamine (SNAP), a NO donor, decreased the activities and the protein levels of catalase, GPX, and Mn-SOD in a dose-dependent manner.	S-Nitroso-N-Acetylpenicillamine	24-55	superoxide dismutase 2	Homo sapiens	146-152
9211496-6	1997	Elevated serum MnSOD correlated with peripheral plasma markers of lipid peroxidation (malondialdehyde) and neutrophil activation (myeloperoxidase) and was associated with decreased plasma ascorbic acid concentrations.	Malondialdehyde	86-101	superoxide dismutase 2	Homo sapiens	15-20
9211496-6	1997	Elevated serum MnSOD correlated with peripheral plasma markers of lipid peroxidation (malondialdehyde) and neutrophil activation (myeloperoxidase) and was associated with decreased plasma ascorbic acid concentrations.	Ascorbic Acid	188-201	superoxide dismutase 2	Homo sapiens	15-20
9109515-2	1997	The 24-h treatment with S-nitroso-N-acetylpenicillamine (SNAP), a NO donor, decreased the activities and the protein levels of catalase, GPX, and Mn-SOD in a dose-dependent manner.	S-Nitroso-N-Acetylpenicillamine	57-61	superoxide dismutase 2	Homo sapiens	146-152
9088787-0	1997	Time course of manganese superoxide dismutase concentrations in serum of alcohol-dependent patients during abstinence.	Alcohols	73-80	superoxide dismutase 2	Homo sapiens	15-45
9116291-1	1997	We have previously reported that intracellular tumor necrosis factor (enTNF) is responsible for resistance, in established cell lines to doxorubicin (DOX), exogenous TNF, and heat stress by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	Doxorubicin	137-148	superoxide dismutase 2	Homo sapiens	199-229
9116291-1	1997	We have previously reported that intracellular tumor necrosis factor (enTNF) is responsible for resistance, in established cell lines to doxorubicin (DOX), exogenous TNF, and heat stress by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	Doxorubicin	137-148	superoxide dismutase 2	Homo sapiens	231-236
9116291-1	1997	We have previously reported that intracellular tumor necrosis factor (enTNF) is responsible for resistance, in established cell lines to doxorubicin (DOX), exogenous TNF, and heat stress by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	Doxorubicin	150-153	superoxide dismutase 2	Homo sapiens	199-229
9116291-1	1997	We have previously reported that intracellular tumor necrosis factor (enTNF) is responsible for resistance, in established cell lines to doxorubicin (DOX), exogenous TNF, and heat stress by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	Doxorubicin	150-153	superoxide dismutase 2	Homo sapiens	231-236
9116291-1	1997	We have previously reported that intracellular tumor necrosis factor (enTNF) is responsible for resistance, in established cell lines to doxorubicin (DOX), exogenous TNF, and heat stress by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	reactive oxygen free radicals	258-287	superoxide dismutase 2	Homo sapiens	199-229
9116291-1	1997	We have previously reported that intracellular tumor necrosis factor (enTNF) is responsible for resistance, in established cell lines to doxorubicin (DOX), exogenous TNF, and heat stress by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals.	reactive oxygen free radicals	258-287	superoxide dismutase 2	Homo sapiens	231-236
9116291-3	1997	Sensitivity to DOX and the expression of enTNF or MnSOD activity were inversely correlated.	Doxorubicin	15-18	superoxide dismutase 2	Homo sapiens	50-55
9095410-5	1997	Soft agar assays demonstrated that the clonogenic fractions of high-expressing MnSOD clones were dramatically reduced.	Agar	5-9	superoxide dismutase 2	Homo sapiens	79-84
9067545-0	1997	Manganese superoxide dismutase expression inhibits soft agar growth in JB6 clone41 mouse epidermal cells.	Agar	56-60	superoxide dismutase 2	Homo sapiens	0-30
9067545-4	1997	Compared with the parental and vector-transfected (gpt) control cells, MnSOD-overexpressing cells had a slower growth rate and their ability to form colonies in soft agar was significantly decreased in response to 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment.	Tetradecanoylphorbol Acetate	214-250	superoxide dismutase 2	Homo sapiens	71-76
9067545-4	1997	Compared with the parental and vector-transfected (gpt) control cells, MnSOD-overexpressing cells had a slower growth rate and their ability to form colonies in soft agar was significantly decreased in response to 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment.	Tetradecanoylphorbol Acetate	252-255	superoxide dismutase 2	Homo sapiens	71-76
9067545-6	1997	Overexpression of MnSOD led to a significant decrease in c-jun and c-fos expression in response to treatment with TPA or the oxidant promoter superoxide.	Tetradecanoylphorbol Acetate	114-117	superoxide dismutase 2	Homo sapiens	18-23
9067545-6	1997	Overexpression of MnSOD led to a significant decrease in c-jun and c-fos expression in response to treatment with TPA or the oxidant promoter superoxide.	Superoxides	142-152	superoxide dismutase 2	Homo sapiens	18-23
9067545-8	1997	A possible mechanism is that elevated MnSOD expression might change the intracellular redox state by altering the balance of reactive oxygen species.	Reactive Oxygen Species	125-148	superoxide dismutase 2	Homo sapiens	38-43
8899800-2	1996	In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD).	Doxorubicin	146-156	superoxide dismutase 2	Homo sapiens	238-268
8903482-1	1996	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme involved in scavenging O2-.	Oxygen	88-90	superoxide dismutase 2	Homo sapiens	0-30
8903482-1	1996	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme involved in scavenging O2-.	Oxygen	88-90	superoxide dismutase 2	Homo sapiens	32-37
8903482-6	1996	Pre-treatment with either actinomycin D or cycloheximide inhibited the induction of MnSOD mRNA by OK432.	Dactinomycin	26-39	superoxide dismutase 2	Homo sapiens	84-89
8903482-6	1996	Pre-treatment with either actinomycin D or cycloheximide inhibited the induction of MnSOD mRNA by OK432.	Cycloheximide	43-56	superoxide dismutase 2	Homo sapiens	84-89
8895350-0	1996	Protection from nicotinamide inhibition of interleukin-1 beta-induced RIN cell nitric oxide formation is associated with induction of MnSOD enzyme activity.	Niacinamide	16-28	superoxide dismutase 2	Homo sapiens	134-139
9038914-3	1997	Investigation of Mn-SOD and Cu,Zn-SOD activities revealed that the lower SOD activity in asthmatics -CS was because of decreased Cu,Zn-SOD activity.	Cesium	101-103	superoxide dismutase 2	Homo sapiens	17-23
9215812-8	1997	MnSOD protects against TNF by decreasing O2- attack on [4Fe-4S] clusters and thus lowering free iron.	Iron	96-100	superoxide dismutase 2	Homo sapiens	0-5
8913477-1	1996	The oxygen free-radical scavenger recombinant human manganese superoxide dismutase (MnSOD) was studied for its effects on influenza virus infections in mice when used alone and in combination with ribavirin.	Oxygen	4-10	superoxide dismutase 2	Homo sapiens	52-82
8913477-1	1996	The oxygen free-radical scavenger recombinant human manganese superoxide dismutase (MnSOD) was studied for its effects on influenza virus infections in mice when used alone and in combination with ribavirin.	Oxygen	4-10	superoxide dismutase 2	Homo sapiens	84-89
8899800-2	1996	In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD).	Doxorubicin	146-156	superoxide dismutase 2	Homo sapiens	270-275
8899800-2	1996	In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD).	Doxorubicin	158-161	superoxide dismutase 2	Homo sapiens	238-268
8899800-2	1996	In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD).	Doxorubicin	158-161	superoxide dismutase 2	Homo sapiens	270-275
8899800-2	1996	In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD).	oxygen free radicals	198-218	superoxide dismutase 2	Homo sapiens	238-268
8899800-2	1996	In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD).	oxygen free radicals	198-218	superoxide dismutase 2	Homo sapiens	270-275
8876227-6	1996	Immunoprecipitation and amino acid sequencing techniques identified manganese superoxide dismutase, the major antioxidant enzyme in mitochondria, as one of the targets of tyrosine nitration.	Tyrosine	171-179	superoxide dismutase 2	Homo sapiens	68-98
8918266-1	1996	By utilizing the oxygen-sensitive Escherichia coli Mn-superoxide dismutase (Mn-SOD) promoter, we have developed a vector system that expresses high levels of cloned foreign genes.	Oxygen	17-23	superoxide dismutase 2	Homo sapiens	76-82
8876227-8	1996	Exposure of recombinant human manganese superoxide dismutase to peroxynitrite resulted in a dose-dependent (IC50 = 10 microM) decrease in enzymatic activity and concomitant increase in tyrosine nitration.	Peroxynitrous Acid	64-77	superoxide dismutase 2	Homo sapiens	30-60
8876227-8	1996	Exposure of recombinant human manganese superoxide dismutase to peroxynitrite resulted in a dose-dependent (IC50 = 10 microM) decrease in enzymatic activity and concomitant increase in tyrosine nitration.	Tyrosine	185-193	superoxide dismutase 2	Homo sapiens	30-60
8876227-10	1996	In addition, inactivation of manganese superoxide dismutase by peroxynitrite may represent a general mechanism that progressively increases the production of peroxynitrite, leading to irreversible oxidative injury to mitochondria.	Peroxynitrous Acid	63-76	superoxide dismutase 2	Homo sapiens	29-59
8876227-10	1996	In addition, inactivation of manganese superoxide dismutase by peroxynitrite may represent a general mechanism that progressively increases the production of peroxynitrite, leading to irreversible oxidative injury to mitochondria.	Peroxynitrous Acid	158-171	superoxide dismutase 2	Homo sapiens	29-59
8897928-2	1996	After exposure to norepinephrine (NE; 0.2 microM) for 24 h, the manganese superoxide dismutase (Mn-SOD) content and activity in the cells were increased from 0.61 +/- 0.03 to 0.87 +/- 0.04 microgram/dish and 22 +/- 1 to 55 +/- 4 U/dish, respectively.	Norepinephrine	18-32	superoxide dismutase 2	Homo sapiens	64-94
8897928-2	1996	After exposure to norepinephrine (NE; 0.2 microM) for 24 h, the manganese superoxide dismutase (Mn-SOD) content and activity in the cells were increased from 0.61 +/- 0.03 to 0.87 +/- 0.04 microgram/dish and 22 +/- 1 to 55 +/- 4 U/dish, respectively.	Norepinephrine	18-32	superoxide dismutase 2	Homo sapiens	96-102
8897928-4	1996	Prazosin (2 microM) abolished the increase in Mn-SOD activity (U/mg total protein).	Prazosin	0-8	superoxide dismutase 2	Homo sapiens	46-52
8897928-6	1996	When antisense oligodeoxyribonucleotides to Mn-SOD were added to myocyte cultures, the increase in Mn-SOD activity (U/mg total protein) and the attenuation of CK release after the addition of NE in the presence of propranolol and yohimbine were not observed.	Oligodeoxyribonucleotides	15-40	superoxide dismutase 2	Homo sapiens	44-50
8897928-6	1996	When antisense oligodeoxyribonucleotides to Mn-SOD were added to myocyte cultures, the increase in Mn-SOD activity (U/mg total protein) and the attenuation of CK release after the addition of NE in the presence of propranolol and yohimbine were not observed.	Oligodeoxyribonucleotides	15-40	superoxide dismutase 2	Homo sapiens	99-105
8897928-6	1996	When antisense oligodeoxyribonucleotides to Mn-SOD were added to myocyte cultures, the increase in Mn-SOD activity (U/mg total protein) and the attenuation of CK release after the addition of NE in the presence of propranolol and yohimbine were not observed.	Propranolol	214-225	superoxide dismutase 2	Homo sapiens	44-50
8897928-6	1996	When antisense oligodeoxyribonucleotides to Mn-SOD were added to myocyte cultures, the increase in Mn-SOD activity (U/mg total protein) and the attenuation of CK release after the addition of NE in the presence of propranolol and yohimbine were not observed.	Yohimbine	230-239	superoxide dismutase 2	Homo sapiens	44-50
8806673-5	1996	We here identify diallelic polymorphism (Ala-9Val) in the MTS of human MnSOD in a Japanese population.	ala-9val	41-49	superoxide dismutase 2	Homo sapiens	71-76
8702551-3	1996	Mn-SOD is a nuclear-encoded mitochondrial matrix protein and serves a protective function by detoxifying superoxide.	Superoxides	105-115	superoxide dismutase 2	Homo sapiens	0-6
8702551-8	1996	The effect of Mn-SOD overexpression on IL-1alpha expression can be overcome by treatment with the protein kinase C activator, phorbol 12-myristate 13-acetate.	Tetradecanoylphorbol Acetate	126-157	superoxide dismutase 2	Homo sapiens	14-20
8702551-10	1996	These findings indicate that both Mn-SOD and O2 may regulate the levels of a cellular oxidant involved in both basal and TNF-induced IL-1alpha expression, presumably superoxide.	Superoxides	166-176	superoxide dismutase 2	Homo sapiens	34-40
8755643-8	1996	However, the observed superoxide production rates are modulated by the variant induction of MnSOD which decreases the rates, sometimes below those seen in control fibroblast mitochondria.	Superoxides	22-32	superoxide dismutase 2	Homo sapiens	92-97
8663465-1	1996	The depletion of superoxide catalyzed by human manganese superoxide dismutase (MnSOD) was observed spectrophotometrically by measuring the absorbance of superoxide at 250-280 nm following pulse radiolysis and by stopped-flow spectrophotometry.	Superoxides	17-27	superoxide dismutase 2	Homo sapiens	47-77
8663465-1	1996	The depletion of superoxide catalyzed by human manganese superoxide dismutase (MnSOD) was observed spectrophotometrically by measuring the absorbance of superoxide at 250-280 nm following pulse radiolysis and by stopped-flow spectrophotometry.	Superoxides	17-27	superoxide dismutase 2	Homo sapiens	79-84
8663465-1	1996	The depletion of superoxide catalyzed by human manganese superoxide dismutase (MnSOD) was observed spectrophotometrically by measuring the absorbance of superoxide at 250-280 nm following pulse radiolysis and by stopped-flow spectrophotometry.	Superoxides	57-67	superoxide dismutase 2	Homo sapiens	79-84
8764104-1	1996	Manganese superoxide dismutase (MnSOD) is a superoxide anion scavenger located in mitochondria.	Superoxides	44-60	superoxide dismutase 2	Homo sapiens	0-30
8764104-1	1996	Manganese superoxide dismutase (MnSOD) is a superoxide anion scavenger located in mitochondria.	Superoxides	44-60	superoxide dismutase 2	Homo sapiens	32-37
8764104-2	1996	Increased expression of MnSOD can diminish oxygen radical-mediated injuries and the cytotoxic effects of tumor necrosis factor alpha, ionizing radiation, and certain chemotherapeutic agents.	Reactive Oxygen Species	43-57	superoxide dismutase 2	Homo sapiens	24-29
8665512-1	1996	Manganese superoxide dismutase (Mn-SOD) inactivates the radiation effect by removal of radiation-induced toxic superoxide radicals.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-38
8760145-2	1996	In this study, we tested the hypothesis that ROS are directly involved in the induction of the mitochondrial antioxidant manganese superoxide dismutase (MnSOD) and mediate the induction of MnSOD by tumor necrosis factor-alpha (TNF-alpha).	Reactive Oxygen Species	45-48	superoxide dismutase 2	Homo sapiens	153-158
8760145-2	1996	In this study, we tested the hypothesis that ROS are directly involved in the induction of the mitochondrial antioxidant manganese superoxide dismutase (MnSOD) and mediate the induction of MnSOD by tumor necrosis factor-alpha (TNF-alpha).	Reactive Oxygen Species	45-48	superoxide dismutase 2	Homo sapiens	189-194
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Acetylcysteine	80-99	superoxide dismutase 2	Homo sapiens	151-156
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Acetylcysteine	101-104	superoxide dismutase 2	Homo sapiens	151-156
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Masoprocol	110-135	superoxide dismutase 2	Homo sapiens	151-156
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Masoprocol	137-141	superoxide dismutase 2	Homo sapiens	151-156
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Reactive Oxygen Species	193-196	superoxide dismutase 2	Homo sapiens	151-156
8760145-4	1996	Treatment of H441 cells with the exogenous oxidants hydrogen peroxide (H2O2) and diamide increased MnSOD mRNA, supporting the hypothesis that ROS directly affect expression of MnSOD.	Hydrogen Peroxide	52-69	superoxide dismutase 2	Homo sapiens	99-104
8760145-4	1996	Treatment of H441 cells with the exogenous oxidants hydrogen peroxide (H2O2) and diamide increased MnSOD mRNA, supporting the hypothesis that ROS directly affect expression of MnSOD.	Hydrogen Peroxide	52-69	superoxide dismutase 2	Homo sapiens	176-181
8760145-4	1996	Treatment of H441 cells with the exogenous oxidants hydrogen peroxide (H2O2) and diamide increased MnSOD mRNA, supporting the hypothesis that ROS directly affect expression of MnSOD.	Hydrogen Peroxide	71-75	superoxide dismutase 2	Homo sapiens	99-104
8760145-4	1996	Treatment of H441 cells with the exogenous oxidants hydrogen peroxide (H2O2) and diamide increased MnSOD mRNA, supporting the hypothesis that ROS directly affect expression of MnSOD.	Hydrogen Peroxide	71-75	superoxide dismutase 2	Homo sapiens	176-181
8760145-4	1996	Treatment of H441 cells with the exogenous oxidants hydrogen peroxide (H2O2) and diamide increased MnSOD mRNA, supporting the hypothesis that ROS directly affect expression of MnSOD.	Diamide	81-88	superoxide dismutase 2	Homo sapiens	99-104
8760145-4	1996	Treatment of H441 cells with the exogenous oxidants hydrogen peroxide (H2O2) and diamide increased MnSOD mRNA, supporting the hypothesis that ROS directly affect expression of MnSOD.	Diamide	81-88	superoxide dismutase 2	Homo sapiens	176-181
8760145-4	1996	Treatment of H441 cells with the exogenous oxidants hydrogen peroxide (H2O2) and diamide increased MnSOD mRNA, supporting the hypothesis that ROS directly affect expression of MnSOD.	Reactive Oxygen Species	142-145	superoxide dismutase 2	Homo sapiens	99-104
8760145-4	1996	Treatment of H441 cells with the exogenous oxidants hydrogen peroxide (H2O2) and diamide increased MnSOD mRNA, supporting the hypothesis that ROS directly affect expression of MnSOD.	Reactive Oxygen Species	142-145	superoxide dismutase 2	Homo sapiens	176-181
8760145-5	1996	The temporal pattern of MnSOD induction differed for TNF-alpha and H2O2, suggesting distinct signaling pathways.	Hydrogen Peroxide	67-71	superoxide dismutase 2	Homo sapiens	24-29
8760145-10	1996	We conclude that ROS directly alter MnSOD expression and are involved in the induction of MnSOD by TNF-alpha.	Reactive Oxygen Species	17-20	superoxide dismutase 2	Homo sapiens	36-41
8760145-10	1996	We conclude that ROS directly alter MnSOD expression and are involved in the induction of MnSOD by TNF-alpha.	Reactive Oxygen Species	17-20	superoxide dismutase 2	Homo sapiens	90-95
8665527-8	1996	A possible mechanism is that overexpression of MnSOD might alter the intracellular redox state by modulation of the balance of reactive oxygen species.	Reactive Oxygen Species	127-150	superoxide dismutase 2	Homo sapiens	47-52
8602839-1	1996	Human manganese-containing superoxide dismutase (MnSOD) is a nuclear encoded mitochondrial protein that scavenges potentially toxic superoxide radicals by dismuting O2- to O2 plus H2O2.	Superoxides	27-37	superoxide dismutase 2	Homo sapiens	49-54
8817062-4	1996	Similarly MnSOD specific activity was increased by TNF (290% increase) and the amosite+TNF combination (313% increase) but not by amosite alone.	Asbestos, Amosite	79-86	superoxide dismutase 2	Homo sapiens	10-15
8817062-4	1996	Similarly MnSOD specific activity was increased by TNF (290% increase) and the amosite+TNF combination (313% increase) but not by amosite alone.	Asbestos, Amosite	130-137	superoxide dismutase 2	Homo sapiens	10-15
21594386-2	1996	The known function of MnSOD is to remove superoxide radicals generated in the mitochondria.	Superoxides	41-51	superoxide dismutase 2	Homo sapiens	22-27
8605177-1	1996	Human manganese superoxide dismutase (MnSOD) is a homotetrameric enzyme which protects mitochondria against oxygen-mediated free radical damage.	Oxygen	108-114	superoxide dismutase 2	Homo sapiens	38-43
8605177-9	1996	Rapid inactivation of Ile58Thr MnSOD at the elevated temperatures associated with fever and inflammation could provide an early advantage by killing infected cells, but also would increase superoxide-mediated oxidative damage and perhaps contribute to late-onset diseases.	Superoxides	189-199	superoxide dismutase 2	Homo sapiens	31-36
8602839-1	1996	Human manganese-containing superoxide dismutase (MnSOD) is a nuclear encoded mitochondrial protein that scavenges potentially toxic superoxide radicals by dismuting O2- to O2 plus H2O2.	Superoxides	165-167	superoxide dismutase 2	Homo sapiens	6-47
8602839-1	1996	Human manganese-containing superoxide dismutase (MnSOD) is a nuclear encoded mitochondrial protein that scavenges potentially toxic superoxide radicals by dismuting O2- to O2 plus H2O2.	Superoxides	165-167	superoxide dismutase 2	Homo sapiens	49-54
8602839-1	1996	Human manganese-containing superoxide dismutase (MnSOD) is a nuclear encoded mitochondrial protein that scavenges potentially toxic superoxide radicals by dismuting O2- to O2 plus H2O2.	Superoxides	172-174	superoxide dismutase 2	Homo sapiens	6-47
8602839-1	1996	Human manganese-containing superoxide dismutase (MnSOD) is a nuclear encoded mitochondrial protein that scavenges potentially toxic superoxide radicals by dismuting O2- to O2 plus H2O2.	Superoxides	172-174	superoxide dismutase 2	Homo sapiens	49-54
8602839-1	1996	Human manganese-containing superoxide dismutase (MnSOD) is a nuclear encoded mitochondrial protein that scavenges potentially toxic superoxide radicals by dismuting O2- to O2 plus H2O2.	Hydrogen Peroxide	180-184	superoxide dismutase 2	Homo sapiens	6-47
8602839-1	1996	Human manganese-containing superoxide dismutase (MnSOD) is a nuclear encoded mitochondrial protein that scavenges potentially toxic superoxide radicals by dismuting O2- to O2 plus H2O2.	Hydrogen Peroxide	180-184	superoxide dismutase 2	Homo sapiens	49-54
8602757-1	1996	Superoxide dismutases (SODs) are metalloenzymes that detoxify superoxide radicals, and occur in cytosolic (Cu,Zn-SOD) and mitochondrial (Mn-SOD) forms in multiple tissues, including brain.	Superoxides	62-72	superoxide dismutase 2	Homo sapiens	137-143
8602757-6	1996	Our findings clearly indicate the importance of selegiline on measured Cu,Zn-SOD and Mn-SOD activity in peripheral lymphocytes.	Selegiline	48-58	superoxide dismutase 2	Homo sapiens	85-91
8643079-8	1996	In phosphate-buffered saline (PSB), HQ underwent a slow autoxidation to BQ, which was accelerated by Cu/Zn-SOD, Mn-SOD, or Fe-SOD with similar efficiency.	quinone	72-74	superoxide dismutase 2	Homo sapiens	112-118
8661822-7	1996	Up-regulation of Mn-SOD mRNA in gastric carcinoma tissue most likely serves as a protective mechanism against superoxide radicals and TNF cytotoxicity.	Superoxides	110-120	superoxide dismutase 2	Homo sapiens	17-23
7493040-2	1995	Skin is endowed with antioxidant enzymes including superoxide dismutases (SOD): cytosolic copper zinc SOD and mitochondrial manganese SOD.	Copper	90-96	superoxide dismutase 2	Homo sapiens	74-77
8856983-3	1996	TNF or LT pretreatment, which can induce the synthesis of "protective" proteins such as mitochondrial manganese superoxide dismutase (MnSOD), protects animals from lethal doses of radiation or the chemotherapeutic drug doxorubicin.	Doxorubicin	219-230	superoxide dismutase 2	Homo sapiens	102-132
8856983-3	1996	TNF or LT pretreatment, which can induce the synthesis of "protective" proteins such as mitochondrial manganese superoxide dismutase (MnSOD), protects animals from lethal doses of radiation or the chemotherapeutic drug doxorubicin.	Doxorubicin	219-230	superoxide dismutase 2	Homo sapiens	134-139
8582655-3	1995	In this study, in vitro CSH administration significantly increased manganese superoxide dismutase (MnSOD) activity in cultured astroglia.	csh	24-27	superoxide dismutase 2	Homo sapiens	67-97
8582655-3	1995	In this study, in vitro CSH administration significantly increased manganese superoxide dismutase (MnSOD) activity in cultured astroglia.	csh	24-27	superoxide dismutase 2	Homo sapiens	99-104
8582655-5	1995	Systemic administration of CSH also significantly augmented MnSOD activity in the intact diencephalon.	csh	27-30	superoxide dismutase 2	Homo sapiens	60-65
7593237-2	1995	SOD-1 (a copper and zinc containing form of SOD) and SOD-2 (a manganese containing form of the enzyme) activities were both observed to be significantly lower in cell lines derived from fetal skin than in lines established from postnatal skin (ages 17-94 years).	Manganese	62-71	superoxide dismutase 2	Homo sapiens	53-58
7487113-7	1995	In order to investigate the mechanism of the cellular adaptive response to ethanol-induced oxidative stress, the effects of short-term ethanol exposure on MnSOD RNA, protein, and activity were determined in a human hepatoma cell line (HepG2).	Ethanol	135-142	superoxide dismutase 2	Homo sapiens	155-160
7487113-8	1995	We found that exposure to ethanol (25 mM concentration) for 72 h increased the protein level and enzyme activity of MnSOD.	Ethanol	26-33	superoxide dismutase 2	Homo sapiens	116-121
7487113-12	1995	Thus it appears that both TNF and ethanol are capable of increasing MnSOD activity presumably via enhanced oxidative stress.	Ethanol	34-41	superoxide dismutase 2	Homo sapiens	68-73
7487113-13	1995	However, unlike TNF, acute ethanol administration increases the activity of MnSOD without increasing MnSOD mRNA.	Ethanol	27-34	superoxide dismutase 2	Homo sapiens	76-81
7487113-14	1995	The increase in MnSOD after a short-term dose of ethanol is diminished with repeated ethanol administrations.	Ethanol	49-56	superoxide dismutase 2	Homo sapiens	16-21
7487113-14	1995	The increase in MnSOD after a short-term dose of ethanol is diminished with repeated ethanol administrations.	Ethanol	85-92	superoxide dismutase 2	Homo sapiens	16-21
7487113-16	1995	If this adaptive response of MnSOD is lessened, it may have implications in the increased toxicity due to prolonged ethanol exposure.	Ethanol	116-123	superoxide dismutase 2	Homo sapiens	29-34
8886804-2	1996	Manganese superoxide dismutase (MnSOD), a mitochondrial superoxide radical scavenging enzyme, is low in most tumors but is known to be induced by asbestos fibers and certain cytokines.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
8886804-3	1996	Induction of MnSOD may be associated in asbestos-related pulmonary diseases in vivo.	Asbestos	40-48	superoxide dismutase 2	Homo sapiens	13-18
8886804-8	1996	Cytotoxicity experiments, which were conducted in four cell lines, indicated that cells containing high MnSOD mRNA level and activity were resistant to the mitochondrial superoxide-producing agent menadione.	Superoxides	170-180	superoxide dismutase 2	Homo sapiens	104-109
8886804-8	1996	Cytotoxicity experiments, which were conducted in four cell lines, indicated that cells containing high MnSOD mRNA level and activity were resistant to the mitochondrial superoxide-producing agent menadione.	Vitamin K 3	197-206	superoxide dismutase 2	Homo sapiens	104-109
8541726-3	1995	Manganese-containing superoxide dismutase (MnSOD) belongs to a family of metalloproteins that catalyse the metabolization of oxygen radicals in order to protect these cells from radical damage.	Reactive Oxygen Species	125-140	superoxide dismutase 2	Homo sapiens	0-41
8574013-4	1995	Cu/Zn- and Mn-SOD reactivity was detectable in hepatocytes with a heavy and a low iron burden, but Cu/Zn-SOD staining was more intense than that of Mn-SOD in the three groups analysed.	Iron	82-86	superoxide dismutase 2	Homo sapiens	11-17
8574013-6	1995	The findings suggest that the two SOD"s may be differentially expressed in states of hepatic iron overload, and that low expression of the inducible radical scavenger, Mn-SOD, may play a role in chronic iron toxicity.	Iron	93-97	superoxide dismutase 2	Homo sapiens	34-37
8574013-6	1995	The findings suggest that the two SOD"s may be differentially expressed in states of hepatic iron overload, and that low expression of the inducible radical scavenger, Mn-SOD, may play a role in chronic iron toxicity.	Iron	203-207	superoxide dismutase 2	Homo sapiens	168-174
8541726-3	1995	Manganese-containing superoxide dismutase (MnSOD) belongs to a family of metalloproteins that catalyse the metabolization of oxygen radicals in order to protect these cells from radical damage.	Reactive Oxygen Species	125-140	superoxide dismutase 2	Homo sapiens	43-48
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Superoxides	100-118	superoxide dismutase 2	Homo sapiens	0-30
7673115-11	1995	In the presence of SIN-1, Mn-SOD increased accumulation of H2O2 in a concentration-dependent manner.	Hydrogen Peroxide	59-63	superoxide dismutase 2	Homo sapiens	26-32
8580367-8	1995	MnSOD acts as a scaveneger of toxic superoxide radicals and its induction by TNF paralleled arachidonic acid release.	Superoxides	36-46	superoxide dismutase 2	Homo sapiens	0-5
8580367-8	1995	MnSOD acts as a scaveneger of toxic superoxide radicals and its induction by TNF paralleled arachidonic acid release.	Arachidonic Acid	92-108	superoxide dismutase 2	Homo sapiens	0-5
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Superoxides	100-118	superoxide dismutase 2	Homo sapiens	32-38
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Superoxides	120-122	superoxide dismutase 2	Homo sapiens	0-30
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Superoxides	120-122	superoxide dismutase 2	Homo sapiens	32-38
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Superoxides	184-186	superoxide dismutase 2	Homo sapiens	0-30
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Superoxides	184-186	superoxide dismutase 2	Homo sapiens	32-38
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Hydrogen Peroxide	192-209	superoxide dismutase 2	Homo sapiens	0-30
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Hydrogen Peroxide	192-209	superoxide dismutase 2	Homo sapiens	32-38
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Hydrogen Peroxide	211-215	superoxide dismutase 2	Homo sapiens	0-30
7622845-1	1995	Manganese superoxide dismutase (Mn SOD), mitochondrial enzyme, defends against the toxic effects of superoxide radical (O2.-) in pathological processes by catalyzing the conversion of O2.- to hydrogen peroxide (H2O2).	Hydrogen Peroxide	211-215	superoxide dismutase 2	Homo sapiens	32-38
7622845-4	1995	NADH diaphorase enzymatic activity co-migrated with complexes of Mn SOD on a non-denaturing gel.	NAD	0-4	superoxide dismutase 2	Homo sapiens	65-71
7476933-5	1995	In contrast, thiol oxidizing or alkylating agents inhibited both NF-kappa B activation and elevated MnSOD expression in response to TNF alpha or IL-1.	Sulfhydryl Compounds	13-18	superoxide dismutase 2	Homo sapiens	100-105
8775911-8	1995	The superoxide radical-SOD system might play an important role in ovulation and in the luteal function of the human ovary.	Superoxides	4-14	superoxide dismutase 2	Homo sapiens	23-26
7797591-3	1995	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme involved in scavenging O2..-.	Superoxides	88-90	superoxide dismutase 2	Homo sapiens	0-30
7476933-0	1995	Thiol modulation of TNF alpha and IL-1 induced MnSOD gene expression and activation of NF-kappa B.	Sulfhydryl Compounds	0-5	superoxide dismutase 2	Homo sapiens	47-52
7476933-4	1995	Activation of NF-kB and increased MnSOD expression were potentiated by thiol reducing agents.	Sulfhydryl Compounds	71-76	superoxide dismutase 2	Homo sapiens	34-39
7797591-9	1995	Inhibition of the cyclo-oxygenase pathway with indomethacin augmented the induction MnSOD mRNA by irradiation and prostaglandin E2 inhibited the accumulation of MnSOD mRNA by irradiation.	Dinoprostone	114-130	superoxide dismutase 2	Homo sapiens	161-166
7797591-3	1995	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme involved in scavenging O2..-.	Superoxides	88-90	superoxide dismutase 2	Homo sapiens	32-37
7797591-12	1995	These results suggest that induction of the MnSOD gene after irradiation is regulated, at least in part, by IL-1 production and that increased levels of MnSOD transcripts also occur through a pathway of endogenous prostaglandin E2 production.	Dinoprostone	214-230	superoxide dismutase 2	Homo sapiens	153-158
7797591-9	1995	Inhibition of the cyclo-oxygenase pathway with indomethacin augmented the induction MnSOD mRNA by irradiation and prostaglandin E2 inhibited the accumulation of MnSOD mRNA by irradiation.	Indomethacin	47-59	superoxide dismutase 2	Homo sapiens	84-89
7761099-7	1995	The clonogenic fraction in soft agar culture was also decreased after MnSOD cDNA transfection.	Agar	32-36	superoxide dismutase 2	Homo sapiens	70-75
7665413-11	1995	Arterial O2-to-inspired O2 fraction ratio was significantly improved at 6 and 12 h after smoke insufflation in SOD compared with CON at the same time points.	Oxygen	9-11	superoxide dismutase 2	Homo sapiens	111-114
7665413-11	1995	Arterial O2-to-inspired O2 fraction ratio was significantly improved at 6 and 12 h after smoke insufflation in SOD compared with CON at the same time points.	Oxygen	24-26	superoxide dismutase 2	Homo sapiens	111-114
7599209-5	1995	MnSOD, identified as one of the protective proteins, is a mitochondrial enzyme that scavenges superoxide radicals (O2-).	Superoxides	94-104	superoxide dismutase 2	Homo sapiens	0-5
7599209-5	1995	MnSOD, identified as one of the protective proteins, is a mitochondrial enzyme that scavenges superoxide radicals (O2-).	Superoxides	115-117	superoxide dismutase 2	Homo sapiens	0-5
7539260-1	1995	We presently investigated the effects of pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of nuclear factor kappa B (NF-kappa B), on the induction of nitric oxide synthase (iNOS) and manganese superoxide dismutase (MnSOD) mRNAs by IL-1 beta in insulin-producing RIN cells.	pyrrolidine dithiocarbamic acid	41-68	superoxide dismutase 2	Homo sapiens	189-219
7539260-1	1995	We presently investigated the effects of pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of nuclear factor kappa B (NF-kappa B), on the induction of nitric oxide synthase (iNOS) and manganese superoxide dismutase (MnSOD) mRNAs by IL-1 beta in insulin-producing RIN cells.	pyrrolidine dithiocarbamic acid	41-68	superoxide dismutase 2	Homo sapiens	221-226
7539260-1	1995	We presently investigated the effects of pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of nuclear factor kappa B (NF-kappa B), on the induction of nitric oxide synthase (iNOS) and manganese superoxide dismutase (MnSOD) mRNAs by IL-1 beta in insulin-producing RIN cells.	pyrrolidine dithiocarbamic acid	70-74	superoxide dismutase 2	Homo sapiens	189-219
7539260-1	1995	We presently investigated the effects of pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of nuclear factor kappa B (NF-kappa B), on the induction of nitric oxide synthase (iNOS) and manganese superoxide dismutase (MnSOD) mRNAs by IL-1 beta in insulin-producing RIN cells.	pyrrolidine dithiocarbamic acid	70-74	superoxide dismutase 2	Homo sapiens	221-226
7775261-2	1995	Based on our previous finding that endogenous TNF (enTNF) acts as an intracellular resistance factor against exogenous TNF by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD), we examined the suppression of these resistance factors by chemotherapeutic drugs and the resulting increase in TNF cytotoxicity.	oxygen free radicals	137-157	superoxide dismutase 2	Homo sapiens	177-207
7775261-2	1995	Based on our previous finding that endogenous TNF (enTNF) acts as an intracellular resistance factor against exogenous TNF by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD), we examined the suppression of these resistance factors by chemotherapeutic drugs and the resulting increase in TNF cytotoxicity.	oxygen free radicals	137-157	superoxide dismutase 2	Homo sapiens	209-214
7700080-4	1995	Persistence of this differential sensitivity when MnSOD is inhibited by sodium nitroprusside (SNP) suggests that the greater susceptibility of drug-resistant cells to TNF alpha was not entirely due to their decreased level of MnSOD activity.	Nitroprusside	72-92	superoxide dismutase 2	Homo sapiens	50-55
7739117-5	1995	Marked induction of Mn-SOD and Cu/Zn-SOD mRNA was found in the heart with viral myocarditis and oxygen radicals may play an important role in the pathogenesis of viral myocarditis.	Reactive Oxygen Species	96-111	superoxide dismutase 2	Homo sapiens	20-26
7484097-4	1995	These results suggest that the increased Mn SOD immunoreactivity in MKHD reflects enzyme induction as a protective mechanism against the highly toxic superoxide anion generated under the disease conditions.	Superoxides	150-166	superoxide dismutase 2	Homo sapiens	41-47
7859743-8	1995	Decreased Mn-SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione.	Glutathione	68-79	superoxide dismutase 2	Homo sapiens	10-16
7859743-8	1995	Decreased Mn-SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione.	Glutathione	118-129	superoxide dismutase 2	Homo sapiens	10-16
7856748-9	1995	In senile plaques, copper, zinc-superoxide dismutase-positive globular structures were surrounded by astrocytes highly enriched in manganese-superoxide dismutase.	Copper	19-25	superoxide dismutase 2	Homo sapiens	131-161
7964476-5	1994	In vitro, the autoantibodies were shown to inhibit the dismutation of superoxide radicals by blocking MnSOD.	Superoxides	70-80	superoxide dismutase 2	Homo sapiens	102-107
7989127-8	1994	The higher SOD2 and lower G6PD activity observed in FUra-resistant cell in comparison with parental cells at all times after sub-culture could be characteristic both of differentiative and of differentiated cells.	Fluorouracil	52-56	superoxide dismutase 2	Homo sapiens	11-15
7702755-1	1994	Human manganese superoxide dismutase (MnSOD) is one of the major cellular defense enzymes that protects against toxic effects of superoxide radicals.	Superoxides	16-26	superoxide dismutase 2	Homo sapiens	38-43
8077189-10	1994	Manganese superoxide dismutase (MnSOD) is thought to be the sole enzymic scavenger of superoxide in mammalian mitochondria.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
7932852-3	1994	One of the antioxidant enzymes that is protective against reactive oxygen-induced damage is manganese superoxide dismutase (MnSOD), which is located in the mitochondria of mammalian cells.	Oxygen	67-73	superoxide dismutase 2	Homo sapiens	92-122
7932852-3	1994	One of the antioxidant enzymes that is protective against reactive oxygen-induced damage is manganese superoxide dismutase (MnSOD), which is located in the mitochondria of mammalian cells.	Oxygen	67-73	superoxide dismutase 2	Homo sapiens	124-129
8037686-0	1994	Induction of manganese superoxide dismutase mRNA by okadaic acid and protein synthesis inhibitors.	Okadaic Acid	52-64	superoxide dismutase 2	Homo sapiens	13-43
7923586-4	1994	The observed decreases in total cellular SOD and GPX activities following ciprofibrate treatment were due to significant decreases in cytosolic CuZn SOD and GPX, whereas mitochondrial levels of Mn SOD and GPX were relatively unchanged.	ciprofibrate	74-86	superoxide dismutase 2	Homo sapiens	41-44
7923586-4	1994	The observed decreases in total cellular SOD and GPX activities following ciprofibrate treatment were due to significant decreases in cytosolic CuZn SOD and GPX, whereas mitochondrial levels of Mn SOD and GPX were relatively unchanged.	ciprofibrate	74-86	superoxide dismutase 2	Homo sapiens	194-200
7914182-2	1994	Cells producing endogenous tumor necrosis factor (enTNF) show resistance to the cytotoxicity of exogenous TNF and heat by inducing manganous superoxide dismutase (MnSOD) to scavenge the reactive oxygen molecules.	reactive oxygen	186-201	superoxide dismutase 2	Homo sapiens	131-161
7914182-2	1994	Cells producing endogenous tumor necrosis factor (enTNF) show resistance to the cytotoxicity of exogenous TNF and heat by inducing manganous superoxide dismutase (MnSOD) to scavenge the reactive oxygen molecules.	reactive oxygen	186-201	superoxide dismutase 2	Homo sapiens	163-168
7914182-6	1994	The stable transformants became resistant to adriamycin with increased levels of MnSOD.	Doxorubicin	45-55	superoxide dismutase 2	Homo sapiens	81-86
7914182-9	1994	These results indicate that enTNF exerts its intracellular protective effect against adriamycin-induced cytotoxicity by the same mechanism as that against exogenous TNF and heat, namely scavenging reactive oxygen with induced MnSOD.	Doxorubicin	85-95	superoxide dismutase 2	Homo sapiens	226-231
8037686-1	1994	We have reported that the phorbol ester phorbol 12-myristate 13-acetate (PMA) enhances the expression of manganese superoxide dismutase (Mn-SOD) mRNA [Fujii and Taniguchi (1991) J. Biol.	Phorbol Esters	26-39	superoxide dismutase 2	Homo sapiens	137-143
8037686-1	1994	We have reported that the phorbol ester phorbol 12-myristate 13-acetate (PMA) enhances the expression of manganese superoxide dismutase (Mn-SOD) mRNA [Fujii and Taniguchi (1991) J. Biol.	Tetradecanoylphorbol Acetate	40-71	superoxide dismutase 2	Homo sapiens	105-135
8037686-1	1994	We have reported that the phorbol ester phorbol 12-myristate 13-acetate (PMA) enhances the expression of manganese superoxide dismutase (Mn-SOD) mRNA [Fujii and Taniguchi (1991) J. Biol.	Tetradecanoylphorbol Acetate	40-71	superoxide dismutase 2	Homo sapiens	137-143
8037686-1	1994	We have reported that the phorbol ester phorbol 12-myristate 13-acetate (PMA) enhances the expression of manganese superoxide dismutase (Mn-SOD) mRNA [Fujii and Taniguchi (1991) J. Biol.	Tetradecanoylphorbol Acetate	73-76	superoxide dismutase 2	Homo sapiens	105-135
8037686-1	1994	We have reported that the phorbol ester phorbol 12-myristate 13-acetate (PMA) enhances the expression of manganese superoxide dismutase (Mn-SOD) mRNA [Fujii and Taniguchi (1991) J. Biol.	Phorbol Esters	26-39	superoxide dismutase 2	Homo sapiens	105-135
8037686-1	1994	We have reported that the phorbol ester phorbol 12-myristate 13-acetate (PMA) enhances the expression of manganese superoxide dismutase (Mn-SOD) mRNA [Fujii and Taniguchi (1991) J. Biol.	Tetradecanoylphorbol Acetate	73-76	superoxide dismutase 2	Homo sapiens	137-143
8024580-1	1994	On the basis of the well-known effect of ethanol poisoning on the prooxidant/antioxidant balance of human and rodent liver we tested the response of the mitochondrial manganese-containing superoxide dismutase (MnSOD) in the liver of rats following an acute ethanol load or chronically intoxicated with an alcohol-supplemented solid diet for three weeks.	Ethanol	41-48	superoxide dismutase 2	Homo sapiens	210-215
8037686-4	1994	Okadaic acid, an inhibitor of type I and type IIa phosphatases, was also found to induce Mn-SOD mRNA at submicromolar concentrations in HeLa cells.	Okadaic Acid	0-12	superoxide dismutase 2	Homo sapiens	89-95
8037686-6	1994	When the effect of cycloheximide on the decay of Mn-SOD mRNA was examined by inhibiting mRNA synthesis with actinomycin D, cycloheximide had virtually no effect on mRNA stability, suggesting that accumulation of the mRNA was caused by activation by this reagent of transcription of the gene.	Cycloheximide	19-32	superoxide dismutase 2	Homo sapiens	49-55
8037686-7	1994	PMA pretreatment of HeLa cells markedly enhanced cycloheximide-dependent superinduction of Mn-SOD mRNA.	Cycloheximide	49-62	superoxide dismutase 2	Homo sapiens	91-97
8023358-3	1994	In the present study we examined whether oxygen radicals also induce the expression of manganese superoxide dismutase messenger RNA in the postischemic brain.	Reactive Oxygen Species	41-56	superoxide dismutase 2	Homo sapiens	87-117
8024580-1	1994	On the basis of the well-known effect of ethanol poisoning on the prooxidant/antioxidant balance of human and rodent liver we tested the response of the mitochondrial manganese-containing superoxide dismutase (MnSOD) in the liver of rats following an acute ethanol load or chronically intoxicated with an alcohol-supplemented solid diet for three weeks.	Ethanol	257-264	superoxide dismutase 2	Homo sapiens	167-208
8024580-1	1994	On the basis of the well-known effect of ethanol poisoning on the prooxidant/antioxidant balance of human and rodent liver we tested the response of the mitochondrial manganese-containing superoxide dismutase (MnSOD) in the liver of rats following an acute ethanol load or chronically intoxicated with an alcohol-supplemented solid diet for three weeks.	Ethanol	257-264	superoxide dismutase 2	Homo sapiens	210-215
8024580-1	1994	On the basis of the well-known effect of ethanol poisoning on the prooxidant/antioxidant balance of human and rodent liver we tested the response of the mitochondrial manganese-containing superoxide dismutase (MnSOD) in the liver of rats following an acute ethanol load or chronically intoxicated with an alcohol-supplemented solid diet for three weeks.	Alcohols	305-312	superoxide dismutase 2	Homo sapiens	210-215
8118652-4	1994	Dosage-dependent increases in steady-state mRNA levels of MnSOD and HO were observed in HMC exposed to asbestos or X/XO.	Asbestos	103-111	superoxide dismutase 2	Homo sapiens	58-63
8118652-9	1994	In contrast, X/XO caused striking elevations in MnSOD protein levels in HAL cells.	hal	72-75	superoxide dismutase 2	Homo sapiens	48-53
7905787-0	1994	Resistance to TNF-alpha and adriamycin in the human breast cancer MCF-7 cell line: relationship to MDR1, MnSOD, and TNF gene expression.	Doxorubicin	28-38	superoxide dismutase 2	Homo sapiens	105-110
7509102-1	1993	The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique.	Superoxides	110-129	superoxide dismutase 2	Homo sapiens	45-68
7509102-1	1993	The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique.	Superoxides	110-129	superoxide dismutase 2	Homo sapiens	70-73
7509102-1	1993	The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique.	Superoxides	131-133	superoxide dismutase 2	Homo sapiens	45-68
7509102-1	1993	The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique.	Superoxides	131-133	superoxide dismutase 2	Homo sapiens	70-73
8238402-2	1993	The Mn-SOD in human endothelial cells was markedly induced by the cytokines tumor necrosis factor (TNF), interleukin-1, and lipopolysaccharide as well as by phorbol esters [12-O-tetradecanoylphorbol 13-acetate (TPA)].	Phorbol Esters	157-171	superoxide dismutase 2	Homo sapiens	4-10
7509102-1	1993	The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique.	Superoxides	139-141	superoxide dismutase 2	Homo sapiens	45-68
7509102-1	1993	The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique.	Superoxides	139-141	superoxide dismutase 2	Homo sapiens	70-73
7509102-1	1993	The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique.	Hydrogen Peroxide	146-150	superoxide dismutase 2	Homo sapiens	45-68
7509102-1	1993	The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique.	Hydrogen Peroxide	146-150	superoxide dismutase 2	Homo sapiens	70-73
8257593-3	1993	Expression of MnSOD may be critical in determining the degree of tissue injury during re-oxygenation because the mitochondrial electron transport system produces reactive oxygen species (ROS) both during hypoxia and re-oxygenation.	Reactive Oxygen Species	162-185	superoxide dismutase 2	Homo sapiens	14-19
8257593-3	1993	Expression of MnSOD may be critical in determining the degree of tissue injury during re-oxygenation because the mitochondrial electron transport system produces reactive oxygen species (ROS) both during hypoxia and re-oxygenation.	Reactive Oxygen Species	187-190	superoxide dismutase 2	Homo sapiens	14-19
7915978-3	1993	Since beta cells contain low amounts of the superoxide radical scavenger enzyme manganese superoxide dismutase (MnSOD), this may leave beta cells more susceptible to IL-1 than other cell types.	Superoxides	44-54	superoxide dismutase 2	Homo sapiens	112-117
8238402-2	1993	The Mn-SOD in human endothelial cells was markedly induced by the cytokines tumor necrosis factor (TNF), interleukin-1, and lipopolysaccharide as well as by phorbol esters [12-O-tetradecanoylphorbol 13-acetate (TPA)].	Tetradecanoylphorbol Acetate	173-209	superoxide dismutase 2	Homo sapiens	4-10
8238402-2	1993	The Mn-SOD in human endothelial cells was markedly induced by the cytokines tumor necrosis factor (TNF), interleukin-1, and lipopolysaccharide as well as by phorbol esters [12-O-tetradecanoylphorbol 13-acetate (TPA)].	Tetradecanoylphorbol Acetate	211-214	superoxide dismutase 2	Homo sapiens	4-10
8232185-1	1993	The localization of Cu/Zn and Mn superoxide dismutase (SOD), which catalyzes the dismutation of superoxide radicals (O2-) to O2 and H2O2, in various thyroid disorders was studied by an immunohistochemical technique in 20% formalin fixed paraffin embedded thin sections using anti-human Cu/Zn and Mn-SOD antibodies.	Superoxides	33-43	superoxide dismutase 2	Homo sapiens	296-302
8260539-3	1993	On the other hand, TNF or radiation treatment can stimulate the expression of a mitochondrial superoxide scavenging enzyme, manganese superoxide dismutase (MnSOD), which can lower the cytotoxic effects of both agents.	Superoxides	94-104	superoxide dismutase 2	Homo sapiens	124-154
8260539-3	1993	On the other hand, TNF or radiation treatment can stimulate the expression of a mitochondrial superoxide scavenging enzyme, manganese superoxide dismutase (MnSOD), which can lower the cytotoxic effects of both agents.	Superoxides	94-104	superoxide dismutase 2	Homo sapiens	156-161
8232185-1	1993	The localization of Cu/Zn and Mn superoxide dismutase (SOD), which catalyzes the dismutation of superoxide radicals (O2-) to O2 and H2O2, in various thyroid disorders was studied by an immunohistochemical technique in 20% formalin fixed paraffin embedded thin sections using anti-human Cu/Zn and Mn-SOD antibodies.	Superoxides	117-119	superoxide dismutase 2	Homo sapiens	30-53
8232185-1	1993	The localization of Cu/Zn and Mn superoxide dismutase (SOD), which catalyzes the dismutation of superoxide radicals (O2-) to O2 and H2O2, in various thyroid disorders was studied by an immunohistochemical technique in 20% formalin fixed paraffin embedded thin sections using anti-human Cu/Zn and Mn-SOD antibodies.	Superoxides	125-127	superoxide dismutase 2	Homo sapiens	30-53
8232185-1	1993	The localization of Cu/Zn and Mn superoxide dismutase (SOD), which catalyzes the dismutation of superoxide radicals (O2-) to O2 and H2O2, in various thyroid disorders was studied by an immunohistochemical technique in 20% formalin fixed paraffin embedded thin sections using anti-human Cu/Zn and Mn-SOD antibodies.	Hydrogen Peroxide	132-136	superoxide dismutase 2	Homo sapiens	30-53
8232185-1	1993	The localization of Cu/Zn and Mn superoxide dismutase (SOD), which catalyzes the dismutation of superoxide radicals (O2-) to O2 and H2O2, in various thyroid disorders was studied by an immunohistochemical technique in 20% formalin fixed paraffin embedded thin sections using anti-human Cu/Zn and Mn-SOD antibodies.	Formaldehyde	222-230	superoxide dismutase 2	Homo sapiens	30-53
8232185-1	1993	The localization of Cu/Zn and Mn superoxide dismutase (SOD), which catalyzes the dismutation of superoxide radicals (O2-) to O2 and H2O2, in various thyroid disorders was studied by an immunohistochemical technique in 20% formalin fixed paraffin embedded thin sections using anti-human Cu/Zn and Mn-SOD antibodies.	Paraffin	237-245	superoxide dismutase 2	Homo sapiens	30-53
8353281-11	1993	Further studies showed that the antisense oligonucleotides entered the cells and resulted in decreased levels of Mn-SOD RNA.	Oligonucleotides	42-58	superoxide dismutase 2	Homo sapiens	113-119
8372889-8	1993	CONCLUSIONS: These data show that reactive oxygen produced in adenomyosis may induce Mn-SOD in ectopic endometrium, which results in the release of relatively large amounts of this protein into the peritoneal fluid.	reactive oxygen	34-49	superoxide dismutase 2	Homo sapiens	85-91
8323302-2	1993	The results showed that treatment with BSO, NEM, or diamide can increase MnSOD activity in the human fibroblast cells.	Buthionine Sulfoximine	39-42	superoxide dismutase 2	Homo sapiens	73-78
8317554-1	1993	Several enzymes, including superoxide dismutase (SOD), catalase, glutathione peroxidase, and D-glucose-6-phosphate dehydrogenase are capable of scavenging reactive oxygen species in in vivo.	Reactive Oxygen Species	155-178	superoxide dismutase 2	Homo sapiens	49-52
8317554-3	1993	Basal activity of copper-zinc SOD, and manganese SOD showed little variation with age.	Copper	18-24	superoxide dismutase 2	Homo sapiens	30-33
8317554-5	1993	Both manganese SOD and copper, zinc SOD activities were significantly induced by paraquat, interleukin-1, tumor necrosis factor, adriamycin, and bleomycin in lymphocytes and neutrophils from asymptomatic non-aged adults, whereas neither activity was induced in aged individuals.	Doxorubicin	129-139	superoxide dismutase 2	Homo sapiens	15-18
8317554-5	1993	Both manganese SOD and copper, zinc SOD activities were significantly induced by paraquat, interleukin-1, tumor necrosis factor, adriamycin, and bleomycin in lymphocytes and neutrophils from asymptomatic non-aged adults, whereas neither activity was induced in aged individuals.	Bleomycin	145-154	superoxide dismutase 2	Homo sapiens	15-18
8323302-0	1993	Thiol-modulating agents increase manganese superoxide dismutase activity in human lung fibroblasts.	Sulfhydryl Compounds	0-5	superoxide dismutase 2	Homo sapiens	33-63
8323302-2	1993	The results showed that treatment with BSO, NEM, or diamide can increase MnSOD activity in the human fibroblast cells.	Ethylmaleimide	44-47	superoxide dismutase 2	Homo sapiens	73-78
8323302-2	1993	The results showed that treatment with BSO, NEM, or diamide can increase MnSOD activity in the human fibroblast cells.	Diamide	52-59	superoxide dismutase 2	Homo sapiens	73-78
8516341-2	1993	Evidence suggests that both CuZnSOD and MnSOD are important in pulmonary defense against oxygen toxicity.	Oxygen	89-95	superoxide dismutase 2	Homo sapiens	40-45
8394950-8	1993	Besides reducing the excessive O2- formation, methylprednisolone induced an increase in polymorph expression of the gene encoding for manganese superoxide dismutase (Mn-SOD) enzyme.	Superoxides	31-33	superoxide dismutase 2	Homo sapiens	134-164
8394950-8	1993	Besides reducing the excessive O2- formation, methylprednisolone induced an increase in polymorph expression of the gene encoding for manganese superoxide dismutase (Mn-SOD) enzyme.	Superoxides	31-33	superoxide dismutase 2	Homo sapiens	166-172
8394950-8	1993	Besides reducing the excessive O2- formation, methylprednisolone induced an increase in polymorph expression of the gene encoding for manganese superoxide dismutase (Mn-SOD) enzyme.	Methylprednisolone	46-64	superoxide dismutase 2	Homo sapiens	134-164
8394950-8	1993	Besides reducing the excessive O2- formation, methylprednisolone induced an increase in polymorph expression of the gene encoding for manganese superoxide dismutase (Mn-SOD) enzyme.	Methylprednisolone	46-64	superoxide dismutase 2	Homo sapiens	166-172
8394950-10	1993	Methylprednisolone normalizes the abnormal generation of O2-, likely through its ability to up-regulate the gene for Mn-SOD, a potent antioxidant enzyme.	Methylprednisolone	0-18	superoxide dismutase 2	Homo sapiens	117-123
8394950-10	1993	Methylprednisolone normalizes the abnormal generation of O2-, likely through its ability to up-regulate the gene for Mn-SOD, a potent antioxidant enzyme.	Superoxides	57-59	superoxide dismutase 2	Homo sapiens	117-123
8516341-4	1993	Likewise, transgenic overexpression of MnSOD, or induction of endogenous MnSOD by endotoxin, tumor necrosis factor, or interleukin 1, also protects animals against oxygen toxicity.	Oxygen	164-170	superoxide dismutase 2	Homo sapiens	39-44
8516341-4	1993	Likewise, transgenic overexpression of MnSOD, or induction of endogenous MnSOD by endotoxin, tumor necrosis factor, or interleukin 1, also protects animals against oxygen toxicity.	Oxygen	164-170	superoxide dismutase 2	Homo sapiens	73-78
1394426-1	1992	The 2.2 A resolution crystal structure of recombinant human manganese superoxide dismutase, a homotetrameric enzyme that protects mitochondria against oxygen-mediated free radical damage, has been determined.	Oxygen	151-157	superoxide dismutase 2	Homo sapiens	60-90
8392494-9	1993	Inhibition of MnSOD activity in PMN secondary to cytokine exposure in the asthmatic lung could explain, at least in part, the increased generation of superoxide from PMN obtained from asthmatics.	Superoxides	150-160	superoxide dismutase 2	Homo sapiens	14-19
8440412-4	1993	In addition, Chinese hamster ovary (CHO) cells transfected with sense MnSOD cDNA showed increased survival after treatment with doxorubicin, mitomycin C, and gamma (gamma) radiation in vitro.	Doxorubicin	128-139	superoxide dismutase 2	Homo sapiens	70-75
8440412-4	1993	In addition, Chinese hamster ovary (CHO) cells transfected with sense MnSOD cDNA showed increased survival after treatment with doxorubicin, mitomycin C, and gamma (gamma) radiation in vitro.	Mitomycin	141-152	superoxide dismutase 2	Homo sapiens	70-75
8440412-5	1993	It is hypothesized that mitochondrial MnSOD, by scavenging oxygen radicals induced by cytokines, some cytotoxic drugs, and ionizing radiation, is protective and promotes the survival of cells from the lethal effects of these treatments.	Oxygen	59-65	superoxide dismutase 2	Homo sapiens	38-43
8333551-1	1993	Manganese superoxide dismutase (Mn SOD) is an important component of antioxidant defense in aerobic cells because of its location in the mitochondria, a significant source of oxygen radicals and an important target of oxidant injury.	Reactive Oxygen Species	175-190	superoxide dismutase 2	Homo sapiens	32-38
8333551-4	1993	Acute survival during paraquat exposure (0-500 microM) was significantly improved in CHO cells expressing human Mn SOD, with 71% of recombinant CHO cells surviving at the 50% lethal dose (LD50) for wild-type CHO controls.	Paraquat	22-30	superoxide dismutase 2	Homo sapiens	112-118
8333551-4	1993	Acute survival during paraquat exposure (0-500 microM) was significantly improved in CHO cells expressing human Mn SOD, with 71% of recombinant CHO cells surviving at the 50% lethal dose (LD50) for wild-type CHO controls.	cho	85-88	superoxide dismutase 2	Homo sapiens	112-118
8495200-6	1993	The monomer-monomer interactions typical of bacterial Fe- and Mn-containing SODs are retained in the human enzyme, but the dimer-dimer interactions that form the tetramer are very different from those found in the structure of MnSOD from T. thermophilus.	Iron	54-56	superoxide dismutase 2	Homo sapiens	227-232
8495200-9	1993	The metal-ligand interactions, determined by refinement and verified by computation of omit maps, are identical to those observed in T. thermophilus MnSOD.	Metals	4-9	superoxide dismutase 2	Homo sapiens	149-154
8370552-7	1993	In the carrageenan-induced synovitis model, Mn SOD (25 and 50 micrograms; intra-articular administration) exacerbated the inflammation at 48 hours.	Carrageenan	7-18	superoxide dismutase 2	Homo sapiens	44-50
8264340-9	1993	Owing to the second messenger function of ROS in activating transcription factors (NF-kB, AP-1) and to the ability of Mn to facilitate the dismutation of O2- to H2O2 and of Fe to participate in the Fenton reaction, we propose that in the early stage of carcinogenesis an impairment of the signal transduction machinery, related to the metal deficiency, might limit the binding to DNA of transcription factors and cause the defect in the MnSOD gene expression.	Reactive Oxygen Species	42-45	superoxide dismutase 2	Homo sapiens	437-442
8264340-9	1993	Owing to the second messenger function of ROS in activating transcription factors (NF-kB, AP-1) and to the ability of Mn to facilitate the dismutation of O2- to H2O2 and of Fe to participate in the Fenton reaction, we propose that in the early stage of carcinogenesis an impairment of the signal transduction machinery, related to the metal deficiency, might limit the binding to DNA of transcription factors and cause the defect in the MnSOD gene expression.	Iron	173-175	superoxide dismutase 2	Homo sapiens	437-442
1337859-6	1992	Biochemical examinations showed a clear induction of heat shock protein 72 and a significant increase in manganese-containing superoxide dismutase in the hippocampus in animals treated with diethyldithiocarbamate 4 days prior to ischemia.	Ditiocarb	190-212	superoxide dismutase 2	Homo sapiens	105-146
1313774-3	1992	The purpose of this study was to establish whether MnSOD was increased in cells selected for resistance to cytolysis by TNF in combination with cycloheximide.	Cycloheximide	144-157	superoxide dismutase 2	Homo sapiens	51-56
1306294-5	1992	Tumor necrosis factor-alpha (TNF), lipopolysaccharide, IL-1 and phorbol ester induced the m-RNA of Mn-SOD as well as protein levels in TNF-resistant cells.	Phorbol Esters	64-77	superoxide dismutase 2	Homo sapiens	99-105
1616052-0	1992	Effects of TNF-alpha and phorbol ester on human surfactant protein and MnSOD gene transcription in vitro.	Phorbol Esters	25-38	superoxide dismutase 2	Homo sapiens	71-76
1582797-1	1992	Human retinal pigment epithelium (RPE) contains two genetically distinct forms of superoxide dismutase (SOD) enzymes that scavenge harmful superoxide anions.	Superoxides	139-156	superoxide dismutase 2	Homo sapiens	104-107
1582797-2	1992	Biochemical and immunochemical techniques were used to compare levels of copper-zinc- and manganese-containing forms of SOD (CuZn-SOD and Mn-SOD) in human adult and fetal RPE cells.	Copper	73-79	superoxide dismutase 2	Homo sapiens	120-123
1582797-2	1992	Biochemical and immunochemical techniques were used to compare levels of copper-zinc- and manganese-containing forms of SOD (CuZn-SOD and Mn-SOD) in human adult and fetal RPE cells.	Manganese	90-99	superoxide dismutase 2	Homo sapiens	120-123
1582797-2	1992	Biochemical and immunochemical techniques were used to compare levels of copper-zinc- and manganese-containing forms of SOD (CuZn-SOD and Mn-SOD) in human adult and fetal RPE cells.	Manganese	90-99	superoxide dismutase 2	Homo sapiens	130-133
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	5,5-dimethyl-1-pyrroline-1-oxide	102-134	superoxide dismutase 2	Homo sapiens	51-57
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	5,5-dimethyl-1-pyrroline-1-oxide	136-140	superoxide dismutase 2	Homo sapiens	51-57
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	Superoxides	146-162	superoxide dismutase 2	Homo sapiens	51-57
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	Superoxides	164-166	superoxide dismutase 2	Homo sapiens	51-57
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	Superoxides	179-181	superoxide dismutase 2	Homo sapiens	51-57
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	ko2	198-201	superoxide dismutase 2	Homo sapiens	51-57
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	potassium superoxide	203-223	superoxide dismutase 2	Homo sapiens	51-57
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	Dimethyl Sulfoxide	228-247	superoxide dismutase 2	Homo sapiens	51-57
1311175-3	1992	Enzymic reactions were studied in which Cu,Zn-SOD, Mn-SOD and Fe-SOD each competed with the spin trap 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) for superoxide anion (O2-) at pH 7.8 O2- from dissolved KO2 (potassium superoxide) in dimethyl sulphoxide was added directly to the enzyme solutions containing DMPO.	5,5-dimethyl-1-pyrroline-1-oxide	302-306	superoxide dismutase 2	Homo sapiens	51-57
1311175-4	1992	The results show that, in this competition reaction system, the kinetics of the reactions between the enzymes and O2- follow a function y = f[( SOD]0.5).	Superoxides	114-116	superoxide dismutase 2	Homo sapiens	144-147
1616052-6	1992	The time course and extent of increased MnSOD gene transcription by TNF-alpha and TPA were distinct.	Tetradecanoylphorbol Acetate	82-85	superoxide dismutase 2	Homo sapiens	40-45
1550052-4	1992	Manganese supplementation resulted in significant increases in lymphocyte MnSOD activity and serum manganese concentrations from baseline values but no changes in urinary manganese excretion or in any indices of iron status.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	74-79
1550052-6	1992	This work demonstrated that lymphocyte MnSOD activity can be used with serum manganese concentrations to monitor manganese exposure in humans.	Manganese	77-86	superoxide dismutase 2	Homo sapiens	39-44
1550052-6	1992	This work demonstrated that lymphocyte MnSOD activity can be used with serum manganese concentrations to monitor manganese exposure in humans.	Manganese	113-122	superoxide dismutase 2	Homo sapiens	39-44
1744113-0	1991	Phorbol ester induces manganese-superoxide dismutase in tumor necrosis factor-resistant cells.	Phorbol Esters	0-13	superoxide dismutase 2	Homo sapiens	22-52
1761541-7	1991	MnSOD mRNA was selectively induced in confluent epithelial cells exposed to the reactive oxygen species-generating system, xanthine/xanthine oxidase, while steady-state levels of GPX, catalase, and CuZnSOD mRNA remained unchanged.	Reactive Oxygen Species	80-103	superoxide dismutase 2	Homo sapiens	0-5
1761541-10	1991	Induction of MnSOD gene expression was prevented by addition of actinomycin D and cycloheximide.	Dactinomycin	64-77	superoxide dismutase 2	Homo sapiens	13-18
1761541-10	1991	Induction of MnSOD gene expression was prevented by addition of actinomycin D and cycloheximide.	Cycloheximide	82-95	superoxide dismutase 2	Homo sapiens	13-18
1744113-1	1991	The effects of phorbol ester (TPA) and other known stimulators such as tumor necrosis factor (TNF), interleukin-1, and lipopolysaccharide on induction of mRNA for manganese-superoxide dismutase (Mn-SOD) were investigated in various cell lines.	Phorbol Esters	15-28	superoxide dismutase 2	Homo sapiens	163-193
1744113-1	1991	The effects of phorbol ester (TPA) and other known stimulators such as tumor necrosis factor (TNF), interleukin-1, and lipopolysaccharide on induction of mRNA for manganese-superoxide dismutase (Mn-SOD) were investigated in various cell lines.	Tetradecanoylphorbol Acetate	30-33	superoxide dismutase 2	Homo sapiens	163-193
1744113-2	1991	TPA enhanced Mn-SOD mRNA expression in TNF-resistant cell lines including HeLa cells, in which the other reagents also induced expression of the gene, but did not affect TNF-sensitive cells, in which the other stimulators did not alter expression of the gene.	Tetradecanoylphorbol Acetate	0-3	superoxide dismutase 2	Homo sapiens	13-19
1744113-3	1991	HeLa cells which had been desensitized to TPA by pretreatment with TPA for 24 h expressed Mn-SOD mRNA at a slightly higher level than the cells without TPA treatment.	Tetradecanoylphorbol Acetate	42-45	superoxide dismutase 2	Homo sapiens	90-96
1744113-3	1991	HeLa cells which had been desensitized to TPA by pretreatment with TPA for 24 h expressed Mn-SOD mRNA at a slightly higher level than the cells without TPA treatment.	Tetradecanoylphorbol Acetate	67-70	superoxide dismutase 2	Homo sapiens	90-96
1744113-3	1991	HeLa cells which had been desensitized to TPA by pretreatment with TPA for 24 h expressed Mn-SOD mRNA at a slightly higher level than the cells without TPA treatment.	Tetradecanoylphorbol Acetate	67-70	superoxide dismutase 2	Homo sapiens	90-96
1744113-4	1991	TPA-pretreated cells stimulated with TNF, however, expressed Mn-SOD mRNA at about twice the level of TNF-stimulated, TPA-untreated cells.	Tetradecanoylphorbol Acetate	0-3	superoxide dismutase 2	Homo sapiens	61-67
1793616-1	1991	Manganese-superoxide dismutase (MnSOD) in human fibroblast and liver lysates was found to bind copper avidly under the conditions of a copper blotting technique which also detects known copper-binding proteins.	Copper	95-101	superoxide dismutase 2	Homo sapiens	32-37
1959661-0	1991	Overproduction of human Mn-superoxide dismutase modulates paraquat-mediated toxicity in mammalian cells.	Paraquat	58-66	superoxide dismutase 2	Homo sapiens	24-47
1793616-0	1991	Human manganese superoxide dismutase is readily detectable by a copper blotting technique.	Copper	64-70	superoxide dismutase 2	Homo sapiens	6-36
1793616-1	1991	Manganese-superoxide dismutase (MnSOD) in human fibroblast and liver lysates was found to bind copper avidly under the conditions of a copper blotting technique which also detects known copper-binding proteins.	Copper	95-101	superoxide dismutase 2	Homo sapiens	0-30
1793616-1	1991	Manganese-superoxide dismutase (MnSOD) in human fibroblast and liver lysates was found to bind copper avidly under the conditions of a copper blotting technique which also detects known copper-binding proteins.	Copper	135-141	superoxide dismutase 2	Homo sapiens	0-30
1793616-1	1991	Manganese-superoxide dismutase (MnSOD) in human fibroblast and liver lysates was found to bind copper avidly under the conditions of a copper blotting technique which also detects known copper-binding proteins.	Copper	135-141	superoxide dismutase 2	Homo sapiens	32-37
1793616-1	1991	Manganese-superoxide dismutase (MnSOD) in human fibroblast and liver lysates was found to bind copper avidly under the conditions of a copper blotting technique which also detects known copper-binding proteins.	Copper	135-141	superoxide dismutase 2	Homo sapiens	0-30
1793616-1	1991	Manganese-superoxide dismutase (MnSOD) in human fibroblast and liver lysates was found to bind copper avidly under the conditions of a copper blotting technique which also detects known copper-binding proteins.	Copper	135-141	superoxide dismutase 2	Homo sapiens	32-37
1793616-3	1991	Copper blotting provides a sensitive way to detect MnSOD in human tissues, and may be generally applicable to studies of copper-binding by biological molecules.	Copper	0-6	superoxide dismutase 2	Homo sapiens	51-56
1793616-3	1991	Copper blotting provides a sensitive way to detect MnSOD in human tissues, and may be generally applicable to studies of copper-binding by biological molecules.	Copper	121-127	superoxide dismutase 2	Homo sapiens	51-56
1959661-1	1991	Manganese superoxide dismutase (MnSOD) is a nuclear encoded mitochondrial matrix enzyme that functions to scavenge superoxide radicals.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
1654848-1	1991	Stable nitroxide radicals have been previously shown to function as superoxide dismutase (SOD)2 mimics and to protect mammalian cells against superoxide and hydrogen peroxide-mediated oxidative stress.	Superoxides	68-78	superoxide dismutase 2	Homo sapiens	90-95
1682406-0	1991	Elevated level of serum Mn-superoxide dismutase in patients with primary biliary cirrhosis: possible involvement of free radicals in the pathogenesis in primary biliary cirrhosis.	Free Radicals	116-129	superoxide dismutase 2	Homo sapiens	24-47
1682406-12	1991	These data suggested that free radicals including superoxide anion are possibly involved in the pathogenesis of the disease and Mn-SOD may play some role in a protection against the superoxide anion.	Superoxides	182-198	superoxide dismutase 2	Homo sapiens	128-134
1654848-1	1991	Stable nitroxide radicals have been previously shown to function as superoxide dismutase (SOD)2 mimics and to protect mammalian cells against superoxide and hydrogen peroxide-mediated oxidative stress.	nitroxyl	7-25	superoxide dismutase 2	Homo sapiens	90-95
1654848-1	1991	Stable nitroxide radicals have been previously shown to function as superoxide dismutase (SOD)2 mimics and to protect mammalian cells against superoxide and hydrogen peroxide-mediated oxidative stress.	Hydrogen Peroxide	157-174	superoxide dismutase 2	Homo sapiens	90-95
2058689-4	1991	The induction of Mn SOD by LPS was blocked by both a RNA synthesis inhibitor, actinomycin D, and a protein synthesis inhibitor, cycloheximide.	Dactinomycin	78-91	superoxide dismutase 2	Homo sapiens	17-23
1668725-9	1991	TNF-alpha induces manganese-containing superoxide dismutase (MnSOD) which also uses O2- to produce cytotoxic concentrations of hydrogen peroxide.	Superoxides	84-86	superoxide dismutase 2	Homo sapiens	18-59
1668725-9	1991	TNF-alpha induces manganese-containing superoxide dismutase (MnSOD) which also uses O2- to produce cytotoxic concentrations of hydrogen peroxide.	Superoxides	84-86	superoxide dismutase 2	Homo sapiens	61-66
1668725-9	1991	TNF-alpha induces manganese-containing superoxide dismutase (MnSOD) which also uses O2- to produce cytotoxic concentrations of hydrogen peroxide.	Hydrogen Peroxide	127-144	superoxide dismutase 2	Homo sapiens	18-59
1668725-9	1991	TNF-alpha induces manganese-containing superoxide dismutase (MnSOD) which also uses O2- to produce cytotoxic concentrations of hydrogen peroxide.	Hydrogen Peroxide	127-144	superoxide dismutase 2	Homo sapiens	61-66
1904900-11	1991	The induction of Mn-SOD by IFN-gamma and its synergistic induction by IFN-gamma in combination with TNF and IL-1 should protect healthy cells from the toxicity of O2- during an immune response, and may provide a mechanism for selective killing of infected cells.	Oxygen	163-165	superoxide dismutase 2	Homo sapiens	17-23
2058689-4	1991	The induction of Mn SOD by LPS was blocked by both a RNA synthesis inhibitor, actinomycin D, and a protein synthesis inhibitor, cycloheximide.	Cycloheximide	128-141	superoxide dismutase 2	Homo sapiens	17-23
1850207-2	1991	Manganese superoxide dismutase (Mn-SOD) is a superoxide anion (O2-.)	Superoxides	45-61	superoxide dismutase 2	Homo sapiens	0-30
2023255-1	1991	Human liver manganese superoxide dismutase has been purified by a short procedure that includes a tri-phase partitioning step to provide materials that can be crystallized from ammonium sulfate.	Ammonium Sulfate	177-193	superoxide dismutase 2	Homo sapiens	12-42
1850207-15	1991	Our results suggest that the induction of Mn-SOD by TNF-alpha in pulmonary adenocarcinoma cells is pretranslationally mediated and that increasing Mn-SOD activity with TNF-alpha confers protection against O2 radicals.	Superoxides	205-207	superoxide dismutase 2	Homo sapiens	147-153
1850207-2	1991	Manganese superoxide dismutase (Mn-SOD) is a superoxide anion (O2-.)	Superoxides	45-61	superoxide dismutase 2	Homo sapiens	32-38
1850207-2	1991	Manganese superoxide dismutase (Mn-SOD) is a superoxide anion (O2-.)	Superoxides	63-65	superoxide dismutase 2	Homo sapiens	0-30
1850207-2	1991	Manganese superoxide dismutase (Mn-SOD) is a superoxide anion (O2-.)	Superoxides	63-65	superoxide dismutase 2	Homo sapiens	32-38
1850207-9	1991	Actinomycin D blocked the induction of Mn-SOD mRNA by TNF-alpha, but cycloheximide did not.	Dactinomycin	0-13	superoxide dismutase 2	Homo sapiens	39-45
1988135-1	1991	Manganese superoxide dismutase (MnSOD) is a member of a family of metalloenzymes that catalyze the dismutation of the superoxide anion to H2O2.	Superoxides	118-134	superoxide dismutase 2	Homo sapiens	0-30
1988135-1	1991	Manganese superoxide dismutase (MnSOD) is a member of a family of metalloenzymes that catalyze the dismutation of the superoxide anion to H2O2.	Superoxides	118-134	superoxide dismutase 2	Homo sapiens	32-37
1988135-1	1991	Manganese superoxide dismutase (MnSOD) is a member of a family of metalloenzymes that catalyze the dismutation of the superoxide anion to H2O2.	Hydrogen Peroxide	138-142	superoxide dismutase 2	Homo sapiens	0-30
1988135-1	1991	Manganese superoxide dismutase (MnSOD) is a member of a family of metalloenzymes that catalyze the dismutation of the superoxide anion to H2O2.	Hydrogen Peroxide	138-142	superoxide dismutase 2	Homo sapiens	32-37
1646752-2	1991	To assay MnSOD, Cu,ZnSOD can be inhibited selectively by millimolar concentrations of cyanide ion.	Cyanides	86-93	superoxide dismutase 2	Homo sapiens	9-14
1648113-1	1991	A method for copper- and manganese-containing superoxide dismutase (Cu- and MnSOD) assay in tissue homogenates such as liver and brain, based on the measurement of the longitudinal nuclear relaxation time (T1) of F-, has been developed as a preliminary approach to in vivo measurement of these enzymes.	Copper	13-19	superoxide dismutase 2	Homo sapiens	68-81
1648113-2	1991	The relaxation rate of F-, which increases linearly with the SOD concentration, also depends on the oxidation state of the metal ion present in the active site of the enzyme.	Metals	123-128	superoxide dismutase 2	Homo sapiens	61-64
1648113-5	1991	The contribution of the two types of SOD to the F- relaxation rate in the homogenates was measured by addition of either diethyldithiocarbamate or cyanide, both of which selectively inhibit the CuSOD.	Ditiocarb	121-143	superoxide dismutase 2	Homo sapiens	37-40
1648113-5	1991	The contribution of the two types of SOD to the F- relaxation rate in the homogenates was measured by addition of either diethyldithiocarbamate or cyanide, both of which selectively inhibit the CuSOD.	Cyanides	147-154	superoxide dismutase 2	Homo sapiens	37-40
1646752-3	1991	However, calculation of MnSOD activity from the differential cyanide inhibition assay is complex and small experimental errors can cause large errors in the calculated MnSOD activity.	Cyanides	61-68	superoxide dismutase 2	Homo sapiens	24-29
1646752-4	1991	We have assessed how interaction of cyanide and hydrogen peroxide with cytochrome c can lead to further errors in the xanthine oxidase-cytochrome c assay for SOD.	Cyanides	36-43	superoxide dismutase 2	Homo sapiens	158-161
1646752-4	1991	We have assessed how interaction of cyanide and hydrogen peroxide with cytochrome c can lead to further errors in the xanthine oxidase-cytochrome c assay for SOD.	Hydrogen Peroxide	48-65	superoxide dismutase 2	Homo sapiens	158-161
1725166-0	1991	Protective effects of human recombinant MnSOD in adjuvant arthritis and bleomycin-induced lung fibrosis.	Bleomycin	72-81	superoxide dismutase 2	Homo sapiens	40-45
2372299-5	1990	These results suggest that 1,25(OH)2D3 may reduce the susceptibility to TNF cytotoxicity of U-937 cells by enhancing the ability of inducing MnSOD by TNF.	Calcitriol	27-38	superoxide dismutase 2	Homo sapiens	141-146
1725166-1	1991	We have previously shown that human recombinant methionyl manganese superoxide dismutase (MnSOD) is more efficient than CuZnSOD as an anti-inflammatory agent in a model of acute inflammation (Carrageenan-induced paw edema).	Carrageenan	192-203	superoxide dismutase 2	Homo sapiens	48-88
1725166-1	1991	We have previously shown that human recombinant methionyl manganese superoxide dismutase (MnSOD) is more efficient than CuZnSOD as an anti-inflammatory agent in a model of acute inflammation (Carrageenan-induced paw edema).	Carrageenan	192-203	superoxide dismutase 2	Homo sapiens	90-95
1725166-9	1991	MnSOD (50 mg/kg, s.c.), administered 2 h before and then 2 and 4 days after bleomycin, markedly inhibited lung fibrosis, as evident from lung weight and collagen content measured by the 3rd week.	Bleomycin	76-85	superoxide dismutase 2	Homo sapiens	0-5
2276325-1	1990	Manganese-containing superoxide dismutase (Mn-SOD) activity in lung cancer tissue from 5 lung cancer patients was measured by nitrite formation method, and lipid peroxide (LPO) was measured spectrophotometrically by thiobarbituric acid reaction.	Nitrites	126-133	superoxide dismutase 2	Homo sapiens	0-41
2276325-1	1990	Manganese-containing superoxide dismutase (Mn-SOD) activity in lung cancer tissue from 5 lung cancer patients was measured by nitrite formation method, and lipid peroxide (LPO) was measured spectrophotometrically by thiobarbituric acid reaction.	Nitrites	126-133	superoxide dismutase 2	Homo sapiens	43-49
2060854-3	1991	At subcellular level, evidence for the participation of peroxisomal SOD in the molecular mechanism of plant tolerance to Cu is presented, and the activated oxygen-dependent toxicity of a xenobiotic (clofibrate) in plant peroxisomes is examined.	Copper	121-123	superoxide dismutase 2	Homo sapiens	68-71
2071038-1	1991	The light absorption spectral properties of recombinant human MnSOD, which contains an N-terminal additional methionyl residue, were investigated as a function of pH in the range 4.5-10.5.	methionyl	109-118	superoxide dismutase 2	Homo sapiens	62-67
2071038-6	1991	The gel permeation properties of MnSOD were investigated: the enzyme is a tetramer, with a subunit of 22.2 kD; however, it elutes from a Superose 12 column (Pharmacia) with an apparent molecular weight of approximately 60 kD.	Superose 12	137-148	superoxide dismutase 2	Homo sapiens	33-38
2269295-7	1990	Incubation of Mn-SOD in 1% SDS for 2 or 3 days at 25 degrees C or 5 min at 100 degrees C gave material showing two prominent components on polyacrylamide gel electrophoresis in the presence of 0.1% SDS.	Sodium Dodecyl Sulfate	27-30	superoxide dismutase 2	Homo sapiens	14-20
2269295-7	1990	Incubation of Mn-SOD in 1% SDS for 2 or 3 days at 25 degrees C or 5 min at 100 degrees C gave material showing two prominent components on polyacrylamide gel electrophoresis in the presence of 0.1% SDS.	polyacrylamide	139-153	superoxide dismutase 2	Homo sapiens	14-20
2269295-7	1990	Incubation of Mn-SOD in 1% SDS for 2 or 3 days at 25 degrees C or 5 min at 100 degrees C gave material showing two prominent components on polyacrylamide gel electrophoresis in the presence of 0.1% SDS.	Sodium Dodecyl Sulfate	198-201	superoxide dismutase 2	Homo sapiens	14-20
2286014-3	1990	The antibody IgG, purified by the use of Mn SOD-coupled Sepharose, showed a single band on the immunoblotting test with a crude liver extract.	Sepharose	56-65	superoxide dismutase 2	Homo sapiens	41-47
1964798-5	1990	Glucocorticoid may reduce TNF cytotoxicity by inhibiting phospholipase A2 and 1,25-dihydroxyvitamin D3 by inducing MnSOD in combination with TNF.	Calcitriol	78-102	superoxide dismutase 2	Homo sapiens	115-120
2406241-6	1990	The induction of Mn-SOD mRNA levels by LPS is completely inhibited by actinomycin.	Dactinomycin	70-81	superoxide dismutase 2	Homo sapiens	17-23
2163738-2	1990	It was observed that activities of total SOD, Cu, Zn-SOD and Mn-SOD in HCC tissue were lower than those in normal liver tissues respectively (P less than 0.001 & 0.01 less than P less than 0.05).	Adenosine Monophosphate	161-164	superoxide dismutase 2	Homo sapiens	61-67
25157103-2	2014	The level of basal reactive oxygen species (ROS) is extremely low in transformed cells in correlation with elevated expressions of both antioxidant enzymes (catalase, SOD1, and SOD2) and antiapoptotic proteins (Bcl-2/Bcl-xL).	Reactive Oxygen Species	19-42	superoxide dismutase 2	Homo sapiens	177-181
33761612-4	2021	Previously, we have observed that the plasma concentration/activity of superoxide dismutase isozymes differs in the context of obesity and/or rs2234694 (SOD1) and rs4880 (SOD2) and that the concentrations of SOD1, SOD2, SOD3 are correlated with each other.	Superoxides	71-81	superoxide dismutase 2	Homo sapiens	171-175
33761612-4	2021	Previously, we have observed that the plasma concentration/activity of superoxide dismutase isozymes differs in the context of obesity and/or rs2234694 (SOD1) and rs4880 (SOD2) and that the concentrations of SOD1, SOD2, SOD3 are correlated with each other.	Superoxides	71-81	superoxide dismutase 2	Homo sapiens	214-218
33761612-6	2021	In this study, the variability of concentration/activity of superoxide dismutase isozymes in plasma is considered in the context of type 2 diabetes and/or SNPs: rs2234694 (SOD1), rs5746105 (SOD2), rs4880 (SOD2), rs927450 (SOD2), rs8192287 (SOD3).	Superoxides	60-70	superoxide dismutase 2	Homo sapiens	190-194
33761612-6	2021	In this study, the variability of concentration/activity of superoxide dismutase isozymes in plasma is considered in the context of type 2 diabetes and/or SNPs: rs2234694 (SOD1), rs5746105 (SOD2), rs4880 (SOD2), rs927450 (SOD2), rs8192287 (SOD3).	Superoxides	60-70	superoxide dismutase 2	Homo sapiens	205-209
33761612-6	2021	In this study, the variability of concentration/activity of superoxide dismutase isozymes in plasma is considered in the context of type 2 diabetes and/or SNPs: rs2234694 (SOD1), rs5746105 (SOD2), rs4880 (SOD2), rs927450 (SOD2), rs8192287 (SOD3).	Superoxides	60-70	superoxide dismutase 2	Homo sapiens	205-209
33807856-11	2021	Elevated levels of ROS were also reported in diTFPP/C2-ceramide-treated cells, and the expression of the ROS-associated proteins SOD1, SOD2, and catalase was upregulated after diTFPP/C2-ceramide treatment.	Reactive Oxygen Species	19-22	superoxide dismutase 2	Homo sapiens	135-139
33807856-11	2021	Elevated levels of ROS were also reported in diTFPP/C2-ceramide-treated cells, and the expression of the ROS-associated proteins SOD1, SOD2, and catalase was upregulated after diTFPP/C2-ceramide treatment.	ditfpp	45-51	superoxide dismutase 2	Homo sapiens	135-139
33807856-11	2021	Elevated levels of ROS were also reported in diTFPP/C2-ceramide-treated cells, and the expression of the ROS-associated proteins SOD1, SOD2, and catalase was upregulated after diTFPP/C2-ceramide treatment.	N-acetylsphingosine	52-63	superoxide dismutase 2	Homo sapiens	135-139
33807856-11	2021	Elevated levels of ROS were also reported in diTFPP/C2-ceramide-treated cells, and the expression of the ROS-associated proteins SOD1, SOD2, and catalase was upregulated after diTFPP/C2-ceramide treatment.	ditfpp	176-182	superoxide dismutase 2	Homo sapiens	135-139
33807856-11	2021	Elevated levels of ROS were also reported in diTFPP/C2-ceramide-treated cells, and the expression of the ROS-associated proteins SOD1, SOD2, and catalase was upregulated after diTFPP/C2-ceramide treatment.	N-acetylsphingosine	183-194	superoxide dismutase 2	Homo sapiens	135-139
33824320-4	2021	Here, neutron diffraction of two redox-controlled manganese superoxide dismutase crystals reveal the all-atom structures of Mn3+ and Mn2+ enzyme forms.	manganese(III) acetate dihydrate	124-128	superoxide dismutase 2	Homo sapiens	50-80
33824320-4	2021	Here, neutron diffraction of two redox-controlled manganese superoxide dismutase crystals reveal the all-atom structures of Mn3+ and Mn2+ enzyme forms.	Manganese(2+)	133-137	superoxide dismutase 2	Homo sapiens	50-80
33824320-7	2021	We report a concerted proton and electron transfer mechanism for human manganese superoxide dismutase from the direct visualization of active site protons in Mn3+ and Mn2+ redox states.	manganese(III) acetate dihydrate	158-162	superoxide dismutase 2	Homo sapiens	71-101
33824320-7	2021	We report a concerted proton and electron transfer mechanism for human manganese superoxide dismutase from the direct visualization of active site protons in Mn3+ and Mn2+ redox states.	Manganese(2+)	167-171	superoxide dismutase 2	Homo sapiens	71-101
25157103-2	2014	The level of basal reactive oxygen species (ROS) is extremely low in transformed cells in correlation with elevated expressions of both antioxidant enzymes (catalase, SOD1, and SOD2) and antiapoptotic proteins (Bcl-2/Bcl-xL).	Reactive Oxygen Species	44-47	superoxide dismutase 2	Homo sapiens	177-181
34954231-7	2022	Our in vitro study further demonstrated that ALO protected beta-cells from STZ/hydrogen peroxide-induced oxidative damage as manifested by increased expression of MnSOD and CAT.	Streptozocin	75-78	superoxide dismutase 2	Homo sapiens	163-168
22723845-0	2012	Human SOD2 modification by dopamine quinones affects enzymatic activity by promoting its aggregation: possible implications for Parkinson"s disease.	Dopamine	27-35	superoxide dismutase 2	Homo sapiens	6-10
22723845-4	2012	Superoxide dismutase 2 (SOD2) is a mitochondrial enzyme that converts superoxide radicals to molecular oxygen and hydrogen peroxide, providing a first line of defense against ROS.	Superoxides	70-80	superoxide dismutase 2	Homo sapiens	0-22
22723845-4	2012	Superoxide dismutase 2 (SOD2) is a mitochondrial enzyme that converts superoxide radicals to molecular oxygen and hydrogen peroxide, providing a first line of defense against ROS.	Superoxides	70-80	superoxide dismutase 2	Homo sapiens	24-28
22723845-4	2012	Superoxide dismutase 2 (SOD2) is a mitochondrial enzyme that converts superoxide radicals to molecular oxygen and hydrogen peroxide, providing a first line of defense against ROS.	Oxygen	103-109	superoxide dismutase 2	Homo sapiens	0-22
22723845-4	2012	Superoxide dismutase 2 (SOD2) is a mitochondrial enzyme that converts superoxide radicals to molecular oxygen and hydrogen peroxide, providing a first line of defense against ROS.	Oxygen	103-109	superoxide dismutase 2	Homo sapiens	24-28
22723845-4	2012	Superoxide dismutase 2 (SOD2) is a mitochondrial enzyme that converts superoxide radicals to molecular oxygen and hydrogen peroxide, providing a first line of defense against ROS.	Hydrogen Peroxide	114-131	superoxide dismutase 2	Homo sapiens	0-22
22723845-4	2012	Superoxide dismutase 2 (SOD2) is a mitochondrial enzyme that converts superoxide radicals to molecular oxygen and hydrogen peroxide, providing a first line of defense against ROS.	Hydrogen Peroxide	114-131	superoxide dismutase 2	Homo sapiens	24-28
22723845-4	2012	Superoxide dismutase 2 (SOD2) is a mitochondrial enzyme that converts superoxide radicals to molecular oxygen and hydrogen peroxide, providing a first line of defense against ROS.	Reactive Oxygen Species	175-178	superoxide dismutase 2	Homo sapiens	0-22
22723845-4	2012	Superoxide dismutase 2 (SOD2) is a mitochondrial enzyme that converts superoxide radicals to molecular oxygen and hydrogen peroxide, providing a first line of defense against ROS.	Reactive Oxygen Species	175-178	superoxide dismutase 2	Homo sapiens	24-28
22723845-6	2012	Using radioactive DA, we demonstrated that SOD2 is a target of DAQs.	Dopamine	18-20	superoxide dismutase 2	Homo sapiens	43-47
22723845-6	2012	Using radioactive DA, we demonstrated that SOD2 is a target of DAQs.	dopamine quinone	63-67	superoxide dismutase 2	Homo sapiens	43-47
22723845-7	2012	Exposure to micromolar DAQ concentrations induces a loss of up to 50% of SOD2 enzymatic activity in a dose-dependent manner, which is correlated to the concomitant formation of protein aggregates, while the coordination geometry of the active site appears unaffected by DAQ modifications.	dopamine quinone	23-26	superoxide dismutase 2	Homo sapiens	73-77
22723845-7	2012	Exposure to micromolar DAQ concentrations induces a loss of up to 50% of SOD2 enzymatic activity in a dose-dependent manner, which is correlated to the concomitant formation of protein aggregates, while the coordination geometry of the active site appears unaffected by DAQ modifications.	dopamine quinone	270-273	superoxide dismutase 2	Homo sapiens	73-77
22723845-8	2012	Our findings support a model in which DAQ-mediated SOD2 inactivation increases mitochondrial ROS production, suggesting a link between oxidative stress and mitochondrial dysfunction.	dopamine quinone	38-41	superoxide dismutase 2	Homo sapiens	51-55
22723845-8	2012	Our findings support a model in which DAQ-mediated SOD2 inactivation increases mitochondrial ROS production, suggesting a link between oxidative stress and mitochondrial dysfunction.	Reactive Oxygen Species	93-96	superoxide dismutase 2	Homo sapiens	51-55
34954231-7	2022	Our in vitro study further demonstrated that ALO protected beta-cells from STZ/hydrogen peroxide-induced oxidative damage as manifested by increased expression of MnSOD and CAT.	Hydrogen Peroxide	79-96	superoxide dismutase 2	Homo sapiens	163-168
34858880-9	2021	Knowing that TcSODA is acetylated at lysine residues K44 and K97, and that K97 is located at a similar region in the protein structure as K68 in human manganese superoxide dismutase (MnSOD), responsible for regulating MnSOD activity, we generated mutated versions of TcSODA at K44 and K97 and found that replacing K97 by glutamine, which mimics an acetylated lysine, negatively affects the enzyme activity in vitro.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	138-141	superoxide dismutase 2	Homo sapiens	151-181
34968705-2	2022	By regulating superoxide levels, manganese superoxide dismutase plays important roles in numerous biochemical and molecular events essential for the survival of aerobic life.	Superoxides	14-24	superoxide dismutase 2	Homo sapiens	33-63
34958669-1	2022	Superoxide dismutase 2 (SOD2) catalyzes the dismutation of superoxide to hydrogen peroxide in mitochondria limiting mitochondrial damage.	Superoxides	59-69	superoxide dismutase 2	Homo sapiens	0-22
34958669-1	2022	Superoxide dismutase 2 (SOD2) catalyzes the dismutation of superoxide to hydrogen peroxide in mitochondria limiting mitochondrial damage.	Superoxides	59-69	superoxide dismutase 2	Homo sapiens	24-28
34958669-1	2022	Superoxide dismutase 2 (SOD2) catalyzes the dismutation of superoxide to hydrogen peroxide in mitochondria limiting mitochondrial damage.	Hydrogen Peroxide	73-90	superoxide dismutase 2	Homo sapiens	0-22
34958669-1	2022	Superoxide dismutase 2 (SOD2) catalyzes the dismutation of superoxide to hydrogen peroxide in mitochondria limiting mitochondrial damage.	Hydrogen Peroxide	73-90	superoxide dismutase 2	Homo sapiens	24-28
34958669-7	2022	SOD2V16A increases hydrogen peroxide and mitochondrial reactive oxygen species (ROS) production compared to controls.	Hydrogen Peroxide	19-36	superoxide dismutase 2	Homo sapiens	0-4
34958669-7	2022	SOD2V16A increases hydrogen peroxide and mitochondrial reactive oxygen species (ROS) production compared to controls.	Reactive Oxygen Species	55-78	superoxide dismutase 2	Homo sapiens	0-4
34958669-7	2022	SOD2V16A increases hydrogen peroxide and mitochondrial reactive oxygen species (ROS) production compared to controls.	Reactive Oxygen Species	80-83	superoxide dismutase 2	Homo sapiens	0-4
34667598-0	2021	Influence of the SOD2 A16V gene polymorphism on alterations of redox markers and erythrocyte membrane fatty acid profiles in patients with multiple chemical sensitivity.	Fatty Acids	102-112	superoxide dismutase 2	Homo sapiens	17-21
34667598-2	2021	Recently, a single nucleotide polymorphism of the gene coding for mitochondrial superoxide dismutase (SOD2), namely the missense substitution A16V (C47>T) resulting in alteration of SOD2 enzyme activity, has been reported to be associated with MCS.	Superoxides	80-90	superoxide dismutase 2	Homo sapiens	102-106
34667598-2	2021	Recently, a single nucleotide polymorphism of the gene coding for mitochondrial superoxide dismutase (SOD2), namely the missense substitution A16V (C47>T) resulting in alteration of SOD2 enzyme activity, has been reported to be associated with MCS.	Superoxides	80-90	superoxide dismutase 2	Homo sapiens	182-186
34869361-5	2021	Subsequently, we administered adeno-associated virus-SIRT3 to the posterior semicircular canals and found that SIRT3 overexpression significantly attenuated hair cell injury and that this protective effect of SIRT3 could be blocked by 2-methoxyestradiol, a SOD2 inhibitor.	2-Methoxyestradiol	235-253	superoxide dismutase 2	Homo sapiens	257-261
34582115-8	2022	We observed higher levels of 8-OHdG in patients with MnSOD and XRCC1 mutant genotypes and higher XRCC1 levels in patients with NOX p22 fox mutant genotypes rather than controls.	8-ohdg	29-35	superoxide dismutase 2	Homo sapiens	53-58
34826419-10	2022	Notably, ROS production and SOD2 expression was significantly elevated in both pterygium and conjunctival cells after hydroxychloroquine treatment.	Hydroxychloroquine	118-136	superoxide dismutase 2	Homo sapiens	28-32
34547605-1	2021	Mononuclear manganese(III) peroxido complexes are candidates for the reaction intermediates in manganese containing proteins, such as manganese superoxide dismutase (Mn-SOD) etc.	manganese(iii) peroxido complexes	12-45	superoxide dismutase 2	Homo sapiens	134-164
34547605-1	2021	Mononuclear manganese(III) peroxido complexes are candidates for the reaction intermediates in manganese containing proteins, such as manganese superoxide dismutase (Mn-SOD) etc.	manganese(iii) peroxido complexes	12-45	superoxide dismutase 2	Homo sapiens	166-172
34547605-1	2021	Mononuclear manganese(III) peroxido complexes are candidates for the reaction intermediates in manganese containing proteins, such as manganese superoxide dismutase (Mn-SOD) etc.	Manganese	95-104	superoxide dismutase 2	Homo sapiens	134-164
34547605-1	2021	Mononuclear manganese(III) peroxido complexes are candidates for the reaction intermediates in manganese containing proteins, such as manganese superoxide dismutase (Mn-SOD) etc.	Manganese	95-104	superoxide dismutase 2	Homo sapiens	166-172
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	119-131	superoxide dismutase 2	Homo sapiens	58-62
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	133-136	superoxide dismutase 2	Homo sapiens	58-62
34944579-6	2021	Spectroscopic data are combined with rigid body protein-protein docking to assess the potential structure of the FXN-SOD2 complex, which leaves the metal binding region of FXN accessible to the solvent.	Metals	148-153	superoxide dismutase 2	Homo sapiens	117-121
34941679-6	2021	Furthermore, reactive oxygen species (ROS) generation was significantly decreased and the mRNA levels of CAT, SOD2 and GSH-PX were obviously increased in the 200 muM GSP cotreatment group.	Grape Seed Proanthocyanidins	166-169	superoxide dismutase 2	Homo sapiens	110-114
34766239-7	2022	In the presence of HUMSC-CM, increases in superoxide dismutase 1 (SOD1), superoxide dismutase 2 (SOD2), glutathione peroxidase (GPX), and glutathione (GSH) levels were found to contribute to a reduction in reactive oxygen species (ROS) levels.	Reactive Oxygen Species	206-229	superoxide dismutase 2	Homo sapiens	97-101
34858880-9	2021	Knowing that TcSODA is acetylated at lysine residues K44 and K97, and that K97 is located at a similar region in the protein structure as K68 in human manganese superoxide dismutase (MnSOD), responsible for regulating MnSOD activity, we generated mutated versions of TcSODA at K44 and K97 and found that replacing K97 by glutamine, which mimics an acetylated lysine, negatively affects the enzyme activity in vitro.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	138-141	superoxide dismutase 2	Homo sapiens	183-188
34858880-9	2021	Knowing that TcSODA is acetylated at lysine residues K44 and K97, and that K97 is located at a similar region in the protein structure as K68 in human manganese superoxide dismutase (MnSOD), responsible for regulating MnSOD activity, we generated mutated versions of TcSODA at K44 and K97 and found that replacing K97 by glutamine, which mimics an acetylated lysine, negatively affects the enzyme activity in vitro.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	138-141	superoxide dismutase 2	Homo sapiens	218-223
34858880-9	2021	Knowing that TcSODA is acetylated at lysine residues K44 and K97, and that K97 is located at a similar region in the protein structure as K68 in human manganese superoxide dismutase (MnSOD), responsible for regulating MnSOD activity, we generated mutated versions of TcSODA at K44 and K97 and found that replacing K97 by glutamine, which mimics an acetylated lysine, negatively affects the enzyme activity in vitro.	tcsoda	267-273	superoxide dismutase 2	Homo sapiens	151-181
34858880-9	2021	Knowing that TcSODA is acetylated at lysine residues K44 and K97, and that K97 is located at a similar region in the protein structure as K68 in human manganese superoxide dismutase (MnSOD), responsible for regulating MnSOD activity, we generated mutated versions of TcSODA at K44 and K97 and found that replacing K97 by glutamine, which mimics an acetylated lysine, negatively affects the enzyme activity in vitro.	tcsoda	267-273	superoxide dismutase 2	Homo sapiens	218-223
34858880-9	2021	Knowing that TcSODA is acetylated at lysine residues K44 and K97, and that K97 is located at a similar region in the protein structure as K68 in human manganese superoxide dismutase (MnSOD), responsible for regulating MnSOD activity, we generated mutated versions of TcSODA at K44 and K97 and found that replacing K97 by glutamine, which mimics an acetylated lysine, negatively affects the enzyme activity in vitro.	K97	314-317	superoxide dismutase 2	Homo sapiens	218-223
34858880-9	2021	Knowing that TcSODA is acetylated at lysine residues K44 and K97, and that K97 is located at a similar region in the protein structure as K68 in human manganese superoxide dismutase (MnSOD), responsible for regulating MnSOD activity, we generated mutated versions of TcSODA at K44 and K97 and found that replacing K97 by glutamine, which mimics an acetylated lysine, negatively affects the enzyme activity in vitro.	Glutamine	321-330	superoxide dismutase 2	Homo sapiens	218-223
34684868-6	2021	PKE decreased the apoptosis of SW1353 cells treated with H2O2 and could upregulate the gene expression of antioxidant enzymes (SOD-2, GPx, and CAT) and the Bcl-2/Bax ratio, as well as regulate PARP, thus conferring resistance to H2O2 attack.	Hydrogen Peroxide	57-61	superoxide dismutase 2	Homo sapiens	127-132
34790286-0	2021	Circular RNA circPHKA2 Relieves OGD-Induced Human Brain Microvascular Endothelial Cell Injuries through Competitively Binding miR-574-5p to Modulate SOD2.	mir-574-5p	126-136	superoxide dismutase 2	Homo sapiens	149-153
34722507-9	2021	DFO, N-acetylcysteine (NAC), and overexpression of superoxide dismutase 2 (SOD2) decreased ROS generation, autophagy, and cell death.	Reactive Oxygen Species	91-94	superoxide dismutase 2	Homo sapiens	51-73
34722507-9	2021	DFO, N-acetylcysteine (NAC), and overexpression of superoxide dismutase 2 (SOD2) decreased ROS generation, autophagy, and cell death.	Reactive Oxygen Species	91-94	superoxide dismutase 2	Homo sapiens	75-79
34676202-11	2021	In metformin-treated samples, the CEBPA, TP53 and USF1 transcription factors appeared to be involved in the regulation of several factors (SOD1, SOD2, CAT, GLRX, GSTP1) blocking ROS.	Metformin	3-12	superoxide dismutase 2	Homo sapiens	145-149
34676202-11	2021	In metformin-treated samples, the CEBPA, TP53 and USF1 transcription factors appeared to be involved in the regulation of several factors (SOD1, SOD2, CAT, GLRX, GSTP1) blocking ROS.	Reactive Oxygen Species	178-181	superoxide dismutase 2	Homo sapiens	145-149
34402900-2	2021	Manganese (Mn) is critical for CL function as it is a cofactor for Mn superoxide dismutase (MnSOD) and enzymes involved in cholesterol synthesis.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	67-90
34630071-7	2021	Mechanistically, the expression of NADPH oxidase 1 (Nox1) was found to be suppressed and antioxidant enzymes including catalase, superoxide dismutase 2 (SOD-2), and heme oxygenase-1(HO-1) were enhanced following RH treatment, suggesting RH exhibited antioxidant activity by reducing the generation of reactive oxygen species (ROS) as well as enhancing the depletion of ROS.	rhapontin	212-214	superoxide dismutase 2	Homo sapiens	129-151
34630071-7	2021	Mechanistically, the expression of NADPH oxidase 1 (Nox1) was found to be suppressed and antioxidant enzymes including catalase, superoxide dismutase 2 (SOD-2), and heme oxygenase-1(HO-1) were enhanced following RH treatment, suggesting RH exhibited antioxidant activity by reducing the generation of reactive oxygen species (ROS) as well as enhancing the depletion of ROS.	rhapontin	212-214	superoxide dismutase 2	Homo sapiens	153-158
34273538-5	2021	H2O2 emission decreased 60.4% after the intervention (Succinate 3 mmol l-1), concurrent with a 35.1% increase in protein levels of the antioxidant manganese superoxide dismutase (MnSOD) and a trend towards increased levels of the antioxidant catalase (p = 0.06, 72.9%).	Hydrogen Peroxide	0-4	superoxide dismutase 2	Homo sapiens	147-177
34273538-5	2021	H2O2 emission decreased 60.4% after the intervention (Succinate 3 mmol l-1), concurrent with a 35.1% increase in protein levels of the antioxidant manganese superoxide dismutase (MnSOD) and a trend towards increased levels of the antioxidant catalase (p = 0.06, 72.9%).	Hydrogen Peroxide	0-4	superoxide dismutase 2	Homo sapiens	179-184
34260893-6	2021	The mRNA expression levels of Cat and MnSod were increased when the nanoformulation was compared to the doxorubicin solution.	Doxorubicin	104-115	superoxide dismutase 2	Homo sapiens	38-43
34487292-9	2021	The intracellular antioxidant enzymes HO-1 and SOD-2 were upregulated by neoxanthin pretreatment.	neoxanthin	73-83	superoxide dismutase 2	Homo sapiens	47-52
34539974-11	2021	Progesterone replacement therapy induced a significant increase in MnSOD, P53, sestrin 2 (SENS2), and TERF2 mRNA expression when compared to basal conditions.	Progesterone	0-12	superoxide dismutase 2	Homo sapiens	67-72
34402900-2	2021	Manganese (Mn) is critical for CL function as it is a cofactor for Mn superoxide dismutase (MnSOD) and enzymes involved in cholesterol synthesis.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	92-97
34401649-7	2021	Results: The mRNA expression levels of NRF2, SOD2, GPX4, and CAT (p < 0.05 for all) and significantly increased after treatment with DPP.	dipalmitoylphosphatidylserine	133-136	superoxide dismutase 2	Homo sapiens	45-49
34362891-5	2021	By the Paleoproterozoic, they became genetically capable of using iron, nickel, and manganese as cofactors (FeSOD, NiSOD, and MnSOD respectively).	Iron	66-70	superoxide dismutase 2	Homo sapiens	126-131
34362891-5	2021	By the Paleoproterozoic, they became genetically capable of using iron, nickel, and manganese as cofactors (FeSOD, NiSOD, and MnSOD respectively).	Nickel	72-78	superoxide dismutase 2	Homo sapiens	126-131
34362891-5	2021	By the Paleoproterozoic, they became genetically capable of using iron, nickel, and manganese as cofactors (FeSOD, NiSOD, and MnSOD respectively).	Manganese	84-93	superoxide dismutase 2	Homo sapiens	126-131
34401649-10	2021	Conclusion: DPP can increase the expressions of NRF2, GPX4, SOD2, and CAT genes and also improve the semen quality in infertile men.	dipalmitoylphosphatidylserine	12-15	superoxide dismutase 2	Homo sapiens	60-64
34106394-11	2021	NaB also suppressed the BAX nuclear translocation and modulated Nrf-2, HO-1 and MnSOD expression in neuroblastoma cells.	nab	0-3	superoxide dismutase 2	Homo sapiens	80-85
34253201-0	2021	Correction to: Associations between prenatal exposure to cadmium and lead with neural tube defect risks are modified by single-nucleotide polymorphisms of fetal MTHFR and SOD2: a case-control study.	Cadmium	57-64	superoxide dismutase 2	Homo sapiens	171-175
34349641-5	2021	In the present study, we found that SOD2 was downregulated and O2  - was upregulated in H2O2-induced H9C2 cardiac myocyte injury in vitro and myocardial I/R injury in vivo, while such alterations were reversed by ASIV.	Hydrogen Peroxide	88-92	superoxide dismutase 2	Homo sapiens	36-40
34270583-13	2021	If DD fibroblasts were treated with the pharmacological inhibitor SB431542, myofibrogenesis was inhibited, but MnSOD expression was simultaneously elevated, which ought to affect ROS level by raising intracellular H2O2 amount.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	66-74	superoxide dismutase 2	Homo sapiens	111-116
34270583-13	2021	If DD fibroblasts were treated with the pharmacological inhibitor SB431542, myofibrogenesis was inhibited, but MnSOD expression was simultaneously elevated, which ought to affect ROS level by raising intracellular H2O2 amount.	Reactive Oxygen Species	179-182	superoxide dismutase 2	Homo sapiens	111-116
34270583-13	2021	If DD fibroblasts were treated with the pharmacological inhibitor SB431542, myofibrogenesis was inhibited, but MnSOD expression was simultaneously elevated, which ought to affect ROS level by raising intracellular H2O2 amount.	Hydrogen Peroxide	214-218	superoxide dismutase 2	Homo sapiens	111-116
34356358-7	2021	Our findings indicated that the effects of quercetin on regulating the generation of mtROS were dependent on increased levels of deacetyl-SOD2 through the Nrf2-PGC-1alpha-Sirt1 signaling pathway.	Quercetin	43-52	superoxide dismutase 2	Homo sapiens	138-142
34234193-3	2021	Metformin increased AMPK, p-AMPK (Thr172), FOXO3a, p-FOXO3a (Ser413), and MnSOD levels in HDF, but not in AsPC-1 cells.	Metformin	0-9	superoxide dismutase 2	Homo sapiens	74-79
34211977-4	2021	Luteolin supplementation decreased intracellular reactive oxygen species levels and increased the expression levels of oxidative stress-related genes (SOD1, SOD2, and CAT).	Luteolin	0-8	superoxide dismutase 2	Homo sapiens	157-161
34353693-11	2021	An increase in expression of MnSOD, catalase, and higher levels of tGSH and GSH:GSSG ratios underlie the ROS salvaging activity of picroside II.	Reactive Oxygen Species	105-108	superoxide dismutase 2	Homo sapiens	29-34
34353693-11	2021	An increase in expression of MnSOD, catalase, and higher levels of tGSH and GSH:GSSG ratios underlie the ROS salvaging activity of picroside II.	picroside II	131-143	superoxide dismutase 2	Homo sapiens	29-34
34646076-14	2021	Conclusions: We concluded that d-Leu protects oocytes from psychological stress through the induction of HO-1 and SOD2 expression then by reducing oxidative stress.	D-LEUCINE	31-36	superoxide dismutase 2	Homo sapiens	114-118
34195241-3	2021	The BPC supplementation during gestation of sows downregulated the neonate piglets" jejunal genes involved in oxidation (SOD2) and nutrient transport (SLC16A1/MCT1, SLC11A2/DMT1, and SLC39A/ZIP4), while IFNG and CLDN4 related to immune response and barrier function, respectively, were upregulated (q < 0.10).	bpc	4-7	superoxide dismutase 2	Homo sapiens	121-125
34195288-17	2021	Isovitexin-associated inhibition of stemness in LCSLCs is partly dependent on blockage of the MnSOD/CaMKII/AMPK signaling axis and glycolysis suppression.	isovitexin	0-10	superoxide dismutase 2	Homo sapiens	94-99
34090432-0	2021	Associations between prenatal exposure to cadmium and lead with neural tube defect risks are modified by single-nucleotide polymorphisms of fetal MTHFR and SOD2: a case-control study.	Cadmium	42-49	superoxide dismutase 2	Homo sapiens	156-160
34090432-14	2021	CONCLUSIONS: Prenatal exposure to Cd may be a risk factor for NTDs, and the risk effect may be enhanced in fetuses who carry the G allele of rs4880 in SOD2 and T allele of rs1801133 in MTHFR.	Cadmium	34-36	superoxide dismutase 2	Homo sapiens	151-155
34195288-0	2021	Isovitexin Suppresses Stemness of Lung Cancer Stem-Like Cells through Blockage of MnSOD/CaMKII/AMPK Signaling and Glycolysis Inhibition.	isovitexin	0-10	superoxide dismutase 2	Homo sapiens	82-87
35462098-5	2022	This study found that in HK-2 cells, with the prolongation of high concentration glucose stimulation, the expression level of TFEB showed a trend of first increasing and then decreasing; and nuclear translocation of TFEB expression occurred within 24 h. In high-glucose environment, the expression of pyroptosis-related proteins gradually increased over time, while the expression of anti-oxidative stress proteins superoxide dismutase2(SOD2)and NAD(P)H: quinone oxidoreductase 1(NQO1) showed a trend of first increasing and then decreasing.	Glucose	81-88	superoxide dismutase 2	Homo sapiens	437-441
34195288-3	2021	However, whether isovitexin could inhibit the promotion of stemness of LCSLCs mediated by MnSOD through glycolysis remains unclear.	isovitexin	17-27	superoxide dismutase 2	Homo sapiens	90-95
34195288-4	2021	Objective: Our study was aimed at investigating whether isovitexin inhibits lung cancer stem-like cells (LCSLCs) through MnSOD signaling blockage and glycolysis suppression.	isovitexin	56-66	superoxide dismutase 2	Homo sapiens	121-126
34195288-13	2021	The knockdown of MnSOD significantly augmented isovitexin-associated inhibition of CaMKII/AMPK signaling, glycolysis, and stemness in LCSLCs.	isovitexin	47-57	superoxide dismutase 2	Homo sapiens	17-22
34173113-7	2021	The established features of immune regulation (hyperproduction of IgG to benzene, imbalance of apoptosis markers (CD127-, CD3+CD95+, p53, and TNFR) against the background of altered polymorphism of candidate genes (FOXP3, SOD2) form a complex of genetic and immunological markers of autonomic regulation disorders in men living under conditions of aerogenic exposure to benzene.	Benzene	370-377	superoxide dismutase 2	Homo sapiens	222-226
35594792-4	2022	Using ovarian cancer cells as a model, we demonstrate that an increase in mitochondrial superoxide dismutase SOD2 protein expression is a very early event initiated in response to detachment, an important step during metastasis that has been associated with increased oxidative stress.	Superoxides	88-98	superoxide dismutase 2	Homo sapiens	109-113
35462098-5	2022	This study found that in HK-2 cells, with the prolongation of high concentration glucose stimulation, the expression level of TFEB showed a trend of first increasing and then decreasing; and nuclear translocation of TFEB expression occurred within 24 h. In high-glucose environment, the expression of pyroptosis-related proteins gradually increased over time, while the expression of anti-oxidative stress proteins superoxide dismutase2(SOD2)and NAD(P)H: quinone oxidoreductase 1(NQO1) showed a trend of first increasing and then decreasing.	Glucose	262-269	superoxide dismutase 2	Homo sapiens	437-441
35462098-9	2022	The research results suggested that in HK-2 cells in the high glucose environment, TFEB may affect the pyroptosis by regulating the expression of antioxidant enzymes SOD2 and NQO1, which provides a new therapeutic idea for the treatment of diabetic nephropathy.	Glucose	62-69	superoxide dismutase 2	Homo sapiens	166-170
35631465-8	2022	PDGF-C diminished the oxidative stress induced by high glucose, increasing SOD2 expression and SOD activity, and modulating the Keap1 expression gene.	Glucose	55-62	superoxide dismutase 2	Homo sapiens	75-79
35615960-6	2022	In contrast, the expression of SOD-2 increased by 1.026-fold in the presence of quercetin.	Quercetin	80-89	superoxide dismutase 2	Homo sapiens	31-36
35568871-18	2022	Furthermore, we proved that both SRT1720 and mitoquinone counteracted the effect of CS on NOX4, SOD2, PPARalpha and CPT1a in vivo.	mitoquinone	45-56	superoxide dismutase 2	Homo sapiens	96-100
35453408-5	2022	A decreased interaction between sirtuin 3 and superoxide dismutase 2 (SOD2) induced SOD2 acetylation on lysine 68 and inactivation, leading to mitochondrial oxidative stress and dysfunction and hypertrophy after 24 h of Iso treatment.	Lysine	104-110	superoxide dismutase 2	Homo sapiens	46-68
35624792-1	2022	The superoxide dismutase (SOD) family functions as a reactive oxygen species (ROS)-scavenging system by converting superoxide anions into hydrogen peroxide in the cytosol (SOD1), mitochondria (SOD2), and extracellular matrix (SOD3).	Superoxides	115-132	superoxide dismutase 2	Homo sapiens	193-197
35624792-1	2022	The superoxide dismutase (SOD) family functions as a reactive oxygen species (ROS)-scavenging system by converting superoxide anions into hydrogen peroxide in the cytosol (SOD1), mitochondria (SOD2), and extracellular matrix (SOD3).	Hydrogen Peroxide	138-155	superoxide dismutase 2	Homo sapiens	193-197
35625603-5	2022	CPFX 120 microg/mL induced overexpression of IL-33, CASP-3 and CASP-9 in all cybrids, upregulation of TGF-beta1 and SOD2 in U and J cybrids, respectively, along with decreased expression of IL-6 in J cybrids.	Ciprofloxacin	0-4	superoxide dismutase 2	Homo sapiens	116-120
35513593-8	2022	Clomiphene treatment increased mRNA expression of Bax (4 fold) and SOD-2 (2 fold), which was reversed by co-treatment with estradiol.	Clomiphene	0-10	superoxide dismutase 2	Homo sapiens	67-72
35513593-8	2022	Clomiphene treatment increased mRNA expression of Bax (4 fold) and SOD-2 (2 fold), which was reversed by co-treatment with estradiol.	Estradiol	123-132	superoxide dismutase 2	Homo sapiens	67-72
35513593-9	2022	SOD-2 expression increased in cells treated with letrozole compared to control (4 fold), which was also reversed by estradiol.	Letrozole	49-58	superoxide dismutase 2	Homo sapiens	0-5
35513593-9	2022	SOD-2 expression increased in cells treated with letrozole compared to control (4 fold), which was also reversed by estradiol.	Estradiol	116-125	superoxide dismutase 2	Homo sapiens	0-5
35286965-7	2022	Our experiments have shown that TCS in the nontoxic concentrations of 10 microM exerts an impact on SOD2 mRNA expression and SOD activity in the SCC-15 cell line.	Triclosan	32-35	superoxide dismutase 2	Homo sapiens	100-104
35625856-6	2022	The results showed that excess aldosterone suppressed mitochondrial DNA copy numbers, anti-mitochondrial protein, and SOD2 protein expression in a dose- and time-dependent manner.	Aldosterone	31-42	superoxide dismutase 2	Homo sapiens	118-122
35624792-1	2022	The superoxide dismutase (SOD) family functions as a reactive oxygen species (ROS)-scavenging system by converting superoxide anions into hydrogen peroxide in the cytosol (SOD1), mitochondria (SOD2), and extracellular matrix (SOD3).	Reactive Oxygen Species	53-76	superoxide dismutase 2	Homo sapiens	193-197
35624792-1	2022	The superoxide dismutase (SOD) family functions as a reactive oxygen species (ROS)-scavenging system by converting superoxide anions into hydrogen peroxide in the cytosol (SOD1), mitochondria (SOD2), and extracellular matrix (SOD3).	Reactive Oxygen Species	78-81	superoxide dismutase 2	Homo sapiens	193-197
35469135-0	2022	Modulation of MnSOD and FoxM1 is Involved in Invasion and EMT Suppression by Isovitexin in Hepatocellular Carcinoma Cells (Retraction).	isovitexin	77-87	superoxide dismutase 2	Homo sapiens	14-19
35181309-0	2022	Daidzin targets epithelial-to-mesenchymal transition process by attenuating manganese superoxide dismutase expression and PI3K/Akt/mTOR activation in tumor cells.	daidzin	0-7	superoxide dismutase 2	Homo sapiens	76-106
35181309-2	2022	A few recent studies have reported that manganese superoxide dismutase (MnSOD) can effectively modulate EMT phenotype by influencing cellular redox environment via altering the intracellular ratio between O2- and H2O2.	Oxygen	205-208	superoxide dismutase 2	Homo sapiens	40-70
35181309-2	2022	A few recent studies have reported that manganese superoxide dismutase (MnSOD) can effectively modulate EMT phenotype by influencing cellular redox environment via altering the intracellular ratio between O2- and H2O2.	Oxygen	205-208	superoxide dismutase 2	Homo sapiens	72-77
35181309-2	2022	A few recent studies have reported that manganese superoxide dismutase (MnSOD) can effectively modulate EMT phenotype by influencing cellular redox environment via altering the intracellular ratio between O2- and H2O2.	Hydrogen Peroxide	213-217	superoxide dismutase 2	Homo sapiens	40-70
35181309-2	2022	A few recent studies have reported that manganese superoxide dismutase (MnSOD) can effectively modulate EMT phenotype by influencing cellular redox environment via altering the intracellular ratio between O2- and H2O2.	Hydrogen Peroxide	213-217	superoxide dismutase 2	Homo sapiens	72-77
35181309-15	2022	Our data indicated that DDZ might act as a potent suppressor of EMT by affecting MnSOD expression in tumor cells.	daidzin	24-27	superoxide dismutase 2	Homo sapiens	81-86
35447940-8	2022	Moreover, the expression of the antioxidant enzymes superoxide dismutase (SOD1 and SOD2) in CA1-3 pyramidal cells were gradually and significantly reduced after ischemia.	Superoxides	52-62	superoxide dismutase 2	Homo sapiens	83-87
35447940-9	2022	However, in astaxanthin-treated gerbils, the expression of SOD1 and SOD2 was significantly high compared to in-vehicle-treated gerbils before and after ischemia induction.	astaxanthine	12-23	superoxide dismutase 2	Homo sapiens	68-72
35418125-3	2022	The 2D MOF periodically assembles numbers of manganese porphyrin molecules, which has a metal coordination geometry analogous to those of two typical antioxidases, human mitochondrial manganese superoxide dismutase (Mn-SOD) and human erythrocyte catalase.	manganese porphyrin	45-64	superoxide dismutase 2	Homo sapiens	184-214
35418125-3	2022	The 2D MOF periodically assembles numbers of manganese porphyrin molecules, which has a metal coordination geometry analogous to those of two typical antioxidases, human mitochondrial manganese superoxide dismutase (Mn-SOD) and human erythrocyte catalase.	manganese porphyrin	45-64	superoxide dismutase 2	Homo sapiens	216-222
35418125-3	2022	The 2D MOF periodically assembles numbers of manganese porphyrin molecules, which has a metal coordination geometry analogous to those of two typical antioxidases, human mitochondrial manganese superoxide dismutase (Mn-SOD) and human erythrocyte catalase.	Metals	88-93	superoxide dismutase 2	Homo sapiens	184-214
35418125-3	2022	The 2D MOF periodically assembles numbers of manganese porphyrin molecules, which has a metal coordination geometry analogous to those of two typical antioxidases, human mitochondrial manganese superoxide dismutase (Mn-SOD) and human erythrocyte catalase.	Metals	88-93	superoxide dismutase 2	Homo sapiens	216-222
35453408-5	2022	A decreased interaction between sirtuin 3 and superoxide dismutase 2 (SOD2) induced SOD2 acetylation on lysine 68 and inactivation, leading to mitochondrial oxidative stress and dysfunction and hypertrophy after 24 h of Iso treatment.	Lysine	104-110	superoxide dismutase 2	Homo sapiens	70-74
35453408-5	2022	A decreased interaction between sirtuin 3 and superoxide dismutase 2 (SOD2) induced SOD2 acetylation on lysine 68 and inactivation, leading to mitochondrial oxidative stress and dysfunction and hypertrophy after 24 h of Iso treatment.	Lysine	104-110	superoxide dismutase 2	Homo sapiens	84-88
35453408-5	2022	A decreased interaction between sirtuin 3 and superoxide dismutase 2 (SOD2) induced SOD2 acetylation on lysine 68 and inactivation, leading to mitochondrial oxidative stress and dysfunction and hypertrophy after 24 h of Iso treatment.	Isoproterenol	220-223	superoxide dismutase 2	Homo sapiens	46-68
35453408-5	2022	A decreased interaction between sirtuin 3 and superoxide dismutase 2 (SOD2) induced SOD2 acetylation on lysine 68 and inactivation, leading to mitochondrial oxidative stress and dysfunction and hypertrophy after 24 h of Iso treatment.	Isoproterenol	220-223	superoxide dismutase 2	Homo sapiens	70-74
35453408-5	2022	A decreased interaction between sirtuin 3 and superoxide dismutase 2 (SOD2) induced SOD2 acetylation on lysine 68 and inactivation, leading to mitochondrial oxidative stress and dysfunction and hypertrophy after 24 h of Iso treatment.	Isoproterenol	220-223	superoxide dismutase 2	Homo sapiens	84-88
35183533-6	2022	pHGF was also found to restore the reduced SOD1 and SOD2 protein levels that result from H2O2 exposure and significantly increase the HO-1 protein levels in L-02 cells, thus improving the viability of L-02 cells that have been damaged by H2O2 by reducing the ROS and lipid peroxidation levels.	Hydrogen Peroxide	89-93	superoxide dismutase 2	Homo sapiens	52-56
35433903-7	2022	Moreover, the vitrified parthenogenetic zygotes cultured with Ax exhibited significantly increased mRNA expression of CDX2, SOD2, and GPX4 in their blastocysts.	astaxanthine	62-64	superoxide dismutase 2	Homo sapiens	124-128
35099761-0	2022	Circ-SWT1 Ameliorates H2O2-Induced Apoptosis, Oxidative Stress and Endoplasmic Reticulum Stress in Cardiomyocytes via miR-192-5p/SOD2 Axis.	Hydrogen Peroxide	22-26	superoxide dismutase 2	Homo sapiens	129-133
35099761-13	2022	Moreover, miR-192-5p inhibition protected cardiomyocytes against H2O2-evoked apoptosis, oxidative stress and ER stress, which were abolished by SOD2 silencing.	Hydrogen Peroxide	65-69	superoxide dismutase 2	Homo sapiens	144-148
35099761-14	2022	Circ-SWT1 ameliorates H2O2-induced apoptosis, oxidative stress and ER stress in cardiomyocytes via miR-192-5p/SOD2 axis, suggesting the potential involvement of circ-SWT1 in AMI process.	Hydrogen Peroxide	22-26	superoxide dismutase 2	Homo sapiens	110-114
35453320-5	2022	One example of such an antioxidant enzyme is manganese superoxide dismutase (MnSOD, also referred to as SOD2), which detoxifies superoxide, a ROS that has been shown, when its normal physiological levels are disrupted, to lead to oncogenicity and therapy resistance.	Superoxides	128-138	superoxide dismutase 2	Homo sapiens	45-75
35121188-6	2022	Physiologically speaking, cold activation of manganese superoxide dismutase mediates cold stress signaling and transduces temperature (physical signal) degree into H2O2 fluxes (chemical signal), which in turn may act as a second messenger to induce a series of physiological responses such as cold shock.	Hydrogen Peroxide	164-168	superoxide dismutase 2	Homo sapiens	45-75
35059971-7	2022	The addition of the flavones to the cell cultures at a concentration of 50 micromol/L resulted increase in the expression of the SOD1, SOD2 and GPX1 genes compared to the nontreated cell cultures.	Flavones	20-28	superoxide dismutase 2	Homo sapiens	135-139
35433741-12	2022	Moreover, ISL markedly increased the protein levels of Bcl-2 and SOD2, which were reduced by cisplatin stimulation.	Cisplatin	93-102	superoxide dismutase 2	Homo sapiens	65-69
35453320-5	2022	One example of such an antioxidant enzyme is manganese superoxide dismutase (MnSOD, also referred to as SOD2), which detoxifies superoxide, a ROS that has been shown, when its normal physiological levels are disrupted, to lead to oncogenicity and therapy resistance.	Superoxides	128-138	superoxide dismutase 2	Homo sapiens	77-82
35453320-5	2022	One example of such an antioxidant enzyme is manganese superoxide dismutase (MnSOD, also referred to as SOD2), which detoxifies superoxide, a ROS that has been shown, when its normal physiological levels are disrupted, to lead to oncogenicity and therapy resistance.	Superoxides	128-138	superoxide dismutase 2	Homo sapiens	104-108
35453320-5	2022	One example of such an antioxidant enzyme is manganese superoxide dismutase (MnSOD, also referred to as SOD2), which detoxifies superoxide, a ROS that has been shown, when its normal physiological levels are disrupted, to lead to oncogenicity and therapy resistance.	Reactive Oxygen Species	142-145	superoxide dismutase 2	Homo sapiens	45-75
35453320-5	2022	One example of such an antioxidant enzyme is manganese superoxide dismutase (MnSOD, also referred to as SOD2), which detoxifies superoxide, a ROS that has been shown, when its normal physiological levels are disrupted, to lead to oncogenicity and therapy resistance.	Reactive Oxygen Species	142-145	superoxide dismutase 2	Homo sapiens	77-82
35453320-5	2022	One example of such an antioxidant enzyme is manganese superoxide dismutase (MnSOD, also referred to as SOD2), which detoxifies superoxide, a ROS that has been shown, when its normal physiological levels are disrupted, to lead to oncogenicity and therapy resistance.	Reactive Oxygen Species	142-145	superoxide dismutase 2	Homo sapiens	104-108
35330157-5	2022	Our study also showed that 2FF significantly decreased the overproduction of reactive oxygen species (ROS) induced by H2O2 and the activities of catalase, glutathione and Mn-superoxide dismutase were remarkably increased by 2FF pretreatment.	2-deoxy-2-fluoro-L-fucose	27-30	superoxide dismutase 2	Homo sapiens	171-194
35301432-3	2022	In the present study, we illustrated that HIF-2alpha, but not HIF-1alpha, induces stemness in BCs under hypoxia through SOD2-mtROS-PDI/GRP78-UPRER pathway, linking mitochondrial metabolic state to endoplasmic reticulum (ER) response via mitochondrial reactive oxygen species (mtROS) level.	Reactive Oxygen Species	251-274	superoxide dismutase 2	Homo sapiens	120-124
35330157-5	2022	Our study also showed that 2FF significantly decreased the overproduction of reactive oxygen species (ROS) induced by H2O2 and the activities of catalase, glutathione and Mn-superoxide dismutase were remarkably increased by 2FF pretreatment.	Reactive Oxygen Species	77-100	superoxide dismutase 2	Homo sapiens	171-194
35330157-5	2022	Our study also showed that 2FF significantly decreased the overproduction of reactive oxygen species (ROS) induced by H2O2 and the activities of catalase, glutathione and Mn-superoxide dismutase were remarkably increased by 2FF pretreatment.	Reactive Oxygen Species	102-105	superoxide dismutase 2	Homo sapiens	171-194
35330157-5	2022	Our study also showed that 2FF significantly decreased the overproduction of reactive oxygen species (ROS) induced by H2O2 and the activities of catalase, glutathione and Mn-superoxide dismutase were remarkably increased by 2FF pretreatment.	Hydrogen Peroxide	118-122	superoxide dismutase 2	Homo sapiens	171-194
35330157-5	2022	Our study also showed that 2FF significantly decreased the overproduction of reactive oxygen species (ROS) induced by H2O2 and the activities of catalase, glutathione and Mn-superoxide dismutase were remarkably increased by 2FF pretreatment.	2-deoxy-2-fluoro-L-fucose	224-227	superoxide dismutase 2	Homo sapiens	171-194
35024467-5	2022	Meanwhile, PEITC treatment ameliorated DON-induced an increase of the inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) mRNA levels and intracellular reactive oxygen species (ROS) level, and a decrease of glutathione peroxidase 1 (GPx1), superoxide dismutase 2 (SOD2), catalase (CAT) and heme oxygenase 1 (HO-1) mRNA levels.	phenethyl isothiocyanate	11-16	superoxide dismutase 2	Homo sapiens	280-284
35281469-11	2022	In addition, DEX-induced excessive reactive oxygen species (ROS) generation was an upstream trigger of GDF15-mediated signaling, and D7 ameliorated this DEX-induced redox imbalance by restoring the expression of antioxidants, including superoxide dismutase (SOD) 1, SOD2, and catalase, via regulation of GDF15 expression.	Dexamethasone	13-16	superoxide dismutase 2	Homo sapiens	266-270
35281469-11	2022	In addition, DEX-induced excessive reactive oxygen species (ROS) generation was an upstream trigger of GDF15-mediated signaling, and D7 ameliorated this DEX-induced redox imbalance by restoring the expression of antioxidants, including superoxide dismutase (SOD) 1, SOD2, and catalase, via regulation of GDF15 expression.	Reactive Oxygen Species	60-63	superoxide dismutase 2	Homo sapiens	266-270
35024467-5	2022	Meanwhile, PEITC treatment ameliorated DON-induced an increase of the inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) mRNA levels and intracellular reactive oxygen species (ROS) level, and a decrease of glutathione peroxidase 1 (GPx1), superoxide dismutase 2 (SOD2), catalase (CAT) and heme oxygenase 1 (HO-1) mRNA levels.	phenethyl isothiocyanate	11-16	superoxide dismutase 2	Homo sapiens	256-278
35024467-5	2022	Meanwhile, PEITC treatment ameliorated DON-induced an increase of the inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) mRNA levels and intracellular reactive oxygen species (ROS) level, and a decrease of glutathione peroxidase 1 (GPx1), superoxide dismutase 2 (SOD2), catalase (CAT) and heme oxygenase 1 (HO-1) mRNA levels.	deoxynivalenol	39-42	superoxide dismutase 2	Homo sapiens	256-278
35024467-5	2022	Meanwhile, PEITC treatment ameliorated DON-induced an increase of the inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) mRNA levels and intracellular reactive oxygen species (ROS) level, and a decrease of glutathione peroxidase 1 (GPx1), superoxide dismutase 2 (SOD2), catalase (CAT) and heme oxygenase 1 (HO-1) mRNA levels.	deoxynivalenol	39-42	superoxide dismutase 2	Homo sapiens	280-284
35085532-5	2022	Berberine had an antagonistic effect for the majority of genes mutual for AD and toxic metal mixture: ACHE, APP, BAX, BCL2, CASP3, HMOX1, IL1B, MAPT, SOD2, TNF.	Berberine	0-9	superoxide dismutase 2	Homo sapiens	150-154
35186942-8	2021	Thus, these results revealed that PPARgamma/SOD2 might protect against mitochondrial ROS-dependent apoptosis via inhibiting ATG4D-mediated mitophagy to promote pancreatic cancer proliferation, further improving PDAC chemosensitivity.	Reactive Oxygen Species	85-88	superoxide dismutase 2	Homo sapiens	44-48
35274104-2	2022	Superoxide dismutase 2 (SOD2) is a mitochondrial-localized enzyme that catalyzes the dismutation of superoxide to hydrogen peroxide.	Superoxides	100-110	superoxide dismutase 2	Homo sapiens	0-22
35274104-2	2022	Superoxide dismutase 2 (SOD2) is a mitochondrial-localized enzyme that catalyzes the dismutation of superoxide to hydrogen peroxide.	Superoxides	100-110	superoxide dismutase 2	Homo sapiens	24-28
35274104-2	2022	Superoxide dismutase 2 (SOD2) is a mitochondrial-localized enzyme that catalyzes the dismutation of superoxide to hydrogen peroxide.	Hydrogen Peroxide	114-131	superoxide dismutase 2	Homo sapiens	0-22
35274104-2	2022	Superoxide dismutase 2 (SOD2) is a mitochondrial-localized enzyme that catalyzes the dismutation of superoxide to hydrogen peroxide.	Hydrogen Peroxide	114-131	superoxide dismutase 2	Homo sapiens	24-28
35186942-0	2021	PPARgamma/SOD2 Protects Against Mitochondrial ROS-Dependent Apoptosis via Inhibiting ATG4D-Mediated Mitophagy to Promote Pancreatic Cancer Proliferation.	Reactive Oxygen Species	46-49	superoxide dismutase 2	Homo sapiens	10-14
35251472-10	2022	Furthermore, RvD1 and PD1 facilitated the expression of the oxidative indicator superoxide dismutase 2 (SOD2), inhibited NADPH oxidase 2 (NOX2) expression, and diminished intracellular reactive oxygen species (ROS) levels.	Reactive Oxygen Species	210-213	superoxide dismutase 2	Homo sapiens	104-108
35204257-0	2022	Astaxanthin Sensitizes Low SOD2-Expressing GBM Cell Lines to TRAIL Treatment via Pathway Involving Mitochondrial Membrane Depolarization.	astaxanthine	0-11	superoxide dismutase 2	Homo sapiens	27-31
35204257-7	2022	In addition, while 25 and 50 ng/mL TRAIL treatment increased ROS for both cell lines, pretreatment of 5 microM AXT induced a significant ROS decrease in CRT-MG (p < 0.05) while less effective in U251-MG. We found that in U251-MG, superoxide dismutase (SOD) 2 expression and enzymatic activity were lower compared to CRT-MG and that overexpression of SOD2 in U251-MG abolished AXT sensitization to TRAIL treatment.	axt	111-114	superoxide dismutase 2	Homo sapiens	230-258
35204257-7	2022	In addition, while 25 and 50 ng/mL TRAIL treatment increased ROS for both cell lines, pretreatment of 5 microM AXT induced a significant ROS decrease in CRT-MG (p < 0.05) while less effective in U251-MG. We found that in U251-MG, superoxide dismutase (SOD) 2 expression and enzymatic activity were lower compared to CRT-MG and that overexpression of SOD2 in U251-MG abolished AXT sensitization to TRAIL treatment.	axt	111-114	superoxide dismutase 2	Homo sapiens	350-354
35204257-8	2022	Taken together, these results suggest that while AXT acts as an ROS scavenger in GBM cell lines, it also has some role in decreasing mitochondrial potential together with TRAIL in a pathway that can be inhibited by SOD2.	axt	49-52	superoxide dismutase 2	Homo sapiens	215-219
35204257-8	2022	Taken together, these results suggest that while AXT acts as an ROS scavenger in GBM cell lines, it also has some role in decreasing mitochondrial potential together with TRAIL in a pathway that can be inhibited by SOD2.	Reactive Oxygen Species	64-67	superoxide dismutase 2	Homo sapiens	215-219
35145273-0	2022	FTO promotes Bortezomib resistance via m6A-dependent destabilization of SOD2 expression in multiple myeloma.	Bortezomib	13-23	superoxide dismutase 2	Homo sapiens	72-76
35204196-5	2022	SOD2 overexpression increases glucose transporter GLUT-1 and glucose uptake.	Glucose	30-37	superoxide dismutase 2	Homo sapiens	0-4
35204196-5	2022	SOD2 overexpression increases glucose transporter GLUT-1 and glucose uptake.	Glucose	61-68	superoxide dismutase 2	Homo sapiens	0-4
35110539-9	2022	Moreover, baicalein treatment inhibited ferroptosis in adenine-stimulated PTEC by selectively modulating the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) and thus, suppressing mitochondrial superoxide production and DNA damage.	baicalein	10-19	superoxide dismutase 2	Homo sapiens	142-164
35110539-9	2022	Moreover, baicalein treatment inhibited ferroptosis in adenine-stimulated PTEC by selectively modulating the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) and thus, suppressing mitochondrial superoxide production and DNA damage.	baicalein	10-19	superoxide dismutase 2	Homo sapiens	166-170
35110539-9	2022	Moreover, baicalein treatment inhibited ferroptosis in adenine-stimulated PTEC by selectively modulating the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) and thus, suppressing mitochondrial superoxide production and DNA damage.	Adenine	55-62	superoxide dismutase 2	Homo sapiens	142-164
35110539-9	2022	Moreover, baicalein treatment inhibited ferroptosis in adenine-stimulated PTEC by selectively modulating the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) and thus, suppressing mitochondrial superoxide production and DNA damage.	Adenine	55-62	superoxide dismutase 2	Homo sapiens	166-170
35110539-9	2022	Moreover, baicalein treatment inhibited ferroptosis in adenine-stimulated PTEC by selectively modulating the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) and thus, suppressing mitochondrial superoxide production and DNA damage.	Superoxides	208-218	superoxide dismutase 2	Homo sapiens	142-164
35110539-9	2022	Moreover, baicalein treatment inhibited ferroptosis in adenine-stimulated PTEC by selectively modulating the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) and thus, suppressing mitochondrial superoxide production and DNA damage.	Superoxides	208-218	superoxide dismutase 2	Homo sapiens	166-170
35205334-4	2022	This study aimed to evaluate changes in IL-6 concentration and the concentration/activity of superoxide dismutase isoenzymes (SOD1, SOD2, and SOD3) in the blood of patients with acute pancreatitis (AP) in terms of rs1800795 polymorphism in the IL6 gene.	Superoxides	93-103	superoxide dismutase 2	Homo sapiens	132-136
35155508-7	2021	Collectively, alpha-mangostin was demonstrated to be a prominent ROS suppressor which reversed the reduction of antioxidant enzymes (CAT and SOD2).	mangostin	14-29	superoxide dismutase 2	Homo sapiens	141-145
35044248-13	2022	regarding the activation of antioxidant marker proteins such as SOD2 and SIRT3 were determined using DCFH-DA assay, western blot analysis and immunocytochemistry.	diacetyldichlorofluorescein	101-108	superoxide dismutase 2	Homo sapiens	64-68
35044248-19	2022	may exert its protective effects against ROS through SOD2 and SIRT3 signaling pathways in dexamethasone-induced neurotoxicity.	Reactive Oxygen Species	41-44	superoxide dismutase 2	Homo sapiens	53-57
35044248-19	2022	may exert its protective effects against ROS through SOD2 and SIRT3 signaling pathways in dexamethasone-induced neurotoxicity.	Dexamethasone	90-103	superoxide dismutase 2	Homo sapiens	53-57
35155508-7	2021	Collectively, alpha-mangostin was demonstrated to be a prominent ROS suppressor which reversed the reduction of antioxidant enzymes (CAT and SOD2).	Reactive Oxygen Species	65-68	superoxide dismutase 2	Homo sapiens	141-145
35096052-8	2022	Furthermore, the expression of SIRT3, FOXO3A, and SOD2 proteins declined, except for an initial elevation of SIRT3 between 0 and 0.75 mM H2O2.	Hydrogen Peroxide	137-141	superoxide dismutase 2	Homo sapiens	50-54
35084580-3	2022	13 bibenzyl derivatives from D. officinale were sent for molecular docking, surface plasmon resonance (SPR) assay and after detection of Mn-SOD and SIRT3 activities in or not in HaCaT cells, it was concluded that bibenzyl derivatives did not directly activate Mn-SOD but promoted SIRT3 proteins.	Bibenzyls	3-11	superoxide dismutase 2	Homo sapiens	137-143
35084580-3	2022	13 bibenzyl derivatives from D. officinale were sent for molecular docking, surface plasmon resonance (SPR) assay and after detection of Mn-SOD and SIRT3 activities in or not in HaCaT cells, it was concluded that bibenzyl derivatives did not directly activate Mn-SOD but promoted SIRT3 proteins.	Bibenzyls	3-11	superoxide dismutase 2	Homo sapiens	260-266
35084580-5	2022	The results show that bibenzyl derivatives could directly bind to SIRT3, enhance the deacetylation and then activate Mn-SOD, so as to protect UV-B induced skin photoaging.	Bibenzyls	22-30	superoxide dismutase 2	Homo sapiens	117-123
35162241-8	2022	A low dose of SWCNTs-COOH induced ROS generation and increased the expression of catalase, MnSOD, CuZnSOD, and SOD-2 mRNA but decreased the expression of GPX-2 and GPX-3 mRNA in human monocytes.	Carbonic Acid	21-25	superoxide dismutase 2	Homo sapiens	91-96
35162241-8	2022	A low dose of SWCNTs-COOH induced ROS generation and increased the expression of catalase, MnSOD, CuZnSOD, and SOD-2 mRNA but decreased the expression of GPX-2 and GPX-3 mRNA in human monocytes.	Carbonic Acid	21-25	superoxide dismutase 2	Homo sapiens	111-116
35096612-10	2021	In the finasteride arm, stronger associations were observed among men with lower serum lycopene for NOS3-rs1799983, higher serum alpha-carotene, beta-carotene, and beta-cryptoxanthin for LIG3-rs1052536, or lower serum retinol for SOD2-rs1799725.	Finasteride	7-18	superoxide dismutase 2	Homo sapiens	230-234
35082966-8	2022	Furthermore, in human umbilical vein endothelial cells (HUVECs), colchicine showed antioxidative stress effects through increasing protein expression of glutathione peroxidase-1 (GPx-1), and mRNA levels of forkhead box O3 (FOXO3a) and superoxide dismutase 2 (SOD2).	Colchicine	65-75	superoxide dismutase 2	Homo sapiens	235-257
35082966-8	2022	Furthermore, in human umbilical vein endothelial cells (HUVECs), colchicine showed antioxidative stress effects through increasing protein expression of glutathione peroxidase-1 (GPx-1), and mRNA levels of forkhead box O3 (FOXO3a) and superoxide dismutase 2 (SOD2).	Colchicine	65-75	superoxide dismutase 2	Homo sapiens	259-263
35056649-3	2022	In this work, we focused on determining the effect of kaempferol and its glycoside derivatives on the expression level of genes related to the reduction of oxidative stress-NFE2L2, NQO1, SOD1, SOD2, and HO-1; the enzymatic activity of superoxide dismutases; and the level of glutathione.	kaempferol	54-64	superoxide dismutase 2	Homo sapiens	193-197
35052656-0	2022	Genetic Polymorphisms of MnSOD Modify the Impacts of Environmental Melamine on Oxidative Stress and Early Kidney Injury in Calcium Urolithiasis Patients.	Calcium	123-130	superoxide dismutase 2	Homo sapiens	25-30
35052656-9	2022	In conclusion, the SNPs of MnSOD, rs4880 and rs5746136, influence the risk of oxidative stress and renal tubular injury, respectively, in calcium urolithiasis patients.	Calcium	138-145	superoxide dismutase 2	Homo sapiens	27-32
35017469-7	2022	MnSOD in TNBC cells functions as a prooxidant peroxidase that increases mitochondrial ROS (mROS) and adaptation to oxidative stress under the oncogenic effect.	Reactive Oxygen Species	86-89	superoxide dismutase 2	Homo sapiens	0-5
35017469-11	2022	Quenching mROS with MitoQ, a mitochondria-targeted non-metal-based antioxidant MnSOD mimics, effectively suppresses BCSCs and M2 macrophage invasion exacerbated by MnSOD and MCT-1.	Metals	55-60	superoxide dismutase 2	Homo sapiens	79-84
35052646-7	2022	Furthermore, N-acyl dopamines prevented cell death 24 h after OS induction and promoted the expression of antioxidant enzymes GPX1, GPX7, SOD1, SOD2 and CAT, as well as reduced the BAX/BCL2 mRNA ratio.	n-acyl dopamines	13-29	superoxide dismutase 2	Homo sapiens	144-148
35056649-3	2022	In this work, we focused on determining the effect of kaempferol and its glycoside derivatives on the expression level of genes related to the reduction of oxidative stress-NFE2L2, NQO1, SOD1, SOD2, and HO-1; the enzymatic activity of superoxide dismutases; and the level of glutathione.	Glycosides	73-82	superoxide dismutase 2	Homo sapiens	193-197
4061626-1	1985	Radioimmunoassays for both human copper-zinc and manganous superoxide dismutases (Cu-Zn SOD and Mn SOD, respectively) have been developed, validated, and utilized to measure the concentrations of these enzymes in cultured monocytes.	Copper	33-39	superoxide dismutase 2	Homo sapiens	96-102
34895005-0	2021	Valproic acid promotes SOD2 acetylation: A potential mechanism of valproic acid-induced oxidative stress in developing systems.	Valproic Acid	0-13	superoxide dismutase 2	Homo sapiens	23-27
34895005-0	2021	Valproic acid promotes SOD2 acetylation: A potential mechanism of valproic acid-induced oxidative stress in developing systems.	Valproic Acid	66-79	superoxide dismutase 2	Homo sapiens	23-27
34895005-4	2021	Since VPA is a deacetylase inhibitor, we propose that VPA promotes mitochondrial superoxide dismutase-2 (SOD2) acetylation, decreasing SOD2 activity and increasing oxidant levels.	Valproic Acid	6-9	superoxide dismutase 2	Homo sapiens	105-109
34895005-4	2021	Since VPA is a deacetylase inhibitor, we propose that VPA promotes mitochondrial superoxide dismutase-2 (SOD2) acetylation, decreasing SOD2 activity and increasing oxidant levels.	Valproic Acid	6-9	superoxide dismutase 2	Homo sapiens	135-139
34895005-4	2021	Since VPA is a deacetylase inhibitor, we propose that VPA promotes mitochondrial superoxide dismutase-2 (SOD2) acetylation, decreasing SOD2 activity and increasing oxidant levels.	Valproic Acid	54-57	superoxide dismutase 2	Homo sapiens	105-109
34895005-4	2021	Since VPA is a deacetylase inhibitor, we propose that VPA promotes mitochondrial superoxide dismutase-2 (SOD2) acetylation, decreasing SOD2 activity and increasing oxidant levels.	Valproic Acid	54-57	superoxide dismutase 2	Homo sapiens	135-139
34895005-6	2021	VPA treatments increased oxidant levels, oxidized the glutathione (GSH)/glutathione disulfide (GSSG) redox couple, and decreased total SOD and SOD2 activity in undifferentiated P19 cells but not in differentiated P19 cells.	Valproic Acid	0-3	superoxide dismutase 2	Homo sapiens	143-147
34895005-8	2021	Immunoblot analyses demonstrated that VPA increased acetylation of SOD2 at lysine68 (AcK68 SOD2) in undifferentiated P19 cells but not in differentiated P19 cells.	Valproic Acid	38-41	superoxide dismutase 2	Homo sapiens	67-71
34895005-8	2021	Immunoblot analyses demonstrated that VPA increased acetylation of SOD2 at lysine68 (AcK68 SOD2) in undifferentiated P19 cells but not in differentiated P19 cells.	Valproic Acid	38-41	superoxide dismutase 2	Homo sapiens	91-95
34895005-8	2021	Immunoblot analyses demonstrated that VPA increased acetylation of SOD2 at lysine68 (AcK68 SOD2) in undifferentiated P19 cells but not in differentiated P19 cells.	lysine68	75-83	superoxide dismutase 2	Homo sapiens	67-71
34895005-8	2021	Immunoblot analyses demonstrated that VPA increased acetylation of SOD2 at lysine68 (AcK68 SOD2) in undifferentiated P19 cells but not in differentiated P19 cells.	lysine68	75-83	superoxide dismutase 2	Homo sapiens	91-95
34895005-9	2021	Pretreatments with the Nrf2 inducer, dithiol-3-thione (D3T), in undifferentiated P19 cells prevented increased oxidant levels, GSH/GSSG redox oxidation and restored total SOD and SOD2 activity, correlating with a decrease in AcK68 SOD2 levels.	dithiol-3-thione	37-53	superoxide dismutase 2	Homo sapiens	179-183
34895005-9	2021	Pretreatments with the Nrf2 inducer, dithiol-3-thione (D3T), in undifferentiated P19 cells prevented increased oxidant levels, GSH/GSSG redox oxidation and restored total SOD and SOD2 activity, correlating with a decrease in AcK68 SOD2 levels.	dithiol-3-thione	37-53	superoxide dismutase 2	Homo sapiens	231-235
34895005-9	2021	Pretreatments with the Nrf2 inducer, dithiol-3-thione (D3T), in undifferentiated P19 cells prevented increased oxidant levels, GSH/GSSG redox oxidation and restored total SOD and SOD2 activity, correlating with a decrease in AcK68 SOD2 levels.	d3t	55-58	superoxide dismutase 2	Homo sapiens	179-183
34895005-9	2021	Pretreatments with the Nrf2 inducer, dithiol-3-thione (D3T), in undifferentiated P19 cells prevented increased oxidant levels, GSH/GSSG redox oxidation and restored total SOD and SOD2 activity, correlating with a decrease in AcK68 SOD2 levels.	d3t	55-58	superoxide dismutase 2	Homo sapiens	231-235
34895005-10	2021	In embryos, VPA decreased total SOD and SOD2 activity and increased levels of AcK68 SOD2, and D3T pretreatments prevented VPA effects, increasing total SOD and SOD2 activity and lowering levels of AcK68 SOD2.	Valproic Acid	12-15	superoxide dismutase 2	Homo sapiens	40-44
34895005-10	2021	In embryos, VPA decreased total SOD and SOD2 activity and increased levels of AcK68 SOD2, and D3T pretreatments prevented VPA effects, increasing total SOD and SOD2 activity and lowering levels of AcK68 SOD2.	Valproic Acid	12-15	superoxide dismutase 2	Homo sapiens	84-88
34895005-10	2021	In embryos, VPA decreased total SOD and SOD2 activity and increased levels of AcK68 SOD2, and D3T pretreatments prevented VPA effects, increasing total SOD and SOD2 activity and lowering levels of AcK68 SOD2.	Valproic Acid	12-15	superoxide dismutase 2	Homo sapiens	160-164
34895005-10	2021	In embryos, VPA decreased total SOD and SOD2 activity and increased levels of AcK68 SOD2, and D3T pretreatments prevented VPA effects, increasing total SOD and SOD2 activity and lowering levels of AcK68 SOD2.	Valproic Acid	12-15	superoxide dismutase 2	Homo sapiens	203-207
2607653-4	1989	Minimum detectable amount of SOD by the Mic-NT method and XOD-NTB method was about 15 ng and 200 ng, respectively.	mic-nt	40-46	superoxide dismutase 2	Homo sapiens	29-32
2607653-4	1989	Minimum detectable amount of SOD by the Mic-NT method and XOD-NTB method was about 15 ng and 200 ng, respectively.	xod-ntb	58-65	superoxide dismutase 2	Homo sapiens	29-32
2607653-5	1989	On the other hand, an XOD-NH2OH method which detects SOD activities based on the O2-specific oxidation reaction showed the minimum detectable amount of 2.5 ng.	Oxygen	81-83	superoxide dismutase 2	Homo sapiens	53-56
2607653-6	1989	Consequently, SOD-detecting sensitivity of these methods was found to be in the following order: XOD-NH2OH method greater than Mic-NT method greater than XOD-NTB method.	xod-nh2oh	97-106	superoxide dismutase 2	Homo sapiens	14-17
2607653-6	1989	Consequently, SOD-detecting sensitivity of these methods was found to be in the following order: XOD-NH2OH method greater than Mic-NT method greater than XOD-NTB method.	mic-nt	127-133	superoxide dismutase 2	Homo sapiens	14-17
2607653-6	1989	Consequently, SOD-detecting sensitivity of these methods was found to be in the following order: XOD-NH2OH method greater than Mic-NT method greater than XOD-NTB method.	xod-ntb	154-161	superoxide dismutase 2	Homo sapiens	14-17
2607653-9	1989	The isoenzymes of SOD (Cu, Zn-SOD and Mn-SOD) could be detected separately by 1. deactivating Cu, Zn-SOD with CN- or H2O2 and regarding the remaining activity as Mn-SOD and 2.	Hydrogen Peroxide	117-121	superoxide dismutase 2	Homo sapiens	18-21
2607653-9	1989	The isoenzymes of SOD (Cu, Zn-SOD and Mn-SOD) could be detected separately by 1. deactivating Cu, Zn-SOD with CN- or H2O2 and regarding the remaining activity as Mn-SOD and 2.	Hydrogen Peroxide	117-121	superoxide dismutase 2	Homo sapiens	38-44
2607653-10	1989	by deactivating Mn-SOD selectively through pretreatment of the sample with SDS and regarding the remaining activity as Cu, Zn-SOD.	Sodium Dodecyl Sulfate	75-78	superoxide dismutase 2	Homo sapiens	16-22
2647725-5	1989	All of the above COOH-terminal peptides inhibited the binding whereas the NH2-terminal ones did not, indicating that PG 11 recognizes several peptides of COOH termini of manganese superoxide dismutase.	pg 11	117-122	superoxide dismutase 2	Homo sapiens	170-200
2647725-5	1989	All of the above COOH-terminal peptides inhibited the binding whereas the NH2-terminal ones did not, indicating that PG 11 recognizes several peptides of COOH termini of manganese superoxide dismutase.	Carbonic Acid	17-21	superoxide dismutase 2	Homo sapiens	170-200
2831093-1	1988	cDNAs coding for human manganese-containing superoxide dismutase (Mn SOD) have been isolated from a human liver and a dibutyryl cyclic AMP differentiated U937 cDNA library constructed in vector lambda gtll.	Cyclic AMP	128-138	superoxide dismutase 2	Homo sapiens	23-64
2831093-1	1988	cDNAs coding for human manganese-containing superoxide dismutase (Mn SOD) have been isolated from a human liver and a dibutyryl cyclic AMP differentiated U937 cDNA library constructed in vector lambda gtll.	Cyclic AMP	128-138	superoxide dismutase 2	Homo sapiens	66-72
2831093-4	1988	Differentiation of the U937 cells with dibutyryl cyclic AMP resulted in a 70% decrease in Mn SOD mRNA.	Cyclic AMP	49-59	superoxide dismutase 2	Homo sapiens	90-96
3495372-6	1987	The loss of Mn SOD activity could be mediated by a low intracellular level of superoxide anion due to the scavenger effect of melanin on superoxide anion; in fact, it is well known that the biosynthesis of Mn SOD is induced by intracellular levels of superoxide anion.	Superoxides	78-94	superoxide dismutase 2	Homo sapiens	12-18
3495372-6	1987	The loss of Mn SOD activity could be mediated by a low intracellular level of superoxide anion due to the scavenger effect of melanin on superoxide anion; in fact, it is well known that the biosynthesis of Mn SOD is induced by intracellular levels of superoxide anion.	Superoxides	78-94	superoxide dismutase 2	Homo sapiens	206-212
3495372-6	1987	The loss of Mn SOD activity could be mediated by a low intracellular level of superoxide anion due to the scavenger effect of melanin on superoxide anion; in fact, it is well known that the biosynthesis of Mn SOD is induced by intracellular levels of superoxide anion.	Melanins	126-133	superoxide dismutase 2	Homo sapiens	12-18
3495372-6	1987	The loss of Mn SOD activity could be mediated by a low intracellular level of superoxide anion due to the scavenger effect of melanin on superoxide anion; in fact, it is well known that the biosynthesis of Mn SOD is induced by intracellular levels of superoxide anion.	Melanins	126-133	superoxide dismutase 2	Homo sapiens	206-212
3495372-6	1987	The loss of Mn SOD activity could be mediated by a low intracellular level of superoxide anion due to the scavenger effect of melanin on superoxide anion; in fact, it is well known that the biosynthesis of Mn SOD is induced by intracellular levels of superoxide anion.	Superoxides	137-153	superoxide dismutase 2	Homo sapiens	12-18
3495372-6	1987	The loss of Mn SOD activity could be mediated by a low intracellular level of superoxide anion due to the scavenger effect of melanin on superoxide anion; in fact, it is well known that the biosynthesis of Mn SOD is induced by intracellular levels of superoxide anion.	Superoxides	137-153	superoxide dismutase 2	Homo sapiens	206-212
3495372-6	1987	The loss of Mn SOD activity could be mediated by a low intracellular level of superoxide anion due to the scavenger effect of melanin on superoxide anion; in fact, it is well known that the biosynthesis of Mn SOD is induced by intracellular levels of superoxide anion.	Superoxides	137-153	superoxide dismutase 2	Homo sapiens	12-18
3495372-6	1987	The loss of Mn SOD activity could be mediated by a low intracellular level of superoxide anion due to the scavenger effect of melanin on superoxide anion; in fact, it is well known that the biosynthesis of Mn SOD is induced by intracellular levels of superoxide anion.	Superoxides	137-153	superoxide dismutase 2	Homo sapiens	206-212
34981770-0	2022	Cryotrapping peroxide in the active site of human mitochondrial manganese superoxide dismutase crystals for neutron diffraction.	Peroxides	13-21	superoxide dismutase 2	Homo sapiens	64-94
34981770-7	2022	The resulting neutron diffraction data permitted the visualization of a dioxygen species bound to the MnSOD active-site metal that was indicative of successful cryotrapping.	Oxygen	72-80	superoxide dismutase 2	Homo sapiens	102-107
34981770-7	2022	The resulting neutron diffraction data permitted the visualization of a dioxygen species bound to the MnSOD active-site metal that was indicative of successful cryotrapping.	Metals	120-125	superoxide dismutase 2	Homo sapiens	102-107
2476237-2	1989	Here we demonstrate that manganous superoxide dismutase (MnSOD), a mitochondrial enzyme involved in the scavenging of superoxide radicals (O2-), is such a protein.	Superoxides	35-45	superoxide dismutase 2	Homo sapiens	57-62
2476237-2	1989	Here we demonstrate that manganous superoxide dismutase (MnSOD), a mitochondrial enzyme involved in the scavenging of superoxide radicals (O2-), is such a protein.	Superoxides	139-141	superoxide dismutase 2	Homo sapiens	25-55
2476237-2	1989	Here we demonstrate that manganous superoxide dismutase (MnSOD), a mitochondrial enzyme involved in the scavenging of superoxide radicals (O2-), is such a protein.	Superoxides	139-141	superoxide dismutase 2	Homo sapiens	57-62
2476237-3	1989	Overexpression of MnSOD confers increased resistance to TNF plus cycloheximide on the 293 human embryonic kidney cell line.	Cycloheximide	65-78	superoxide dismutase 2	Homo sapiens	18-23
2476237-4	1989	Conversely, expression of antisense MnSOD RNA renders these cells sensitive to TNF even in the absence of cycloheximide.	Cycloheximide	106-119	superoxide dismutase 2	Homo sapiens	36-41
4026967-6	1985	The increases in chemiluminescence and Mn-SOD activity suggests that the generation of a large amount of activated oxygen is associated with the pathogenesis and progression of alcoholic liver injury in humans.	Oxygen	115-121	superoxide dismutase 2	Homo sapiens	39-45
3838941-6	1985	Human manganese superoxide dismutase was also found to dismute the superoxide radical to hydrogen peroxide and water.	Superoxides	67-85	superoxide dismutase 2	Homo sapiens	6-36
3838941-6	1985	Human manganese superoxide dismutase was also found to dismute the superoxide radical to hydrogen peroxide and water.	Hydrogen Peroxide	89-106	superoxide dismutase 2	Homo sapiens	6-36
3838941-6	1985	Human manganese superoxide dismutase was also found to dismute the superoxide radical to hydrogen peroxide and water.	Water	111-116	superoxide dismutase 2	Homo sapiens	6-36
4039529-7	1985	Thus, the chronic consumption of ethanol results in altered levels of trace minerals and SOD activities in the liver which in turn may contribute to hepatic injury.	Ethanol	33-40	superoxide dismutase 2	Homo sapiens	89-92
4039529-3	1985	The activity of MnSOD was higher in the ethanol-fed group while the activity of CuZnSOD tended to be lower.	Ethanol	40-47	superoxide dismutase 2	Homo sapiens	16-21
4039529-4	1985	The finding of increased activity of MnSOD is consistent with the finding of enlarged mitochondria and increased liver Mn in the ethanol-fed group.	Ethanol	129-136	superoxide dismutase 2	Homo sapiens	37-42
4039529-5	1985	Increased MnSOD may reflect substrate induction, since superoxide anions are generated by ethanol metabolism.	Superoxides	55-72	superoxide dismutase 2	Homo sapiens	10-15
4039529-5	1985	Increased MnSOD may reflect substrate induction, since superoxide anions are generated by ethanol metabolism.	Ethanol	90-97	superoxide dismutase 2	Homo sapiens	10-15
6297065-4	1982	O2 radicals are eliminated by a family of enzymes called superoxide dismutases (SOD).	o2 radicals	0-11	superoxide dismutase 2	Homo sapiens	80-83
6397417-1	1984	A manganese-containing superoxide dismutase (Mn-SOD) was isolated from human liver mitochondria by the procedures including heat treatment, ammonium sulfate precipitation, ion exchange chromatography, gel filtration and isoelectric focusing.	Ammonium Sulfate	140-156	superoxide dismutase 2	Homo sapiens	2-43
6397417-1	1984	A manganese-containing superoxide dismutase (Mn-SOD) was isolated from human liver mitochondria by the procedures including heat treatment, ammonium sulfate precipitation, ion exchange chromatography, gel filtration and isoelectric focusing.	Ammonium Sulfate	140-156	superoxide dismutase 2	Homo sapiens	45-51
6316150-1	1983	Copper, zinc superoxide dismutase (SOD) catalyses the very rapid two-step dismutation of the toxic superoxide radical (O-2) to molecular oxygen and hydrogen peroxide through the alternate reduction and oxidation of the active-site copper.	Copper	0-6	superoxide dismutase 2	Homo sapiens	35-38
6316150-1	1983	Copper, zinc superoxide dismutase (SOD) catalyses the very rapid two-step dismutation of the toxic superoxide radical (O-2) to molecular oxygen and hydrogen peroxide through the alternate reduction and oxidation of the active-site copper.	Superoxides	99-117	superoxide dismutase 2	Homo sapiens	35-38
6316150-1	1983	Copper, zinc superoxide dismutase (SOD) catalyses the very rapid two-step dismutation of the toxic superoxide radical (O-2) to molecular oxygen and hydrogen peroxide through the alternate reduction and oxidation of the active-site copper.	Oxygen	137-143	superoxide dismutase 2	Homo sapiens	35-38
6316150-1	1983	Copper, zinc superoxide dismutase (SOD) catalyses the very rapid two-step dismutation of the toxic superoxide radical (O-2) to molecular oxygen and hydrogen peroxide through the alternate reduction and oxidation of the active-site copper.	Hydrogen Peroxide	148-165	superoxide dismutase 2	Homo sapiens	35-38
6316150-1	1983	Copper, zinc superoxide dismutase (SOD) catalyses the very rapid two-step dismutation of the toxic superoxide radical (O-2) to molecular oxygen and hydrogen peroxide through the alternate reduction and oxidation of the active-site copper.	Copper	231-237	superoxide dismutase 2	Homo sapiens	35-38
6685298-1	1983	Manganese superoxide dismutase (Mn-SOD) studied during ethanol vapor inhalation shows no changes during the inhalation period (4 days) and a transient increase 12 hours after ethanol withdrawal.	Ethanol	55-62	superoxide dismutase 2	Homo sapiens	0-30
6685298-1	1983	Manganese superoxide dismutase (Mn-SOD) studied during ethanol vapor inhalation shows no changes during the inhalation period (4 days) and a transient increase 12 hours after ethanol withdrawal.	Ethanol	55-62	superoxide dismutase 2	Homo sapiens	32-38
6685298-1	1983	Manganese superoxide dismutase (Mn-SOD) studied during ethanol vapor inhalation shows no changes during the inhalation period (4 days) and a transient increase 12 hours after ethanol withdrawal.	Ethanol	175-182	superoxide dismutase 2	Homo sapiens	0-30
6685298-1	1983	Manganese superoxide dismutase (Mn-SOD) studied during ethanol vapor inhalation shows no changes during the inhalation period (4 days) and a transient increase 12 hours after ethanol withdrawal.	Ethanol	175-182	superoxide dismutase 2	Homo sapiens	32-38
6263242-9	1980	However, extensive sonication of spermatozoa released a small amount of a cyanide-insensitive enzyme, presumably a mangano superoxide dismutase, from the mitochondrial matrix.	Cyanides	74-81	superoxide dismutase 2	Homo sapiens	115-143
7248954-0	1981	Copper- and zinc-containing superoxide dismutase and manganese-containing superoxide dismutase in human tissues and human malignant tumors.	Copper	0-6	superoxide dismutase 2	Homo sapiens	53-94
7264869-4	1981	One g-atom each of copper and zinc was contained in the subunit of Cu,Zn-SOD, and one g-atom of manganese was contained in the subunit of Mn-SOD.	Manganese	96-105	superoxide dismutase 2	Homo sapiens	138-144
32712770-6	2021	In contrast, at 10 mumol.L-1 ziram and zinc associated-disulfiram induced expression of several antioxidants genes HMOX1, SOD2, and catalase, which could suggest the induction of oxidative stress.	Ziram	29-34	superoxide dismutase 2	Homo sapiens	122-126
32712770-6	2021	In contrast, at 10 mumol.L-1 ziram and zinc associated-disulfiram induced expression of several antioxidants genes HMOX1, SOD2, and catalase, which could suggest the induction of oxidative stress.	Disulfiram	55-65	superoxide dismutase 2	Homo sapiens	122-126
33743504-10	2021	Both fresh and vitrified oocytes treated with Ax showed significantly higher mRNA levels of GDF9, POU5F1, SOD2, NRF2 and ATG5.	astaxanthine	46-48	superoxide dismutase 2	Homo sapiens	106-110
33400181-8	2021	Our bioinformatics analysis revealed that the oxidative stress genes superoxide dismutase (SOD1, SOD2) and the pro-inflammatory marker tumor necrosis factor (TNF) were identified as the top relevant genes, and the folate metabolism, vitamin B12 metabolism, and the ALS pathways were highly affected by formaldehyde and related to the most brain diseases of interest.	Folic Acid	214-220	superoxide dismutase 2	Homo sapiens	97-101
33400181-8	2021	Our bioinformatics analysis revealed that the oxidative stress genes superoxide dismutase (SOD1, SOD2) and the pro-inflammatory marker tumor necrosis factor (TNF) were identified as the top relevant genes, and the folate metabolism, vitamin B12 metabolism, and the ALS pathways were highly affected by formaldehyde and related to the most brain diseases of interest.	Formaldehyde	302-314	superoxide dismutase 2	Homo sapiens	97-101
34001853-3	2021	Further analysis indicated that mitochondrial superoxide dismutase (SOD)2, which converts O2- into H2O2 remained deacetylated in CLL cells due to SIRT3 overexpression resulting its constitutive activation.	Oxygen	90-93	superoxide dismutase 2	Homo sapiens	46-73
34021366-1	2021	We have generated a mutant of C. elegans manganese superoxide dismutase at histidine 30 by site-directed mutagenesis.	Histidine	75-84	superoxide dismutase 2	Homo sapiens	41-71
34001853-3	2021	Further analysis indicated that mitochondrial superoxide dismutase (SOD)2, which converts O2- into H2O2 remained deacetylated in CLL cells due to SIRT3 overexpression resulting its constitutive activation.	Hydrogen Peroxide	99-103	superoxide dismutase 2	Homo sapiens	46-73
33485979-13	2021	Meanwhile, Scu improved the overload of reactive oxygen species (ROS), superoxide dismutase (SOD) activity and SOD2 protein expression, and reversed the collapse of mitochondrial membrane potential.	scutellarin	11-14	superoxide dismutase 2	Homo sapiens	111-115
34015458-7	2021	Myricetin has also been found to suppress HMW-Abetao-induced mitochondria dysfunction, as demonstrated in decreasing MPT, Mn-SOD, and ATP generation, raising mitochondrial membrane potential, and increasing mitochondrial-ROS generation.	myricetin	0-9	superoxide dismutase 2	Homo sapiens	122-128
33621788-5	2021	Each SOD2 T allele was associated with an odds ratio of being mutation-positive of 1.69 (95%CI: 1.12-2.55, p = 0.013) through 8-oxodG.	8-ohdg	126-133	superoxide dismutase 2	Homo sapiens	5-9
33839528-10	2021	Our results indicated that GH exerted protective effects in cisplatin-induced ovarian granulosa cell apoptosis by alleviating oxidative stress and enhancing mitochondrial function via Sirt3-Sod2 pathway.	Cisplatin	60-69	superoxide dismutase 2	Homo sapiens	190-194
33946939-6	2021	The benefit of NAC was related to the modulation of signaling proteins in the AMPK-SIRT3-SOD2 axis.	Acetylcysteine	15-18	superoxide dismutase 2	Homo sapiens	89-93
33927570-9	2021	Furthermore, the ROS accumulation, upregulated Nox2 expression, downregulated Sirt1, Sirt3, and Mnsod expression in VSMCs under oxLDL stimulation were also relieved after the knockdown of Tlr4.	Reactive Oxygen Species	17-20	superoxide dismutase 2	Homo sapiens	96-101
33900350-3	2021	The induction of reactive oxygen species (ROS) and downregulation of antioxidant defense factors Nrf2 and SOD2 appeared to be an important underlying mechanism and treatment with a non-cytotoxic dose of EGCG effectively reversed the miR483-3p-induced enhancement of HCC cell migration and invasion in vitro.	epigallocatechin gallate	203-207	superoxide dismutase 2	Homo sapiens	106-110
33900350-3	2021	The induction of reactive oxygen species (ROS) and downregulation of antioxidant defense factors Nrf2 and SOD2 appeared to be an important underlying mechanism and treatment with a non-cytotoxic dose of EGCG effectively reversed the miR483-3p-induced enhancement of HCC cell migration and invasion in vitro.	mir483-3p	233-242	superoxide dismutase 2	Homo sapiens	106-110
33924188-7	2021	The treatment also reinstated the TI-induced decrease in superoxide dismutases (SOD1 and SOD2), catalase, and glutathione peroxidase in the CA1 pyramidal cells after TI.	Titanium	34-36	superoxide dismutase 2	Homo sapiens	89-93
33029813-4	2021	The expression of FOXO3a and its target genes, mitochondrial superoxide dismutase (Mn-SOD) and apoptosis repressor with caspase recruitment domain (ARC), increased after MEHP exposure, but the expression of p-FOXO3a protein was decreased.	mono-(2-ethylhexyl)phthalate	170-174	superoxide dismutase 2	Homo sapiens	47-81
33189402-1	2021	Superoxide-hydrogen peroxide (S-HP), triggered by Val16Ala-SOD2 human polymorphism, may influence the risk of depression.	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	59-63
33189402-1	2021	Superoxide-hydrogen peroxide (S-HP), triggered by Val16Ala-SOD2 human polymorphism, may influence the risk of depression.	Hydrogen Peroxide	11-28	superoxide dismutase 2	Homo sapiens	59-63
33189402-1	2021	Superoxide-hydrogen peroxide (S-HP), triggered by Val16Ala-SOD2 human polymorphism, may influence the risk of depression.	s-hp	30-34	superoxide dismutase 2	Homo sapiens	59-63
33834669-9	2021	Sitagliptin suppressed 5 microg mL-1 of LPS-induced IL-6, IL-8, CCL2, and SOD2 gene expression levels in HGF in a concentration-dependent manner.	Sitagliptin Phosphate	0-11	superoxide dismutase 2	Homo sapiens	74-78
33834669-12	2021	Results of qRT-PCR analysis indicated that 0.5 micromol L-1 of sitagliptin and 5 micromol L-1 of BAY11-7082 significantly inhibited LPS-induced IL-6, IL-8, CCL2, and SOD2 gene expressions.	Sitagliptin Phosphate	63-74	superoxide dismutase 2	Homo sapiens	166-170
33834669-12	2021	Results of qRT-PCR analysis indicated that 0.5 micromol L-1 of sitagliptin and 5 micromol L-1 of BAY11-7082 significantly inhibited LPS-induced IL-6, IL-8, CCL2, and SOD2 gene expressions.	3-(4-methylphenylsulfonyl)-2-propenenitrile	97-107	superoxide dismutase 2	Homo sapiens	166-170
33029813-4	2021	The expression of FOXO3a and its target genes, mitochondrial superoxide dismutase (Mn-SOD) and apoptosis repressor with caspase recruitment domain (ARC), increased after MEHP exposure, but the expression of p-FOXO3a protein was decreased.	mono-(2-ethylhexyl)phthalate	170-174	superoxide dismutase 2	Homo sapiens	83-89
33029813-5	2021	Overexpression of FOXO3a decreased the production of ROS and the apoptosis rate induced by MEHP, and the expression of Mn-SOD and ARC was further increased after MEHP exposure.	mono-(2-ethylhexyl)phthalate	162-166	superoxide dismutase 2	Homo sapiens	119-125
33029813-6	2021	In contrast, knockdown of FOXO3a resulted in increased ROS production and apoptosis and suppressed the expression of Mn-SOD and ARC in the presence of MEHP.	mono-(2-ethylhexyl)phthalate	151-155	superoxide dismutase 2	Homo sapiens	117-123
33029813-9	2021	Activation of FOXO3a defends against MEHP-induced oxidative stress and apoptosis by upregulating the expression of Mn-SOD and ARC in AC16 cardiomyocytes.	mono-(2-ethylhexyl)phthalate	37-41	superoxide dismutase 2	Homo sapiens	115-121
33745084-11	2021	SOD2 47CT/TT allele may have greater oxidative stress due to structural change in the protein and decreased H2O2 production.	Hydrogen Peroxide	108-112	superoxide dismutase 2	Homo sapiens	0-4
33745084-20	2021	We believed the deletion GSTT1null/GSTM1null may contribute to the increased of the oxidative stress in SLE patients while carriers of the mutant SOD2 47CT/TT allele may have greater oxidative stress due to structural change in the protein and decreased H2O2 production.	Hydrogen Peroxide	254-258	superoxide dismutase 2	Homo sapiens	146-150
33664465-6	2021	TBM treatment alleviated oxidative stress by decreasing NOX2 and Ac-SOD2/SOD2 and decreased apoptosis by inhibiting cleaved caspse3 and Bax/Bcl-2.	tubeimoside I	0-3	superoxide dismutase 2	Homo sapiens	68-72
33867840-2	2021	We have previously demonstrated that MnSOD lysine-68 (K68) acetylation (K68-Ac) leads to a change in function from a superoxide-scavenging homotetramer to a peroxidase-directed monomer.	Lysine	43-49	superoxide dismutase 2	Homo sapiens	37-42
33867840-2	2021	We have previously demonstrated that MnSOD lysine-68 (K68) acetylation (K68-Ac) leads to a change in function from a superoxide-scavenging homotetramer to a peroxidase-directed monomer.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	54-57	superoxide dismutase 2	Homo sapiens	37-42
33867840-2	2021	We have previously demonstrated that MnSOD lysine-68 (K68) acetylation (K68-Ac) leads to a change in function from a superoxide-scavenging homotetramer to a peroxidase-directed monomer.	Superoxides	117-127	superoxide dismutase 2	Homo sapiens	37-42
33867840-3	2021	Here, we found that estrogen receptor positive (ER+) breast cancer cell lines (MCF7 and T47D), selected for continuous growth in cisplatin (CDDP) and doxorubicin (DXR), exhibited an increase in MnSOD-K68-Ac.	Cisplatin	129-138	superoxide dismutase 2	Homo sapiens	194-199
33867840-3	2021	Here, we found that estrogen receptor positive (ER+) breast cancer cell lines (MCF7 and T47D), selected for continuous growth in cisplatin (CDDP) and doxorubicin (DXR), exhibited an increase in MnSOD-K68-Ac.	Cisplatin	140-144	superoxide dismutase 2	Homo sapiens	194-199
33867840-3	2021	Here, we found that estrogen receptor positive (ER+) breast cancer cell lines (MCF7 and T47D), selected for continuous growth in cisplatin (CDDP) and doxorubicin (DXR), exhibited an increase in MnSOD-K68-Ac.	Doxorubicin	150-161	superoxide dismutase 2	Homo sapiens	194-199
33867840-3	2021	Here, we found that estrogen receptor positive (ER+) breast cancer cell lines (MCF7 and T47D), selected for continuous growth in cisplatin (CDDP) and doxorubicin (DXR), exhibited an increase in MnSOD-K68-Ac.	Doxorubicin	163-166	superoxide dismutase 2	Homo sapiens	194-199
33867840-4	2021	In addition, MnSOD-K68-Ac, as modeled by the expression of a validated acetylation mimic mutant gene (MnSODK68Q ), also led to therapy resistance to CDDP and DXR, altered mitochondrial structure and morphology, and aberrant cellular metabolism.	Cisplatin	149-153	superoxide dismutase 2	Homo sapiens	13-18
33867840-4	2021	In addition, MnSOD-K68-Ac, as modeled by the expression of a validated acetylation mimic mutant gene (MnSODK68Q ), also led to therapy resistance to CDDP and DXR, altered mitochondrial structure and morphology, and aberrant cellular metabolism.	Doxorubicin	158-161	superoxide dismutase 2	Homo sapiens	13-18
33867840-7	2021	Finally, monomeric MnSOD, as modeled by amber codon substitution to generate MnSOD-K68-Ac or MnSOD-K68Q expression in mammalian cells, appeared to incorporate Fe to maximally induce its peroxidase activity.	Iron	159-161	superoxide dismutase 2	Homo sapiens	19-24
33664465-6	2021	TBM treatment alleviated oxidative stress by decreasing NOX2 and Ac-SOD2/SOD2 and decreased apoptosis by inhibiting cleaved caspse3 and Bax/Bcl-2.	tubeimoside I	0-3	superoxide dismutase 2	Homo sapiens	73-77
33099744-3	2021	The current study investigates the role of DNA methylation in SOD2 gene regulation and its involvement in rMTBI-induced persistent neuropathology inflicted by weight drop injury paradigm.	rmtbi	106-111	superoxide dismutase 2	Homo sapiens	62-66
33580500-7	2021	Furthermore, MRJPs administration significantly upregulated the expression of Silent Information Regulator 2 Associated Protein 3, mitochondrial superoxide dismutase (SOD2), and cytochrome c oxidase subunit IV in OA-treated HepG2 cells.	mrjps	13-18	superoxide dismutase 2	Homo sapiens	167-171
33099744-9	2021	The treatment with 5-azacytidine, a pan DNMT inhibitor, normalized DNA methylation levels and revived SOD2 function after the second episode of rMTBI.	rmtbi	144-149	superoxide dismutase 2	Homo sapiens	102-106
33465344-9	2021	Our results emphasize the role of oxidative stress, particularly SOD2, in neurodegeneration triggered by environmental toxic metal mixture and give a new insight into common molecular mechanisms involved in ALS, PD and AD pathology.	Metals	125-130	superoxide dismutase 2	Homo sapiens	65-69
33099744-5	2021	The temporal and episodic increase in ROS levels (oxidative stress) heightened 8-hydroxyguanosine levels indicating oxidative damage after rMTBI that was concomitant with decline in SOD2 function.	ros	38-41	superoxide dismutase 2	Homo sapiens	182-186
33099744-5	2021	The temporal and episodic increase in ROS levels (oxidative stress) heightened 8-hydroxyguanosine levels indicating oxidative damage after rMTBI that was concomitant with decline in SOD2 function.	rmtbi	139-144	superoxide dismutase 2	Homo sapiens	182-186
33099744-6	2021	In parallel, occupancy of DNMT3b at SOD2 promoter was higher post 30 days of the first episode of rMTBI causing hypermethylation at SOD2 promoter.	rmtbi	98-103	superoxide dismutase 2	Homo sapiens	36-40
33099744-6	2021	In parallel, occupancy of DNMT3b at SOD2 promoter was higher post 30 days of the first episode of rMTBI causing hypermethylation at SOD2 promoter.	rmtbi	98-103	superoxide dismutase 2	Homo sapiens	132-136
33099744-7	2021	This epigenetic silencing of SOD2 promoter was sustained after the second episode of rMTBI causing permanent blockade in SOD2 response.	rmtbi	85-90	superoxide dismutase 2	Homo sapiens	29-33
33099744-7	2021	This epigenetic silencing of SOD2 promoter was sustained after the second episode of rMTBI causing permanent blockade in SOD2 response.	rmtbi	85-90	superoxide dismutase 2	Homo sapiens	121-125
33099744-9	2021	The treatment with 5-azacytidine, a pan DNMT inhibitor, normalized DNA methylation levels and revived SOD2 function after the second episode of rMTBI.	Azacitidine	19-32	superoxide dismutase 2	Homo sapiens	102-106
33728027-5	2021	Superoxide dismutase 2 (SOD2), through its preferential localization to the mitochondria, stands at the forefront against mitochondrial ROS in VSMCs and thus potentially modifies the probability of VC initiation or progression.	Reactive Oxygen Species	136-139	superoxide dismutase 2	Homo sapiens	0-22
33624829-4	2021	The mtETC produces reactive oxygen and nitrogen species, which can act as signals or lead to cellular damage, and are thus efficiently removed by mitochondrial antioxidant systems, including Mn-superoxide dismutase, ascorbate-glutathione cycle and thioredoxin-dependent peroxidases.	mtetc	4-9	superoxide dismutase 2	Homo sapiens	191-214
33632046-9	2021	Furthermore, trehalose alleviated oxidative stress in LPS-stimulated PBMCs as it reversed the altered levels of malondialdehyde and total thiols (p <= .05) and restored the activity of antioxidant enzymes glutathione peroxidase and manganese superoxide dismutase (p < .001).Conclusion: The results of this study indicated that trehalose prevented inflammation and oxidative stress in the LPS-stimulated PBMCs, providing evidence for the benefits of trehalose as a potential therapeutic agent in inflammatory conditions.Abbreviations: LPS: Lipopolysaccharide; NAC: N-Acetyl cysteine; ROS: Reactive oxygen species; IL-6: Interleukin-6; TNF-alpha: Tumor necrosis factor-alpha; SOD: Superoxide dismutase; GPx: Glutathione peroxidase; MDA: Malondialdehyde; MAPK: Mitogen-activated protein kinases; JNK: c-Jun N-terminal kinase; NF-kappaB: Nuclear factor kappa-light-chain-enhancer of activated B cells.	Trehalose	13-22	superoxide dismutase 2	Homo sapiens	232-262
33728027-5	2021	Superoxide dismutase 2 (SOD2), through its preferential localization to the mitochondria, stands at the forefront against mitochondrial ROS in VSMCs and thus potentially modifies the probability of VC initiation or progression.	Reactive Oxygen Species	136-139	superoxide dismutase 2	Homo sapiens	24-28
33624829-4	2021	The mtETC produces reactive oxygen and nitrogen species, which can act as signals or lead to cellular damage, and are thus efficiently removed by mitochondrial antioxidant systems, including Mn-superoxide dismutase, ascorbate-glutathione cycle and thioredoxin-dependent peroxidases.	Nitrogen	39-47	superoxide dismutase 2	Homo sapiens	191-214
33728027-7	2021	Apart from the conventional wisdom of attenuating mitochondrial ROS, SOD2 has been found to affect mitophagy and the formation of the autophagosome, suppress JAK/STAT as well as PI3K/Akt signaling, and retard vascular senescence, all of which underlie the beneficial influences on VC exerted by SOD2.	Reactive Oxygen Species	64-67	superoxide dismutase 2	Homo sapiens	69-73
33680286-6	2021	Furthermore, deletion of GCN5L1 could reduce MnSOD acetylation on lysine 68 and activate its activity, thereby scavenging excessive ROS and relieving oxidative stress-induced renal inflammation and fibrosis.	Lysine	66-72	superoxide dismutase 2	Homo sapiens	45-50
33672092-6	2021	We summarize the association findings between drug hypersensitivity reactions and variants in the genes that encode the enzymes related to the redox system such as enzymes related to glutathione: Glutathione S-transferase (GSTM1, GSTP, GSTT1) and glutathione peroxidase (GPX1), thioredoxin reductase (TXNRD1 and TXNRD2), superoxide dismutase (SOD1, SOD2, and SOD3), catalase (CAT), aldo-keto reductase (AKR), and the peroxiredoxin system (PRDX1, PRDX2, PRDX3, PRDX4, PRDX5, PRDX6).	Glutathione	183-194	superoxide dismutase 2	Homo sapiens	349-353
33079465-3	2021	In this work, we show for the first time that a cerium vanadate (CeVO 4 ) nanozyme can substitute the function of superoxide dismutase 1 and 2 (SOD1 and SOD2) in the neuronal cells even when the natural enzyme is down-regulated by specific gene silencing.	dioxo(oxoceriooxy)vanadium	48-63	superoxide dismutase 2	Homo sapiens	153-157
33079465-3	2021	In this work, we show for the first time that a cerium vanadate (CeVO 4 ) nanozyme can substitute the function of superoxide dismutase 1 and 2 (SOD1 and SOD2) in the neuronal cells even when the natural enzyme is down-regulated by specific gene silencing.	cevo 4	65-71	superoxide dismutase 2	Homo sapiens	153-157
33079465-4	2021	The nanozyme prevents the mitochondrial damage in SOD1 and SOD2-depleted cells by regulating the superoxide levels and restores the physiological levels of the anti-apoptotic Bcl-2 family proteins.	Superoxides	97-107	superoxide dismutase 2	Homo sapiens	59-63
33547353-4	2021	Here we report for the first time a one step synthesis in which Manganese Superoxide Dismutase protein plays a key role in the reduction of gold salts via the use of a Good"s buffer (HEPES) to produce gold nanoparticles, compared to other proteins as catalase (CAT) and bovine serum albumin (BSA).We prove that this effect is directly related with the biological activities of the proteins that have an effect on the gold reduction mechanisms.	gold salts	140-150	superoxide dismutase 2	Homo sapiens	64-94
33562298-7	2021	However, co-treatment with TUDCA alleviated inflammatory response induced by IL-1beta, as shown by down regulation of Il-1beta, Il-6, Il-8 and Cox2, and increased the expression of antioxidant enzyme Sod2.	ursodoxicoltaurine	27-32	superoxide dismutase 2	Homo sapiens	200-204
32781281-0	2021	Role of manganese superoxide dismutase (Mn-SOD) against Cr(III)-induced toxicity in bacteria.	tris(1,10-phenanthroline)chromium(III) chloride	56-63	superoxide dismutase 2	Homo sapiens	8-38
32781281-0	2021	Role of manganese superoxide dismutase (Mn-SOD) against Cr(III)-induced toxicity in bacteria.	tris(1,10-phenanthroline)chromium(III) chloride	56-63	superoxide dismutase 2	Homo sapiens	40-46
32781281-3	2021	After exposure to Cr(III), loss of sodA not only led to the excessive generation of ROS, but also enhanced the level of lipid peroxidation and reduced the GSH level, indicating that the deficiency of Mn-SOD decreased the bacterial resistance ability against Cr(III).	tris(1,10-phenanthroline)chromium(III) chloride	18-25	superoxide dismutase 2	Homo sapiens	200-206
32781281-3	2021	After exposure to Cr(III), loss of sodA not only led to the excessive generation of ROS, but also enhanced the level of lipid peroxidation and reduced the GSH level, indicating that the deficiency of Mn-SOD decreased the bacterial resistance ability against Cr(III).	Reactive Oxygen Species	84-87	superoxide dismutase 2	Homo sapiens	200-206
32781281-3	2021	After exposure to Cr(III), loss of sodA not only led to the excessive generation of ROS, but also enhanced the level of lipid peroxidation and reduced the GSH level, indicating that the deficiency of Mn-SOD decreased the bacterial resistance ability against Cr(III).	Glutathione	155-158	superoxide dismutase 2	Homo sapiens	200-206
32781281-3	2021	After exposure to Cr(III), loss of sodA not only led to the excessive generation of ROS, but also enhanced the level of lipid peroxidation and reduced the GSH level, indicating that the deficiency of Mn-SOD decreased the bacterial resistance ability against Cr(III).	tris(1,10-phenanthroline)chromium(III) chloride	258-265	superoxide dismutase 2	Homo sapiens	200-206
32781281-4	2021	The adverse effects of oxidative stress caused by Cr(III) could be recovered by the rescue of Mn-SOD in the sodA-deficient strain.	tris(1,10-phenanthroline)chromium(III) chloride	50-57	superoxide dismutase 2	Homo sapiens	94-100
32781281-4	2021	The adverse effects of oxidative stress caused by Cr(III) could be recovered by the rescue of Mn-SOD in the sodA-deficient strain.	sodium carbonate	108-112	superoxide dismutase 2	Homo sapiens	94-100
32781281-6	2021	Moreover, Mn-SOD might prevent Cr(III) from oxidation on the bacterial surface by combining with Cr(III).	tris(1,10-phenanthroline)chromium(III) chloride	31-38	superoxide dismutase 2	Homo sapiens	10-16
32781281-6	2021	Moreover, Mn-SOD might prevent Cr(III) from oxidation on the bacterial surface by combining with Cr(III).	tris(1,10-phenanthroline)chromium(III) chloride	97-104	superoxide dismutase 2	Homo sapiens	10-16
33547353-4	2021	Here we report for the first time a one step synthesis in which Manganese Superoxide Dismutase protein plays a key role in the reduction of gold salts via the use of a Good"s buffer (HEPES) to produce gold nanoparticles, compared to other proteins as catalase (CAT) and bovine serum albumin (BSA).We prove that this effect is directly related with the biological activities of the proteins that have an effect on the gold reduction mechanisms.	HEPES	183-188	superoxide dismutase 2	Homo sapiens	64-94
33535682-2	2021	Val16A (Ala) SOD2 polymorphism has been associated with increased prostate cancer (PCa) risk.	val16a	0-6	superoxide dismutase 2	Homo sapiens	13-17
33546433-6	2021	Differential array analysis revealed early modulation of stress response gene expression in both A375 melanoma and PANC-1 adenocarcinoma cells elicited by D2O (90%; <=6 h) (upregulated: CDKN1A, DDIT3, EGR1, GADD45A, HMOX1, NFKBIA, or SOD2 (up to 9-fold; p < 0.01)) confirmed by independent RT-qPCR analysis.	Deuterium Oxide	155-158	superoxide dismutase 2	Homo sapiens	234-238
33302636-9	2021	CONCLUSIONS: This study showed for the first time that VC can attenuate the VCM induced nephrotoxicity by decreasing lipid peroxidation and expression of inflammatory cytokines, and increasing superoxide dismutase 2 (SOD2) activity, this effect may relate to the regulation of ROS/NF-kappaB pathway.	Ascorbic Acid	55-57	superoxide dismutase 2	Homo sapiens	193-215
33302636-9	2021	CONCLUSIONS: This study showed for the first time that VC can attenuate the VCM induced nephrotoxicity by decreasing lipid peroxidation and expression of inflammatory cytokines, and increasing superoxide dismutase 2 (SOD2) activity, this effect may relate to the regulation of ROS/NF-kappaB pathway.	Ascorbic Acid	55-57	superoxide dismutase 2	Homo sapiens	217-221
33535682-2	2021	Val16A (Ala) SOD2 polymorphism has been associated with increased prostate cancer (PCa) risk.	Alanine	8-11	superoxide dismutase 2	Homo sapiens	13-17
33535682-3	2021	We hypothesized that SOD2 Ala single nucleotide polymorphism (SNP) may promote EMT.	Alanine	26-29	superoxide dismutase 2	Homo sapiens	21-25
33535682-10	2021	Ala-SOD2 SNP cells exhibited increased levels of total ROS and superoxide and were more sensitive to co-treatment with H2O2 and MSKE, which led to reduced cell growth and increased apoptosis.	Reactive Oxygen Species	55-58	superoxide dismutase 2	Homo sapiens	4-8
33535682-10	2021	Ala-SOD2 SNP cells exhibited increased levels of total ROS and superoxide and were more sensitive to co-treatment with H2O2 and MSKE, which led to reduced cell growth and increased apoptosis.	Superoxides	63-73	superoxide dismutase 2	Homo sapiens	4-8
33535682-10	2021	Ala-SOD2 SNP cells exhibited increased levels of total ROS and superoxide and were more sensitive to co-treatment with H2O2 and MSKE, which led to reduced cell growth and increased apoptosis.	Hydrogen Peroxide	119-123	superoxide dismutase 2	Homo sapiens	4-8
33264651-0	2021	Single-nucleotide polymorphisms (SNPs) of antioxidant enzymes SOD2 and GSTP1 genes and SLE risk and severity in an Egyptian pediatric population.	single-nucleotide	0-17	superoxide dismutase 2	Homo sapiens	62-66
33124528-2	2021	Manganese superoxide dismutase (MnSOD), one of the most important antioxidases in the human body, plays a key role in maintaining the balance of free radicals in the human body.	Free Radicals	145-158	superoxide dismutase 2	Homo sapiens	0-30
33124528-2	2021	Manganese superoxide dismutase (MnSOD), one of the most important antioxidases in the human body, plays a key role in maintaining the balance of free radicals in the human body.	Free Radicals	145-158	superoxide dismutase 2	Homo sapiens	32-37
33359686-5	2021	Further analysis at the 72 h timepoint demonstrated that AntiOxBEN2 and AntiOxCIN4 did not alter mitochondrial membrane potential (Deltapsi), but increased cellular glutathione (GSH) levels, mitochondrial NAD(P)H autofluorescence, and mitochondrial superoxide dismutase 2 (SOD2) protein levels.	antioxben2	57-67	superoxide dismutase 2	Homo sapiens	273-277
33359686-5	2021	Further analysis at the 72 h timepoint demonstrated that AntiOxBEN2 and AntiOxCIN4 did not alter mitochondrial membrane potential (Deltapsi), but increased cellular glutathione (GSH) levels, mitochondrial NAD(P)H autofluorescence, and mitochondrial superoxide dismutase 2 (SOD2) protein levels.	antioxcin4	72-82	superoxide dismutase 2	Homo sapiens	273-277
33359686-10	2021	We conclude that AntiOxBEN2 and AntiOxCIN4 increase ROS levels, which stimulates NRF2 expression and, as a consequence, SOD2 and GSH levels.	ros	52-55	superoxide dismutase 2	Homo sapiens	120-124
33314691-7	2021	Mechanistically, suppression of LETM1 increased the levels of reactive oxygen species (ROS) and mitochondrial ROS by regulation of SOD2, which in turn activated AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR), initiated autophagy, and inhibited proliferation and stemness.	Reactive Oxygen Species	87-90	superoxide dismutase 2	Homo sapiens	131-135
33314691-7	2021	Mechanistically, suppression of LETM1 increased the levels of reactive oxygen species (ROS) and mitochondrial ROS by regulation of SOD2, which in turn activated AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR), initiated autophagy, and inhibited proliferation and stemness.	Reactive Oxygen Species	110-113	superoxide dismutase 2	Homo sapiens	131-135
33201408-0	2021	Dexamethasone upregulates mitochondrial Tom20, Tom70, and MnSOD through SGK1 in the kidney cells.	Dexamethasone	0-13	superoxide dismutase 2	Homo sapiens	58-63
33450375-3	2021	These ROS are converted to a diffusible signaling molecule, hydrogen peroxide (H2O2), by superoxide dismutase (SOD2).	Reactive Oxygen Species	6-9	superoxide dismutase 2	Homo sapiens	111-115
33201408-8	2021	Similarly, dexamethasone significantly increased MnSOD transcripts by 67 +- 15% and protein level only in the mitochondria dose-dependently.	Dexamethasone	11-24	superoxide dismutase 2	Homo sapiens	49-54
33201408-11	2021	Finally, knock-down of Tom20 and Tom70 by their siRNAs reduced dexamethasone-induced increases in the mitochondrial localization of SGK1 and MnSOD proteins.	Dexamethasone	63-76	superoxide dismutase 2	Homo sapiens	141-146
33201408-12	2021	In conclusion, dexamethasone upregulates Tom20, Tom70, and MnSOD, and these effects are dependent on reactive oxygen species and SGK1.	Dexamethasone	15-28	superoxide dismutase 2	Homo sapiens	59-64
33201408-13	2021	Dexamethasone-induced increases of SGK1 and MnSOD mitochondrial localization requires Tom20 and Tom70.	Dexamethasone	0-13	superoxide dismutase 2	Homo sapiens	44-49
33520087-7	2021	More importantly, berbamine increased the intracellular reactive oxygen species (ROS) level through the downregulation of antioxidative genes such as Nrf2, HO-1, SOD2, and GPX-1.	berbamine	18-27	superoxide dismutase 2	Homo sapiens	162-166
33520087-7	2021	More importantly, berbamine increased the intracellular reactive oxygen species (ROS) level through the downregulation of antioxidative genes such as Nrf2, HO-1, SOD2, and GPX-1.	Reactive Oxygen Species	81-84	superoxide dismutase 2	Homo sapiens	162-166
33435886-0	2021	Iron overload adversely effects bone marrow haematogenesis via SIRT-SOD2-mROS in a process ameliorated by curcumin.	Iron	0-4	superoxide dismutase 2	Homo sapiens	68-72
33435886-0	2021	Iron overload adversely effects bone marrow haematogenesis via SIRT-SOD2-mROS in a process ameliorated by curcumin.	Curcumin	106-114	superoxide dismutase 2	Homo sapiens	68-72
33435886-7	2021	Iron loading decreased SIRT3 protein expression, promoted an increase in SOD2, and led to the elevation of mROS.	Iron	0-4	superoxide dismutase 2	Homo sapiens	73-77
33435886-9	2021	Curcumin treatment ameliorated peripheral blood cells generation, enhanced SIRT3 activity, decreased SOD2 acetylation, inhibited mROS production, and suppressed iron loading-induced autophagy.	Curcumin	0-8	superoxide dismutase 2	Homo sapiens	101-105
33435886-10	2021	CONCLUSIONS: Our results suggest that curcumin exerts a protective effect on bone marrow by reducing mROS-stimulated autophagic cell death in a manner dependent on the SIRT3/SOD2 pathway.	Curcumin	38-46	superoxide dismutase 2	Homo sapiens	174-178
33450375-3	2021	These ROS are converted to a diffusible signaling molecule, hydrogen peroxide (H2O2), by superoxide dismutase (SOD2).	Hydrogen Peroxide	60-77	superoxide dismutase 2	Homo sapiens	111-115
33450375-3	2021	These ROS are converted to a diffusible signaling molecule, hydrogen peroxide (H2O2), by superoxide dismutase (SOD2).	Hydrogen Peroxide	79-83	superoxide dismutase 2	Homo sapiens	111-115
33450375-7	2021	Epigenetic silencing of SOD2 by DNA methylation alters H2O2 production, activating hypoxia-inducible factor 1alpha, thereby disrupting mitochondrial metabolism and dynamics, accelerating cell proliferation and inhibiting apoptosis.	Hydrogen Peroxide	55-59	superoxide dismutase 2	Homo sapiens	24-28
33558048-0	2022	Manganese superoxide dismutase induced by lipoteichoic acid isolated from Staphylococcus aureus regulates cytokine production in THP-1 cells.	lipoteichoic acid	42-59	superoxide dismutase 2	Homo sapiens	0-30
33488943-6	2021	Heteronemin treatment also induced the formation of reactive oxygen species (ROS), which are associated with heteronemin-induced cell death, and to trigger ROS removal by mitochondrial SOD2 rather than cytosolic SOD1.	heteronemin	0-11	superoxide dismutase 2	Homo sapiens	185-189
33488943-6	2021	Heteronemin treatment also induced the formation of reactive oxygen species (ROS), which are associated with heteronemin-induced cell death, and to trigger ROS removal by mitochondrial SOD2 rather than cytosolic SOD1.	Reactive Oxygen Species	156-159	superoxide dismutase 2	Homo sapiens	185-189
33220236-5	2021	Our data revealed that esculetin played an antioxidant role not only through its antioxidant activity, but also by highly inducing Nrf-2 translocation to the nucleus, which in turn, enhanced Nrf2 signaling regulated antioxidant genes (HO-1, NQO1, GCLM, SOD1 and SOD2) mRNA expression levels in H2O2-treated HCE cells.	esculetin	23-32	superoxide dismutase 2	Homo sapiens	262-266
33421349-7	2021	In addition, perampanel increased Sirt3 protein expression, enhanced the activities of mitochondrial enzyme IDH2 and SOD2, and preserved BBB function in vitro.	perampanel	13-23	superoxide dismutase 2	Homo sapiens	117-121
33218188-8	2020	Unexpectedly, OE cells showed increased mitochondrial ROS but when challenged with fatty acids and no androgens, the Superoxide dismutase 2 (SOD2) enzyme increased in the OE cells, suggesting better antioxidant defenses with excess CPT1A expression.	Fatty Acids	83-94	superoxide dismutase 2	Homo sapiens	117-139
33250314-8	2021	Moreover, Oligopin  intervention significantly increased plasma total thiol content, TAC, plasma activity of both MnSOD and catalase, and the transcript level of Nrf2, MnSOD, and catalase in comparison with the placebo group.	Oligopin	10-18	superoxide dismutase 2	Homo sapiens	114-119
33250314-8	2021	Moreover, Oligopin  intervention significantly increased plasma total thiol content, TAC, plasma activity of both MnSOD and catalase, and the transcript level of Nrf2, MnSOD, and catalase in comparison with the placebo group.	Oligopin	10-18	superoxide dismutase 2	Homo sapiens	168-173
33130346-5	2020	Additionally, 6a and 6e counteracted H2O2-induced mitochondrial dysfunction, which was supported by maintaining mitochondrial membrane potential, attenuating BAX protein, and increasing BCL-2 protein within the mitochondria as well as upregulating SOD2 mitochondrial antioxidant enzyme.	Hydrogen Peroxide	37-41	superoxide dismutase 2	Homo sapiens	248-252
33090591-4	2020	Cells exposed to high glucose showed lower NF-kappaB and SOD2 methylation levels, increased NF-kappaB and reduced SOD2 expression compared to normal glucose cells.	Glucose	22-29	superoxide dismutase 2	Homo sapiens	114-118
33391410-8	2021	Results: Resveratrol-treated U251 cells, but not resveratrol-treated LN428 cells, exhibited remarkable growth arrest and extensive apoptosis accompanied by elevated intracellular ROS levels and attenuated SOD2 and catalase expression.	Resveratrol	9-20	superoxide dismutase 2	Homo sapiens	205-209
33009206-2	2021	Superoxide anion radicals, the main product of ROS, can be reduced by manganese superoxide dismutase (SOD2) to hydrogen peroxide, which is further reduced by catalase (CAT) and glutathione peroxidase (GPX) to water.	Superoxides	0-16	superoxide dismutase 2	Homo sapiens	70-100
33009206-2	2021	Superoxide anion radicals, the main product of ROS, can be reduced by manganese superoxide dismutase (SOD2) to hydrogen peroxide, which is further reduced by catalase (CAT) and glutathione peroxidase (GPX) to water.	Superoxides	0-16	superoxide dismutase 2	Homo sapiens	102-106
33009206-2	2021	Superoxide anion radicals, the main product of ROS, can be reduced by manganese superoxide dismutase (SOD2) to hydrogen peroxide, which is further reduced by catalase (CAT) and glutathione peroxidase (GPX) to water.	ros	47-50	superoxide dismutase 2	Homo sapiens	70-100
33009206-2	2021	Superoxide anion radicals, the main product of ROS, can be reduced by manganese superoxide dismutase (SOD2) to hydrogen peroxide, which is further reduced by catalase (CAT) and glutathione peroxidase (GPX) to water.	ros	47-50	superoxide dismutase 2	Homo sapiens	102-106
33009206-2	2021	Superoxide anion radicals, the main product of ROS, can be reduced by manganese superoxide dismutase (SOD2) to hydrogen peroxide, which is further reduced by catalase (CAT) and glutathione peroxidase (GPX) to water.	Hydrogen Peroxide	111-128	superoxide dismutase 2	Homo sapiens	70-100
33009206-2	2021	Superoxide anion radicals, the main product of ROS, can be reduced by manganese superoxide dismutase (SOD2) to hydrogen peroxide, which is further reduced by catalase (CAT) and glutathione peroxidase (GPX) to water.	Hydrogen Peroxide	111-128	superoxide dismutase 2	Homo sapiens	102-106
33009206-2	2021	Superoxide anion radicals, the main product of ROS, can be reduced by manganese superoxide dismutase (SOD2) to hydrogen peroxide, which is further reduced by catalase (CAT) and glutathione peroxidase (GPX) to water.	Water	209-214	superoxide dismutase 2	Homo sapiens	70-100
33009206-2	2021	Superoxide anion radicals, the main product of ROS, can be reduced by manganese superoxide dismutase (SOD2) to hydrogen peroxide, which is further reduced by catalase (CAT) and glutathione peroxidase (GPX) to water.	Water	209-214	superoxide dismutase 2	Homo sapiens	102-106
33362719-5	2020	In addition, BA treatment suppresses ERbeta target genes, including superoxide dismutase 2 (SOD2), nuclear respiratory factor-1 (NRF1), cyclooxygenase 2 (COX2), and matrix metalloproteinase-1 (MMP1), subsequently increasing oxidative stress, triggering mitochondrial dysfunction, decreasing elevated proinflammatory cytokines, and eventually suppressing endometriotic cell proliferation, mimicking the effect of ERbeta knockdown.	betulinic acid	13-15	superoxide dismutase 2	Homo sapiens	68-90
33362719-5	2020	In addition, BA treatment suppresses ERbeta target genes, including superoxide dismutase 2 (SOD2), nuclear respiratory factor-1 (NRF1), cyclooxygenase 2 (COX2), and matrix metalloproteinase-1 (MMP1), subsequently increasing oxidative stress, triggering mitochondrial dysfunction, decreasing elevated proinflammatory cytokines, and eventually suppressing endometriotic cell proliferation, mimicking the effect of ERbeta knockdown.	betulinic acid	13-15	superoxide dismutase 2	Homo sapiens	92-96
33090591-4	2020	Cells exposed to high glucose showed lower NF-kappaB and SOD2 methylation levels, increased NF-kappaB and reduced SOD2 expression compared to normal glucose cells.	Glucose	22-29	superoxide dismutase 2	Homo sapiens	57-61
33012204-6	2020	Mitochondrial isolevuglandins in arterioles from hypertensive patients were 250% greater than in arterioles from normotensive subjects, and ex vivo mito2HOBA treatment of arterioles from hypertensive subjects increased deacetylation of a key mitochondrial antioxidant, SOD2 (superoxide dismutase 2).	mito2hoba	148-157	superoxide dismutase 2	Homo sapiens	269-273
33012204-6	2020	Mitochondrial isolevuglandins in arterioles from hypertensive patients were 250% greater than in arterioles from normotensive subjects, and ex vivo mito2HOBA treatment of arterioles from hypertensive subjects increased deacetylation of a key mitochondrial antioxidant, SOD2 (superoxide dismutase 2).	mito2hoba	148-157	superoxide dismutase 2	Homo sapiens	275-297
32900489-6	2020	Furthermore, ADA modulated the expressions of SOD2, HO-1 and Gpx1 as antioxidant enzymes.	adrenic acid	13-16	superoxide dismutase 2	Homo sapiens	46-50
33218188-8	2020	Unexpectedly, OE cells showed increased mitochondrial ROS but when challenged with fatty acids and no androgens, the Superoxide dismutase 2 (SOD2) enzyme increased in the OE cells, suggesting better antioxidant defenses with excess CPT1A expression.	Fatty Acids	83-94	superoxide dismutase 2	Homo sapiens	141-145
33177495-8	2020	Further, this study demonstrates that quercetin reduces ROS via SIRT3-mediated acetylation of SOD2"s K68 residue.	Quercetin	38-47	superoxide dismutase 2	Homo sapiens	94-98
33198315-0	2020	Astaxanthin Counteracts Vascular Calcification In Vitro Through an Early Up-Regulation of SOD2 Based on a Transcriptomic Approach.	astaxanthine	0-11	superoxide dismutase 2	Homo sapiens	90-94
33198315-11	2020	SOD2 knockdown prominently abolished the anti-calcification effect of astaxanthin on HP-treated VSMCs, lending support to our findings.	astaxanthine	70-81	superoxide dismutase 2	Homo sapiens	0-4
33198315-12	2020	In conclusion, we demonstrated for the first time that astaxanthin could be a potential candidate treatment for VC, through inducing the up-regulation of SOD2 early during calcification progression and potentially suppressing vascular senescence.	astaxanthine	55-66	superoxide dismutase 2	Homo sapiens	154-158
32950532-4	2020	VITROCELL  cloud chamber exposure of BEAS-2B monolayers increased mitochondrial protein oxidation, expression of the antioxidant enzyme SOD2, activation of NF-kappaB, and secretion of inflammatory cytokines (IL-6 and IL-8).	beas	37-41	superoxide dismutase 2	Homo sapiens	136-140
33177495-8	2020	Further, this study demonstrates that quercetin reduces ROS via SIRT3-mediated acetylation of SOD2"s K68 residue.	ros	56-59	superoxide dismutase 2	Homo sapiens	94-98
33177495-8	2020	Further, this study demonstrates that quercetin reduces ROS via SIRT3-mediated acetylation of SOD2"s K68 residue.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	101-104	superoxide dismutase 2	Homo sapiens	94-98
33196414-8	2021	The plasma concentration of TBARS was associated with GSTP1 303AG/GG, GSTP1 -16CT/TT, and SOD2 47CT/TT genotypes.	Thiobarbituric Acid Reactive Substances	28-33	superoxide dismutase 2	Homo sapiens	90-94
33196414-12	2021	We observed an association between elevated TBARS levels and the presence of GSTP1 and SOD2 variants in stored RBC.	Thiobarbituric Acid Reactive Substances	44-49	superoxide dismutase 2	Homo sapiens	87-91
32931795-11	2020	Unlike PA, PABut significantly decreased protein levels of NAD+-dependent deacetylase SirT1 and beta-actin accompanied by mild significant upregulation of mitochondrial SOD2 and senescence markers, p16 protein and SA-beta-Gal activity.	pabut	11-16	superoxide dismutase 2	Homo sapiens	169-173
32889510-5	2020	RESULTS: Statistical analyses showed the association of MnSOD Ala16Val polymorphism with cognitive impairment, including praxis, perception, attention, language, executive functions, long-term semantic memory, short-term visual memory, and total memory in patients with epilepsy and Valine-Valine (VV) genotype compared with the control group.	valine-valine	283-296	superoxide dismutase 2	Homo sapiens	56-61
33050459-11	2020	The Manganese diPyridoxyL EthylDiamine (MnPLED)-type mangafodipir (manganese dipyridoxyl diphosphate-MnDPDP), a magnetic resonance imaging (MRI) contrast agent that possesses MnSOD mimetic activity, has shown promising results in various forms of inflammation, in preclinical as well as clinical settings.	manganese dipyridoxyl ethyldiamine	4-38	superoxide dismutase 2	Homo sapiens	175-180
33149812-0	2020	Notoginseng Leaf Triterpenes Ameliorates OGD/R-Induced Neuronal Injury via SIRT1/2/3-Foxo3a-MnSOD/PGC-1alpha Signaling Pathways Mediated by the NAMPT-NAD Pathway.	Triterpenes	17-28	superoxide dismutase 2	Homo sapiens	92-97
33050459-11	2020	The Manganese diPyridoxyL EthylDiamine (MnPLED)-type mangafodipir (manganese dipyridoxyl diphosphate-MnDPDP), a magnetic resonance imaging (MRI) contrast agent that possesses MnSOD mimetic activity, has shown promising results in various forms of inflammation, in preclinical as well as clinical settings.	N,N'-bis(pyridoxal-5-phosphate)ethylenediamine-N,N'-diacetic acid	53-65	superoxide dismutase 2	Homo sapiens	175-180
33050459-11	2020	The Manganese diPyridoxyL EthylDiamine (MnPLED)-type mangafodipir (manganese dipyridoxyl diphosphate-MnDPDP), a magnetic resonance imaging (MRI) contrast agent that possesses MnSOD mimetic activity, has shown promising results in various forms of inflammation, in preclinical as well as clinical settings.	manganese dipyridoxyl diphosphate-mndpdp	67-107	superoxide dismutase 2	Homo sapiens	175-180
32424140-5	2020	Mechanistically, REGgamma interacted with and targeted PP2Acalpha for degradation directly, thereby leading to increase of phosphorylation levels and nuclear export of Forkhead box protein O (FoxO) 3a and subsequent of SOD2 decline, ROS accumulation, and cardiac hypertrophy.	pp2acalpha	55-65	superoxide dismutase 2	Homo sapiens	219-223
32424140-6	2020	Introducing exogenous PP2Acalpha or SOD2 to human cardiomyocytes significantly rescued the REGgamma-mediated ROS accumulation of Ang II stimulation in vitro.	Reactive Oxygen Species	109-112	superoxide dismutase 2	Homo sapiens	36-40
32707370-14	2020	It is of advantage to prevent apoptosis through SIRT3-mediated SOD2 deacetylation that reduces ROS accumulation and restores mitochondrial function.	ros	95-98	superoxide dismutase 2	Homo sapiens	63-67
33039058-7	2020	The results indicated that DpLE causes apoptosis and exerts intracellular ROS-independent anticancer effects on prostate cancer cells, associated with increased SOD-2, cleaved caspase-8, and cleaved-PARP expression and inhibited p-AKT signaling.	dple	27-31	superoxide dismutase 2	Homo sapiens	161-166
32707370-16	2020	CONCLUSION: Theacrine prevents apoptosis of dopaminergic neurons through directly activating SIRT3 which deacetylating SOD2 and restoring mitochondrial functions.	1,3,7,9-tetramethyluric acid	12-21	superoxide dismutase 2	Homo sapiens	119-123
32814232-10	2020	Punicalagin and curcumin also altered antioxidant (SOD2 and catalase) mRNA expression in placenta, VAT and SAT, with minimal effect on hydrogen peroxide concentrations in tissue lysates.	Curcumin	16-24	superoxide dismutase 2	Homo sapiens	51-55
32673443-7	2020	We collected the conditioned medium from lipopolysaccharide-activated phorbol myristate acetate-induced THP1 (M1) cells to stimulate A549 and H1299 cells and observed that THP1-M1 upregulated SOD-2 by secreting TNF-alpha.	Tetradecanoylphorbol Acetate	70-95	superoxide dismutase 2	Homo sapiens	192-197
32961441-7	2020	5-aza-2"-deoxycytidine treatment restored SOD2 expression and ROS levels.	Decitabine	0-22	superoxide dismutase 2	Homo sapiens	42-46
32899983-6	2020	ROS levels in IMR-32 cells increased significantly in a time- and AFB1 concentration-dependent manner, which was associated with the upregulation of NOX2, and downregulation of OXR1, SOD1, and SOD2.	Reactive Oxygen Species	0-3	superoxide dismutase 2	Homo sapiens	193-197
32986362-3	2020	We recently demonstrated that human BCSCs (CD24-/CD44+) could survive better than their counterpart non-BCSCs (CD24-/CD44-) when treated with rotenone, possibly due to lower levels of reactive oxygen species (ROS) production, high expression of antioxidant manganese superoxide dismutase (MnSOD), and anti-apoptotic survivin.	Rotenone	142-150	superoxide dismutase 2	Homo sapiens	257-287
32986362-3	2020	We recently demonstrated that human BCSCs (CD24-/CD44+) could survive better than their counterpart non-BCSCs (CD24-/CD44-) when treated with rotenone, possibly due to lower levels of reactive oxygen species (ROS) production, high expression of antioxidant manganese superoxide dismutase (MnSOD), and anti-apoptotic survivin.	Rotenone	142-150	superoxide dismutase 2	Homo sapiens	289-294
33015038-9	2020	More importantly, caffeine enhanced SIRT3 activity and reduced SOD2 acetylation, thereby leading to increased SOD2 activity, which could be reversed by treatment with the SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP) in vitro and in vivo.	3-TYP	223-228	superoxide dismutase 2	Homo sapiens	110-114
33015038-10	2020	Taken together, our results show that caffeine targets SIRT3 to enhance SOD2 activity and protect skin cells from UV irradiation-induced oxidative stress.	Caffeine	38-46	superoxide dismutase 2	Homo sapiens	72-76
32705806-8	2020	In addition, Andro also reduced TGF-beta1-induced intracellular ROS generation and NOX4 expression, and elevated antioxidant superoxide dismutase 2 (SOD2) expression, demonstrating the inhibiting effect of Andro on TGF-beta1-induced oxidative stress, which is closely linked to EMT.	andrographolide	13-18	superoxide dismutase 2	Homo sapiens	125-147
32705806-8	2020	In addition, Andro also reduced TGF-beta1-induced intracellular ROS generation and NOX4 expression, and elevated antioxidant superoxide dismutase 2 (SOD2) expression, demonstrating the inhibiting effect of Andro on TGF-beta1-induced oxidative stress, which is closely linked to EMT.	andrographolide	13-18	superoxide dismutase 2	Homo sapiens	149-153
32783052-6	2020	Further, SOD2 immunostaining was enhanced in GM and WM from SIV-infected animals.	Gentamicins	45-47	superoxide dismutase 2	Homo sapiens	9-13
32986362-6	2020	RESULTS: Suppression of survivin expression using YM155 could reduce the survival of rotenone-treated BCSCs, which may be associated with oxidative stress modulation, as shown by increased ROS levels and decreased MnSOD expression.	Rotenone	85-93	superoxide dismutase 2	Homo sapiens	214-219
32986362-8	2020	Furthermore, YM155 could modulate oxidative stress in BCSCs by reducing MnSOD expression and increasing ROS levels.	YM 155	13-18	superoxide dismutase 2	Homo sapiens	72-77
33015038-0	2020	Caffeine Targets SIRT3 to Enhance SOD2 Activity in Mitochondria.	Caffeine	0-8	superoxide dismutase 2	Homo sapiens	34-38
33015038-2	2020	Superoxide dismutase (SOD) 2 is a manganese-containing enzyme located in mitochondria that protects cells against oxidative stress by scavenging reactive oxygen species (ROS).	Manganese	34-43	superoxide dismutase 2	Homo sapiens	0-28
33015038-2	2020	Superoxide dismutase (SOD) 2 is a manganese-containing enzyme located in mitochondria that protects cells against oxidative stress by scavenging reactive oxygen species (ROS).	Reactive Oxygen Species	145-168	superoxide dismutase 2	Homo sapiens	0-28
33015038-2	2020	Superoxide dismutase (SOD) 2 is a manganese-containing enzyme located in mitochondria that protects cells against oxidative stress by scavenging reactive oxygen species (ROS).	Reactive Oxygen Species	170-173	superoxide dismutase 2	Homo sapiens	0-28
33015038-4	2020	Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity.	NAD	45-78	superoxide dismutase 2	Homo sapiens	187-191
33015038-4	2020	Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity.	NAD	80-83	superoxide dismutase 2	Homo sapiens	187-191
33015038-5	2020	In this study, we investigated whether the antioxidant effect of caffeine involves modulation of SOD2 by SIRT3 using in vitro and in vivo models.	Caffeine	65-73	superoxide dismutase 2	Homo sapiens	97-101
33015038-9	2020	More importantly, caffeine enhanced SIRT3 activity and reduced SOD2 acetylation, thereby leading to increased SOD2 activity, which could be reversed by treatment with the SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP) in vitro and in vivo.	Caffeine	18-26	superoxide dismutase 2	Homo sapiens	63-67
33015038-9	2020	More importantly, caffeine enhanced SIRT3 activity and reduced SOD2 acetylation, thereby leading to increased SOD2 activity, which could be reversed by treatment with the SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP) in vitro and in vivo.	Caffeine	18-26	superoxide dismutase 2	Homo sapiens	110-114
33015038-9	2020	More importantly, caffeine enhanced SIRT3 activity and reduced SOD2 acetylation, thereby leading to increased SOD2 activity, which could be reversed by treatment with the SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP) in vitro and in vivo.	3-TYP	187-221	superoxide dismutase 2	Homo sapiens	63-67
33015038-9	2020	More importantly, caffeine enhanced SIRT3 activity and reduced SOD2 acetylation, thereby leading to increased SOD2 activity, which could be reversed by treatment with the SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP) in vitro and in vivo.	3-TYP	187-221	superoxide dismutase 2	Homo sapiens	110-114
32412821-4	2020	Results: Kaempferol, in a dose-dependent manner, significantly increased cell survival and reduced levels of reactive oxygen species, malondialdehyde, single-stranded DNA (ssDNA), and lactate dehydrogenase but increased levels of glutathione (GSH) and manganese-superoxide dismutase (MnSOD) in H2O2-treated ARPE-19 cells.	kaempferol	9-19	superoxide dismutase 2	Homo sapiens	252-282
32412821-4	2020	Results: Kaempferol, in a dose-dependent manner, significantly increased cell survival and reduced levels of reactive oxygen species, malondialdehyde, single-stranded DNA (ssDNA), and lactate dehydrogenase but increased levels of glutathione (GSH) and manganese-superoxide dismutase (MnSOD) in H2O2-treated ARPE-19 cells.	kaempferol	9-19	superoxide dismutase 2	Homo sapiens	284-289
32412821-5	2020	It also increased GSH and MnSOD in a dose-dependent manner in control + Kaempferol treated cells.	kaempferol	72-82	superoxide dismutase 2	Homo sapiens	26-31
32552390-10	2020	Spermidine treatment of PBMCs resulted in a significantly increased expression of all genes tested, whereas resveratrol treatment caused a significant increase of SIRT3, FOXO3 and SOD2 mRNA expression.	Resveratrol	108-119	superoxide dismutase 2	Homo sapiens	180-184
32863233-4	2020	We demonstrate for the first time that Mel potentiates the cytotoxic effects of SHK on cancer cells by inducing oxidative stress via inhibition of the SIRT3/SOD2-AKT pathway.	Melatonin	39-42	superoxide dismutase 2	Homo sapiens	157-161
32782570-0	2020	Genistein inhibits lung cancer cell stem-like characteristics by modulating MnSOD and FoxM1 expression.	Genistein	0-9	superoxide dismutase 2	Homo sapiens	76-81
32782570-11	2020	MnSOD and FoxM1 overexpression antagonized the effects of genistein (40 microM), whereas MnSOD and FoxM1 knockdown enhanced the inhibitory effects of genistein (20 microM) on CSLC characteristics of LCSLCs.	Genistein	58-67	superoxide dismutase 2	Homo sapiens	0-5
32782570-11	2020	MnSOD and FoxM1 overexpression antagonized the effects of genistein (40 microM), whereas MnSOD and FoxM1 knockdown enhanced the inhibitory effects of genistein (20 microM) on CSLC characteristics of LCSLCs.	Genistein	150-159	superoxide dismutase 2	Homo sapiens	89-94
32782570-12	2020	Overall, the results suggested that genistein suppressed lung cancer cell CSLC characteristics by modulating MnSOD and FoxM1 expression levels.	Genistein	36-45	superoxide dismutase 2	Homo sapiens	109-114
32863233-0	2020	Melatonin sensitises shikonin-induced cancer cell death mediated by oxidative stress via inhibition of the SIRT3/SOD2-AKT pathway.	Melatonin	0-9	superoxide dismutase 2	Homo sapiens	113-117
32895185-7	2020	GSEA enrichment analysis indicated that SOD2 played an important role in the JAK-STAT signaling pathway.	gsea	0-4	superoxide dismutase 2	Homo sapiens	40-44
32863233-0	2020	Melatonin sensitises shikonin-induced cancer cell death mediated by oxidative stress via inhibition of the SIRT3/SOD2-AKT pathway.	shikonin	21-29	superoxide dismutase 2	Homo sapiens	113-117
32150044-12	2020	Dual inhibition of both miR-24-3p and miR-145-5p prior to hypoxia-reoxygenation caused significant upregulation of SOD2 and HMOX1 protein; fold-change of 3.17 (p<=0.05) and 6.97 (p<=0.05) respectively.	mir-24-3p	24-33	superoxide dismutase 2	Homo sapiens	115-119
32848792-10	2020	FG-4592 could protect cardiomyocytes against DOX-induced apoptosis and ROS production in line with the upregulation of HIF-1alpha and its target genes of Bcl-2 and SOD2.	Doxorubicin	45-48	superoxide dismutase 2	Homo sapiens	164-168
32781658-8	2020	In Western blotting, the expression levels of SOD2 and IL-4 were increased due to pretreatment with CGA and, furthermore, 4-HNE production and IL-4 expressions were inhibited by CGA pretreatment.	4-hydroxy-2-nonenal	122-127	superoxide dismutase 2	Homo sapiens	46-50
32222623-7	2020	Mechanistically, we provide compelling evidence that PM2.5 reduces SOD2 expression through activation of Akt pathway, which leads to a disruption of mitochondrial redox homeostasis characterized by increased accumulation of mitochondrial superoxide.	Superoxides	238-248	superoxide dismutase 2	Homo sapiens	67-71
32658869-0	2020	Mechanistic study of mtROS-JNK-SOD2 signaling in bupivacaine-induced neuron oxidative stress.	Bupivacaine	49-60	superoxide dismutase 2	Homo sapiens	31-35
32305596-7	2020	In the LOAD group, the gene expression of CAT, SOD2 and GPX also showed a significant decrease and an increase in malondialdehyde.	Malondialdehyde	114-129	superoxide dismutase 2	Homo sapiens	47-51
32765079-0	2020	Modulation of MnSOD and FoxM1 Is Involved in Invasion and EMT Suppression by Isovitexin in Hepatocellular Carcinoma Cells.	isovitexin	77-87	superoxide dismutase 2	Homo sapiens	14-19
32765079-2	2020	Isovitexin (ISOV) was recently found to downregulate MnSOD and FoxM1, decreasing stemness in hepatocellular carcinoma (HCC) stem-like cells (HCSLCs).	isovitexin	0-10	superoxide dismutase 2	Homo sapiens	53-58
32765079-2	2020	Isovitexin (ISOV) was recently found to downregulate MnSOD and FoxM1, decreasing stemness in hepatocellular carcinoma (HCC) stem-like cells (HCSLCs).	isovitexin	12-16	superoxide dismutase 2	Homo sapiens	53-58
32765079-6	2020	The suppressive effects of ISOV on the migratory and invasive capabilities and EMT phenotype could be potentiated by MnSOD or FoxM1 knockdown in HCSLCs, and attenuated by MnSOD or FoxM1 overexpression in HCC cells.	isovitexin	27-31	superoxide dismutase 2	Homo sapiens	117-122
32765079-6	2020	The suppressive effects of ISOV on the migratory and invasive capabilities and EMT phenotype could be potentiated by MnSOD or FoxM1 knockdown in HCSLCs, and attenuated by MnSOD or FoxM1 overexpression in HCC cells.	isovitexin	27-31	superoxide dismutase 2	Homo sapiens	171-176
32658869-8	2020	Inhibition of JNK signaling with a small interfering RNA (siRNA) or with sp600125 down-regulated the increase of SOD2 transcription.	pyrazolanthrone	73-81	superoxide dismutase 2	Homo sapiens	113-117
32658869-9	2020	SOD2 gene knock-down exacerbated bupivacaine-induced mtROS generation and neurotoxic injury but had no effect on JNK phosphorylation.	Bupivacaine	33-44	superoxide dismutase 2	Homo sapiens	0-4
32658869-11	2020	Collectively, our results confirm that mtROS stimulates the transcription of SOD2 via activating JNK signaling in bupivacaine-induced oxidative stress.	Bupivacaine	114-125	superoxide dismutase 2	Homo sapiens	77-81
32774685-6	2020	Additionally, H2O2 at 1 mM significantly decreased the mRNA expression levels of Nrf2, CAT, SOD1, SOD2, HO-1, GST-pi, NQO1, and GLCM in ARPE-19 cells; however, treatment with EE-TT reversed the downregulated mRNA expression levels of all these genes induced by H2O2.	Hydrogen Peroxide	14-18	superoxide dismutase 2	Homo sapiens	98-102
32760286-4	2020	Mitochondria maintain an antioxidant enzyme system that eliminates excess ROS; manganese superoxide dismutase (Mn-SOD) is one of the major components of this system, as it catalyzes the first step involved in scavenging ROS.	Reactive Oxygen Species	74-77	superoxide dismutase 2	Homo sapiens	79-109
32760286-4	2020	Mitochondria maintain an antioxidant enzyme system that eliminates excess ROS; manganese superoxide dismutase (Mn-SOD) is one of the major components of this system, as it catalyzes the first step involved in scavenging ROS.	Reactive Oxygen Species	74-77	superoxide dismutase 2	Homo sapiens	111-117
32760286-4	2020	Mitochondria maintain an antioxidant enzyme system that eliminates excess ROS; manganese superoxide dismutase (Mn-SOD) is one of the major components of this system, as it catalyzes the first step involved in scavenging ROS.	Reactive Oxygen Species	220-223	superoxide dismutase 2	Homo sapiens	79-109
32760286-4	2020	Mitochondria maintain an antioxidant enzyme system that eliminates excess ROS; manganese superoxide dismutase (Mn-SOD) is one of the major components of this system, as it catalyzes the first step involved in scavenging ROS.	Reactive Oxygen Species	220-223	superoxide dismutase 2	Homo sapiens	111-117
32658869-1	2020	Manganese superoxide dismutase (SOD2) is a key enzyme to scavenge free radical superoxide in the mitochondrion.	free radical superoxide	66-89	superoxide dismutase 2	Homo sapiens	0-30
32658869-12	2020	Enhancing antioxidant ability of SOD2 might be crucial in combating bupivacaine-induced neurotoxic injury.	Bupivacaine	68-79	superoxide dismutase 2	Homo sapiens	33-37
32658869-1	2020	Manganese superoxide dismutase (SOD2) is a key enzyme to scavenge free radical superoxide in the mitochondrion.	free radical superoxide	66-89	superoxide dismutase 2	Homo sapiens	32-36
32658869-4	2020	The role and the mechanism of SOD2 regulation in bupivacaine-induced oxidative stress remains unclear.	Bupivacaine	49-60	superoxide dismutase 2	Homo sapiens	30-34
32658869-6	2020	The results showed that bupivacaine caused the over-production of mitochondrial reactive oxygen species (mtROS), the activation of C-Jun N-terminal kinase (JNK), and the elevation of SOD2 transcription.	Bupivacaine	24-35	superoxide dismutase 2	Homo sapiens	183-187
32658869-7	2020	Decrease of mtROS with N-acetyl-L-cysteine attenuated the activation of JNK and the increase of SOD2 transcription.	Acetylcysteine	23-42	superoxide dismutase 2	Homo sapiens	96-100
32585852-12	2020	Overall, these data indicate that BRAF pathway inhibitor-resistant cells can compensate for elevated ROS via increased expression of the antioxidant SOD2.	Reactive Oxygen Species	101-104	superoxide dismutase 2	Homo sapiens	149-153
32559843-3	2020	EGCG functions mainly through the regulation of ROS (reactive oxygen species) levels, which affect the expression of catalase (CAT), superoxide dismutase 1(SOD1), superoxide dismutase 2(SOD2), and glutathione peroxidase (GPx), has positive influence on other enzyme activities in germ cells and oocytes, and actively alters antioxidant activities.	epigallocatechin gallate	0-4	superoxide dismutase 2	Homo sapiens	186-190
32559843-3	2020	EGCG functions mainly through the regulation of ROS (reactive oxygen species) levels, which affect the expression of catalase (CAT), superoxide dismutase 1(SOD1), superoxide dismutase 2(SOD2), and glutathione peroxidase (GPx), has positive influence on other enzyme activities in germ cells and oocytes, and actively alters antioxidant activities.	Reactive Oxygen Species	48-51	superoxide dismutase 2	Homo sapiens	186-190
32559843-3	2020	EGCG functions mainly through the regulation of ROS (reactive oxygen species) levels, which affect the expression of catalase (CAT), superoxide dismutase 1(SOD1), superoxide dismutase 2(SOD2), and glutathione peroxidase (GPx), has positive influence on other enzyme activities in germ cells and oocytes, and actively alters antioxidant activities.	Reactive Oxygen Species	53-76	superoxide dismutase 2	Homo sapiens	186-190
32468046-0	2020	Excessive production of mitochondrion-derived reactive oxygen species induced by titanium ions leads to autophagic cell death of osteoblasts via the SIRT3/SOD2 pathway.	Oxygen	55-61	superoxide dismutase 2	Homo sapiens	155-159
32468046-0	2020	Excessive production of mitochondrion-derived reactive oxygen species induced by titanium ions leads to autophagic cell death of osteoblasts via the SIRT3/SOD2 pathway.	Titanium	81-89	superoxide dismutase 2	Homo sapiens	155-159
32468046-10	2020	Therefore, the present results suggested that excessive production of mROS induced by Ti ions led to autophagic cell death of osteoblasts, which is dependent on the SIRT3/SOD2 pathway.	Titanium	86-88	superoxide dismutase 2	Homo sapiens	171-175
32201199-1	2020	Superoxide dismutase 2 (SOD2) is a key enzyme for scavenging reactive oxygen species produced by mitochondria, which plays an important role in maintaining cellular homeostasis.	Reactive Oxygen Species	61-84	superoxide dismutase 2	Homo sapiens	0-22
32201199-1	2020	Superoxide dismutase 2 (SOD2) is a key enzyme for scavenging reactive oxygen species produced by mitochondria, which plays an important role in maintaining cellular homeostasis.	Reactive Oxygen Species	61-84	superoxide dismutase 2	Homo sapiens	24-28
32694997-9	2020	Furthermore, the gene expression of mitochondrial Glrx2 and SOD2 were increased upon lapatinib treatment, which was also observed for the mitochondrial SOD2 protein content.	Lapatinib	85-94	superoxide dismutase 2	Homo sapiens	60-64
32694997-9	2020	Furthermore, the gene expression of mitochondrial Glrx2 and SOD2 were increased upon lapatinib treatment, which was also observed for the mitochondrial SOD2 protein content.	Lapatinib	85-94	superoxide dismutase 2	Homo sapiens	152-156
32527005-5	2020	Antioxidant Mn-activated superoxide dismutase (SOD2) and (m)-aconitase activities were increased in HCM vs. CTRL.	Superoxides	25-35	superoxide dismutase 2	Homo sapiens	47-51
32222469-0	2020	Manganese porphyrin, MnTE-2-PyP, treatment protects the prostate from radiation-induced fibrosis (RIF) by activating the NRF2 signaling pathway and enhancing SOD2 and sirtuin activity.	manganese porphyrin	0-19	superoxide dismutase 2	Homo sapiens	158-162
31820335-12	2020	Further, lutein protected high glucose-mediated down-regulation of a redox-sensitive transcription factor, Nrf2, and antioxidant enzymes, SOD2, HO-1, and catalase.	Lutein	9-15	superoxide dismutase 2	Homo sapiens	138-142
31820335-12	2020	Further, lutein protected high glucose-mediated down-regulation of a redox-sensitive transcription factor, Nrf2, and antioxidant enzymes, SOD2, HO-1, and catalase.	Glucose	31-38	superoxide dismutase 2	Homo sapiens	138-142
31854466-19	2020	Interestingly, we observed that BCI promoted the nucleus translocation of pNrf2, as well as the gene expression levels of pNrf2 and its target genes (Cat, Gclc, Sod1, and Sod2).	baicalein	32-35	superoxide dismutase 2	Homo sapiens	171-175
32525823-10	2020	Dex also recovered the levels of NF-kappaB and COX2, as well as mnSOD, catalase and ROS.	Dexmedetomidine	0-3	superoxide dismutase 2	Homo sapiens	64-69
32466166-9	2020	SOD2 expression was reduced upon exposure to B. burgdorferi, suggesting that B. burgdorferi might be responsible for superoxide reduction.	Superoxides	117-127	superoxide dismutase 2	Homo sapiens	0-4
32222469-10	2020	This decrease in SOD2 K122 acetylation correlates with an increase in SOD2 activity and mitochondrial superoxide scavenging capacity.	Superoxides	102-112	superoxide dismutase 2	Homo sapiens	17-21
32149414-10	2020	First, proper level of SOD2 helped CRC cells maintain mitochondrial function by disposal of superoxide (O2 .- ).	Superoxides	92-102	superoxide dismutase 2	Homo sapiens	23-27
32149414-10	2020	First, proper level of SOD2 helped CRC cells maintain mitochondrial function by disposal of superoxide (O2 .- ).	Oxygen	104-106	superoxide dismutase 2	Homo sapiens	23-27
32149414-11	2020	Second, over-expression of SOD2 induced H2 O2 -mediated tumorigenesis by upregulating AMPK and glycolysis.	Hydrogen Peroxide	40-45	superoxide dismutase 2	Homo sapiens	27-31
32142722-3	2020	Our findings demonstrated that the electron leakage from the impaired ETC, leading to the accumulation of ROS was gradually elevating with increasing concentration of CEES exposure, which decline the activity of superoxide dismutase (SOD), manganese SOD (MnSOD) and copper-zinc SOD (Cu-ZnSOD) in keratinocytes.	Reactive Oxygen Species	106-109	superoxide dismutase 2	Homo sapiens	240-253
32142722-3	2020	Our findings demonstrated that the electron leakage from the impaired ETC, leading to the accumulation of ROS was gradually elevating with increasing concentration of CEES exposure, which decline the activity of superoxide dismutase (SOD), manganese SOD (MnSOD) and copper-zinc SOD (Cu-ZnSOD) in keratinocytes.	2-chloroethyl ethyl sulfide	167-171	superoxide dismutase 2	Homo sapiens	240-253
32142722-3	2020	Our findings demonstrated that the electron leakage from the impaired ETC, leading to the accumulation of ROS was gradually elevating with increasing concentration of CEES exposure, which decline the activity of superoxide dismutase (SOD), manganese SOD (MnSOD) and copper-zinc SOD (Cu-ZnSOD) in keratinocytes.	2-chloroethyl ethyl sulfide	167-171	superoxide dismutase 2	Homo sapiens	255-260
32316287-9	2020	Notably, Mn-TM-2-PyP increased SOD2 expression eight-fold, while resveratrol increased Nrf2 expression three-fold.	manganese tetrakis-(N-methyl-2 pyridyl) porphyrin	9-20	superoxide dismutase 2	Homo sapiens	31-35
32327976-5	2020	Our findings showed that DHT treatment suppresses the expression of estrogen receptor beta (ERbeta) and superoxide dismutase 2 (SOD2) through AR-mediated hypermethylation on the ERbeta promoter, and BBR treatment suppresses AR expression through hypermethylation on the AR promoter.	Dihydrotestosterone	25-28	superoxide dismutase 2	Homo sapiens	104-126
32327976-5	2020	Our findings showed that DHT treatment suppresses the expression of estrogen receptor beta (ERbeta) and superoxide dismutase 2 (SOD2) through AR-mediated hypermethylation on the ERbeta promoter, and BBR treatment suppresses AR expression through hypermethylation on the AR promoter.	Dihydrotestosterone	25-28	superoxide dismutase 2	Homo sapiens	128-132
32327976-5	2020	Our findings showed that DHT treatment suppresses the expression of estrogen receptor beta (ERbeta) and superoxide dismutase 2 (SOD2) through AR-mediated hypermethylation on the ERbeta promoter, and BBR treatment suppresses AR expression through hypermethylation on the AR promoter.	Berberine	199-202	superoxide dismutase 2	Homo sapiens	128-132
32264868-8	2020	EMPA and DAPA (100 muM) significantly reduced SA-induced inflammation (IL1beta, TNFalpha, MCP1), oxidant stress (SOD2, TXN, HO1), but not apoptosis in MAC.	empagliflozin	0-4	superoxide dismutase 2	Homo sapiens	113-117
32264868-8	2020	EMPA and DAPA (100 muM) significantly reduced SA-induced inflammation (IL1beta, TNFalpha, MCP1), oxidant stress (SOD2, TXN, HO1), but not apoptosis in MAC.	dapagliflozin	9-13	superoxide dismutase 2	Homo sapiens	113-117
30937835-6	2020	Additionally, phloretin treatment increased oxidative stress, as demonstrated through lower antioxidant enzymes (catalase, SOD2, Gpx1, Gpx3).	Phloretin	14-23	superoxide dismutase 2	Homo sapiens	123-127
31968997-4	2020	This review discusses how mitochondrial superoxide dismutase (SOD2) plays two critical roles in facilitating redox signaling.	Superoxides	40-50	superoxide dismutase 2	Homo sapiens	62-66
31904901-4	2020	Superoxide anions are metabolized by manganese-dependent superoxide dismutase (SOD2) in the mitochondria.	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	79-83
32228565-5	2020	We evaluated the effects of UPM and/or curcumin on the expression of phosphorylated ERK, Nrf2, HO-1, and SOD2 in fibroblasts by Western blotting.	Curcumin	39-47	superoxide dismutase 2	Homo sapiens	105-109
32228565-10	2020	Nrf2 production was also promoted to increase the expression of HO-1 and SOD2 by curcumin.	Curcumin	81-89	superoxide dismutase 2	Homo sapiens	73-77
32213883-3	2020	Results showed that Seleno-L-methionine did not cause an increase in hydrogen peroxide production at relatively low concentrations, accompanied by a rise in the antioxidant enzymes catalase and MnSOD, and UCP2 protein expression levels.	Selenomethionine	20-39	superoxide dismutase 2	Homo sapiens	194-199
32213883-6	2020	Moreover, at 10 microM, Seleno-L-cystine decreased UCP2 and MnSOD protein expression.	L-Selenocystine	24-40	superoxide dismutase 2	Homo sapiens	60-65
32077682-0	2020	Lipid-Functionalized Graphene Loaded with hMnSOD for Selective Inhibition of Cancer Cells.	Graphite	21-29	superoxide dismutase 2	Homo sapiens	42-48
32218705-6	2020	Aspirin inhibited COX-2 and iNOS without changes in COX-1 expression, increasing anti-oxidant protein (Cu/Zn-SOD and Mn-SOD) expression in presence or absence of Abeta1-42.	Aspirin	0-7	superoxide dismutase 2	Homo sapiens	117-123
31786336-11	2020	In addition, metformin and rotenone (0.1 mumol/L) also reduces reactive oxygen species (ROS) production and increase superoxide dismutase 2 (SOD2) expression.	Metformin	13-22	superoxide dismutase 2	Homo sapiens	117-139
31786336-11	2020	In addition, metformin and rotenone (0.1 mumol/L) also reduces reactive oxygen species (ROS) production and increase superoxide dismutase 2 (SOD2) expression.	Metformin	13-22	superoxide dismutase 2	Homo sapiens	141-145
31786336-11	2020	In addition, metformin and rotenone (0.1 mumol/L) also reduces reactive oxygen species (ROS) production and increase superoxide dismutase 2 (SOD2) expression.	Rotenone	27-35	superoxide dismutase 2	Homo sapiens	117-139
31786336-11	2020	In addition, metformin and rotenone (0.1 mumol/L) also reduces reactive oxygen species (ROS) production and increase superoxide dismutase 2 (SOD2) expression.	Rotenone	27-35	superoxide dismutase 2	Homo sapiens	141-145
31786336-12	2020	Our results establish that metformin AMPK-independently protects against palmitate-induced hepatic cell death by moderate inhibition of the mitochondrial respiratory chain, recovering mitochondrial function, decreasing cellular ROS production, and inducing SOD2 expression, indicating that metformin may have beneficial actions beyond its glucose-lowering effect and also suggests that mitochondrial complex I may be a therapeutic target in NAFLD.	Metformin	27-36	superoxide dismutase 2	Homo sapiens	257-261
31904901-4	2020	Superoxide anions are metabolized by manganese-dependent superoxide dismutase (SOD2) in the mitochondria.	Manganese	37-46	superoxide dismutase 2	Homo sapiens	79-83
31786336-12	2020	Our results establish that metformin AMPK-independently protects against palmitate-induced hepatic cell death by moderate inhibition of the mitochondrial respiratory chain, recovering mitochondrial function, decreasing cellular ROS production, and inducing SOD2 expression, indicating that metformin may have beneficial actions beyond its glucose-lowering effect and also suggests that mitochondrial complex I may be a therapeutic target in NAFLD.	Palmitates	73-82	superoxide dismutase 2	Homo sapiens	257-261
31904901-4	2020	Superoxide anions are metabolized by manganese-dependent superoxide dismutase (SOD2) in the mitochondria.	Superoxides	57-67	superoxide dismutase 2	Homo sapiens	79-83
31904901-5	2020	A functional genetic polymorphism (SOD2, rs4880), responsible of a 40% reduction in enzyme activity, is associated with anti-inflammatory response of rosuvastatin.	rosuvastatin	150-162	superoxide dismutase 2	Homo sapiens	35-39
31904901-6	2020	We investigated the association of Ala-allele of SOD2 rs4880 and both antidepressant efficacy and inflammatory parameters in patients treated for a MDE with antidepressant drugs.	alanyl-alanyl-alanyl-alanine	35-38	superoxide dismutase 2	Homo sapiens	49-53
32141579-5	2020	The regulatory effect of zoledronic acid on the SIRT3/SOD2 pathway was detected by Western blot.	Zoledronic Acid	25-40	superoxide dismutase 2	Homo sapiens	54-58
32271398-11	2020	Also, we found that VO increased the antioxidant enzymes SOD1, SOD2, CAT, GSH, POD production, and suppressed the ROS in the disc.	Vanadium(II) oxide	20-22	superoxide dismutase 2	Homo sapiens	63-67
32271403-13	2020	Besides, high glucose promoted the expression of 8-OH, and inhibited SOD1, SOD2, and CAT mRNA expressions, resulting in the up-regulated ROS level of CHs.	Glucose	14-21	superoxide dismutase 2	Homo sapiens	75-79
32539644-0	2020	Association of arsenic-related AS3MT gene and antioxidant SOD2 gene expression in industrial workers occupationally exposed to arsenic.	Arsenic	127-134	superoxide dismutase 2	Homo sapiens	58-62
32539644-10	2020	This study suggests that decreased AS3MT and SOD2 expression levels may lead to bioaccumulation of As in the body accompanied by increased oxidative stress ultimately inducing DNA damage.	Arsenic	99-101	superoxide dismutase 2	Homo sapiens	45-49
32141579-0	2020	Zoledronic acid accelerates osteogenesis of bone marrow mesenchymal stem cells by attenuating oxidative stress via the SIRT3/SOD2 pathway and thus alleviates osteoporosis.	Zoledronic Acid	0-15	superoxide dismutase 2	Homo sapiens	125-129
32141579-10	2020	Besides, zoledronic acid protected H2O2-induced SIRT3 down-regulation and AC-SOD2/SOD2 up-regulation in BMSCs.	Zoledronic Acid	9-24	superoxide dismutase 2	Homo sapiens	77-81
32141579-1	2020	OBJECTIVE: The aim of this study was to clarify the potential effect of zoledronic acid on alleviating oxidative stress and promoting bone marrow mesenchymal stem cells (BMSCs) osteogenesis through the SIRT3/SOD2 pathway, thus alleviating the progression of osteoporosis.	Zoledronic Acid	72-87	superoxide dismutase 2	Homo sapiens	208-212
32141579-10	2020	Besides, zoledronic acid protected H2O2-induced SIRT3 down-regulation and AC-SOD2/SOD2 up-regulation in BMSCs.	Zoledronic Acid	9-24	superoxide dismutase 2	Homo sapiens	82-86
32141582-5	2020	Furthermore, the expression of antioxidant factor Nrf2, as well as downstream antioxidant genes, including NQO1, SOD1, SOD2, and HO1 was assessed in hydroquinone stimulated ARPE19 cells, in the presence or absence of SAC pretreatment.	hydroquinone	149-161	superoxide dismutase 2	Homo sapiens	119-123
31919630-6	2020	The high SOD2 levels in UFM and PM cells correlated with lower levels of superoxide and reactive oxygen species (ROS), and with morphological anomalies and depolarization of the mitochondrial membrane detected through confocal microscopy.	Superoxides	73-83	superoxide dismutase 2	Homo sapiens	9-13
31919630-6	2020	The high SOD2 levels in UFM and PM cells correlated with lower levels of superoxide and reactive oxygen species (ROS), and with morphological anomalies and depolarization of the mitochondrial membrane detected through confocal microscopy.	Reactive Oxygen Species	88-111	superoxide dismutase 2	Homo sapiens	9-13
31919630-6	2020	The high SOD2 levels in UFM and PM cells correlated with lower levels of superoxide and reactive oxygen species (ROS), and with morphological anomalies and depolarization of the mitochondrial membrane detected through confocal microscopy.	Reactive Oxygen Species	113-116	superoxide dismutase 2	Homo sapiens	9-13
31919630-9	2020	Overall, these data suggest that in PM and UFM carriers, which have high levels of FMR1 transcription and may develop FXTAS, SOD2 overexpression helps to maintain low levels of both superoxide and ROS with signs of mitochondrial degradation.	Superoxides	182-192	superoxide dismutase 2	Homo sapiens	125-129
31919630-9	2020	Overall, these data suggest that in PM and UFM carriers, which have high levels of FMR1 transcription and may develop FXTAS, SOD2 overexpression helps to maintain low levels of both superoxide and ROS with signs of mitochondrial degradation.	Reactive Oxygen Species	197-200	superoxide dismutase 2	Homo sapiens	125-129
31901951-6	2020	We further verified that ACT001 elevated the levels of reactive oxygen species (ROS) by regulating NF-kappaB-targeted MnSOD.	Oxygen	64-70	superoxide dismutase 2	Homo sapiens	118-123
31842414-7	2019	Besides, fucoxanthin promoted the expression of manganese superoxide dismutase, a downstream target of FoxO3alpha.	fucoxanthin	9-20	superoxide dismutase 2	Homo sapiens	48-78
31891227-0	2020	Superoxide imbalance triggered by Val16Ala-SOD2 polymorphism increases the risk of depression and self-reported psychological stress in free-living elderly people.	Superoxides	0-10	superoxide dismutase 2	Homo sapiens	43-47
31891227-2	2020	However, it is still not clear whether the VV-SOD2 genotype that causes higher basal superoxide anion levels has any impact on the risk for depression and self-reported psychological stress in elderly people.	Superoxides	85-101	superoxide dismutase 2	Homo sapiens	46-50
31723239-6	2020	Mechanistically, SIRT3 prevents mitochondrial superoxide surges in detached cells by regulating the manganese superoxide dismutase (SOD2).	Superoxides	100-120	superoxide dismutase 2	Homo sapiens	132-136
32410873-9	2020	Gene expressions of IRGM, CTLA4, FOXO4, SLC26A3, SLC39A4, SOD2, TDO2, and ALDOB were associated with clinical outcomes, such as medical treatment in response to aminosalicylates, histological remission, clinical course, and evolution.	Aminosalicylic Acid	161-177	superoxide dismutase 2	Homo sapiens	58-62
31940867-6	2020	Overall, we found that SOD2 siRNA transfection in the spheroid form of MSCs increases the expression of apoptotic genes and decreases the clearance of mitochondrial reactive oxygen species (ROS).	Oxygen	174-180	superoxide dismutase 2	Homo sapiens	23-27
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Oxygen	129-135	superoxide dismutase 2	Homo sapiens	18-40
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Oxygen	129-135	superoxide dismutase 2	Homo sapiens	42-46
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Oxygen	129-135	superoxide dismutase 2	Homo sapiens	51-81
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Superoxides	254-270	superoxide dismutase 2	Homo sapiens	18-40
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Superoxides	254-270	superoxide dismutase 2	Homo sapiens	42-46
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Superoxides	254-270	superoxide dismutase 2	Homo sapiens	51-81
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Oxygen	272-274	superoxide dismutase 2	Homo sapiens	18-40
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Oxygen	272-274	superoxide dismutase 2	Homo sapiens	42-46
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Oxygen	272-274	superoxide dismutase 2	Homo sapiens	51-81
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Hydrogen Peroxide	284-288	superoxide dismutase 2	Homo sapiens	18-40
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Hydrogen Peroxide	284-288	superoxide dismutase 2	Homo sapiens	42-46
31494578-5	2020	This gene encodes superoxide dismutase 2 (SOD2) or manganese-superoxide dismutase, a mitochondrial matrix protein that scavenges oxygen radicals produced by oxidation-reduction and electron transport reactions occurring in mitochondria via conversion of superoxide anion (O2 - ) into H2O2.	Hydrogen Peroxide	284-288	superoxide dismutase 2	Homo sapiens	51-81
31494578-6	2020	Measurement of hydroethidine oxidation showed a significant increase in O2 -  levels in the patient"s skin fibroblasts, as compared with controls, and this was paralleled by reduced catalytic activity of SOD2 in patient fibroblasts and muscle.	hydroethidine	15-28	superoxide dismutase 2	Homo sapiens	204-208
31494578-6	2020	Measurement of hydroethidine oxidation showed a significant increase in O2 -  levels in the patient"s skin fibroblasts, as compared with controls, and this was paralleled by reduced catalytic activity of SOD2 in patient fibroblasts and muscle.	Oxygen	72-74	superoxide dismutase 2	Homo sapiens	204-208
31494578-8	2020	CONCLUSION: Our results provide evidence that defective SOD2 may lead to toxic increases in the levels of damaging oxygen radicals in the neonatal heart, which can result in rapidly developing heart failure and death.	Oxygen	115-121	superoxide dismutase 2	Homo sapiens	56-60
31648572-7	2020	Abbreviations AKT protein kinase B ARMS alveolar rhabdomyosarcoma ATM ataxia telangiectasia mutated Bax Bcl-2-associated X protein Bcl-2 B-cell lymphoma 2 CDC2 cyclin-dependent kinase 2 Bcl-xL B-cell lymphoma-extra large c-FLIP cellular FLICE-like inhibitory protein CDDP cisplatin COX-2 cyclooxygenase-2 cyt c cytochrome c DNA-PKcs DNA-dependent protein kinase EGFR epidermal growth factor receptor EMT epithelial-mesenchymal transition ERK extracellular signal-regulated kinase ES Ewing`s sarcoma ETS2 erythroblastosis virus transcription factor 2 GBM glioblastoma multiforme HCC hepatocellular carcinoma HNSCC head and neck squamous cell carcinoma IAP inhibitor of apoptosis protein IkappaBalpha inhibitor of kappaB alpha IKK inhibitor of kappaB kinase IR ionizing radiation lncRNA long non-coding RNA luc luciferase Mcl-1 myeloid cell leukemia-1 MDR1 multidrug resistance protein 1 miR microRNA MMP-9 matrix metalloproteinase-9 mTOR mammalian target of rapamycin NB neuroblastoma NF-kappaB nuclear factor-kappaB NPC nasopharyngeal carcinoma NSCLC non-small cell lung cancer OSCC oral squamous cell carcinoma PARP poly-(ADP-ribose)-polymerase pH2AX phosphorylated histone 2AX-immunoreactive PI3K phosphatidylinositol 3-kinase Prp4K Pre-mRNA processing factor 4 kinase RCC renal cell carcinoma ROS reactive oxygen species SCC squamous cell carcinoma SLN solid lipid nanoparticle SOD2 superoxide dismutase 2 TERT telomerase reverse transcriptase TNF-alpha tumor necrosis factor-alpha TxnRd1 thioredoxin reductase-1 VEGF vascular endothelial growth factor XIAP X-linked inhibitor of apoptosis protein DeltaPsim mitochondrial membrane potential.	Cisplatin	267-281	superoxide dismutase 2	Homo sapiens	1381-1385
31648572-7	2020	Abbreviations AKT protein kinase B ARMS alveolar rhabdomyosarcoma ATM ataxia telangiectasia mutated Bax Bcl-2-associated X protein Bcl-2 B-cell lymphoma 2 CDC2 cyclin-dependent kinase 2 Bcl-xL B-cell lymphoma-extra large c-FLIP cellular FLICE-like inhibitory protein CDDP cisplatin COX-2 cyclooxygenase-2 cyt c cytochrome c DNA-PKcs DNA-dependent protein kinase EGFR epidermal growth factor receptor EMT epithelial-mesenchymal transition ERK extracellular signal-regulated kinase ES Ewing`s sarcoma ETS2 erythroblastosis virus transcription factor 2 GBM glioblastoma multiforme HCC hepatocellular carcinoma HNSCC head and neck squamous cell carcinoma IAP inhibitor of apoptosis protein IkappaBalpha inhibitor of kappaB alpha IKK inhibitor of kappaB kinase IR ionizing radiation lncRNA long non-coding RNA luc luciferase Mcl-1 myeloid cell leukemia-1 MDR1 multidrug resistance protein 1 miR microRNA MMP-9 matrix metalloproteinase-9 mTOR mammalian target of rapamycin NB neuroblastoma NF-kappaB nuclear factor-kappaB NPC nasopharyngeal carcinoma NSCLC non-small cell lung cancer OSCC oral squamous cell carcinoma PARP poly-(ADP-ribose)-polymerase pH2AX phosphorylated histone 2AX-immunoreactive PI3K phosphatidylinositol 3-kinase Prp4K Pre-mRNA processing factor 4 kinase RCC renal cell carcinoma ROS reactive oxygen species SCC squamous cell carcinoma SLN solid lipid nanoparticle SOD2 superoxide dismutase 2 TERT telomerase reverse transcriptase TNF-alpha tumor necrosis factor-alpha TxnRd1 thioredoxin reductase-1 VEGF vascular endothelial growth factor XIAP X-linked inhibitor of apoptosis protein DeltaPsim mitochondrial membrane potential.	Sirolimus	957-966	superoxide dismutase 2	Homo sapiens	1381-1385
31648572-7	2020	Abbreviations AKT protein kinase B ARMS alveolar rhabdomyosarcoma ATM ataxia telangiectasia mutated Bax Bcl-2-associated X protein Bcl-2 B-cell lymphoma 2 CDC2 cyclin-dependent kinase 2 Bcl-xL B-cell lymphoma-extra large c-FLIP cellular FLICE-like inhibitory protein CDDP cisplatin COX-2 cyclooxygenase-2 cyt c cytochrome c DNA-PKcs DNA-dependent protein kinase EGFR epidermal growth factor receptor EMT epithelial-mesenchymal transition ERK extracellular signal-regulated kinase ES Ewing`s sarcoma ETS2 erythroblastosis virus transcription factor 2 GBM glioblastoma multiforme HCC hepatocellular carcinoma HNSCC head and neck squamous cell carcinoma IAP inhibitor of apoptosis protein IkappaBalpha inhibitor of kappaB alpha IKK inhibitor of kappaB kinase IR ionizing radiation lncRNA long non-coding RNA luc luciferase Mcl-1 myeloid cell leukemia-1 MDR1 multidrug resistance protein 1 miR microRNA MMP-9 matrix metalloproteinase-9 mTOR mammalian target of rapamycin NB neuroblastoma NF-kappaB nuclear factor-kappaB NPC nasopharyngeal carcinoma NSCLC non-small cell lung cancer OSCC oral squamous cell carcinoma PARP poly-(ADP-ribose)-polymerase pH2AX phosphorylated histone 2AX-immunoreactive PI3K phosphatidylinositol 3-kinase Prp4K Pre-mRNA processing factor 4 kinase RCC renal cell carcinoma ROS reactive oxygen species SCC squamous cell carcinoma SLN solid lipid nanoparticle SOD2 superoxide dismutase 2 TERT telomerase reverse transcriptase TNF-alpha tumor necrosis factor-alpha TxnRd1 thioredoxin reductase-1 VEGF vascular endothelial growth factor XIAP X-linked inhibitor of apoptosis protein DeltaPsim mitochondrial membrane potential.	Poly Adenosine Diphosphate Ribose	1117-1134	superoxide dismutase 2	Homo sapiens	1381-1385
31648572-7	2020	Abbreviations AKT protein kinase B ARMS alveolar rhabdomyosarcoma ATM ataxia telangiectasia mutated Bax Bcl-2-associated X protein Bcl-2 B-cell lymphoma 2 CDC2 cyclin-dependent kinase 2 Bcl-xL B-cell lymphoma-extra large c-FLIP cellular FLICE-like inhibitory protein CDDP cisplatin COX-2 cyclooxygenase-2 cyt c cytochrome c DNA-PKcs DNA-dependent protein kinase EGFR epidermal growth factor receptor EMT epithelial-mesenchymal transition ERK extracellular signal-regulated kinase ES Ewing`s sarcoma ETS2 erythroblastosis virus transcription factor 2 GBM glioblastoma multiforme HCC hepatocellular carcinoma HNSCC head and neck squamous cell carcinoma IAP inhibitor of apoptosis protein IkappaBalpha inhibitor of kappaB alpha IKK inhibitor of kappaB kinase IR ionizing radiation lncRNA long non-coding RNA luc luciferase Mcl-1 myeloid cell leukemia-1 MDR1 multidrug resistance protein 1 miR microRNA MMP-9 matrix metalloproteinase-9 mTOR mammalian target of rapamycin NB neuroblastoma NF-kappaB nuclear factor-kappaB NPC nasopharyngeal carcinoma NSCLC non-small cell lung cancer OSCC oral squamous cell carcinoma PARP poly-(ADP-ribose)-polymerase pH2AX phosphorylated histone 2AX-immunoreactive PI3K phosphatidylinositol 3-kinase Prp4K Pre-mRNA processing factor 4 kinase RCC renal cell carcinoma ROS reactive oxygen species SCC squamous cell carcinoma SLN solid lipid nanoparticle SOD2 superoxide dismutase 2 TERT telomerase reverse transcriptase TNF-alpha tumor necrosis factor-alpha TxnRd1 thioredoxin reductase-1 VEGF vascular endothelial growth factor XIAP X-linked inhibitor of apoptosis protein DeltaPsim mitochondrial membrane potential.	Phosphatidylinositols	1199-1219	superoxide dismutase 2	Homo sapiens	1381-1385
31648572-7	2020	Abbreviations AKT protein kinase B ARMS alveolar rhabdomyosarcoma ATM ataxia telangiectasia mutated Bax Bcl-2-associated X protein Bcl-2 B-cell lymphoma 2 CDC2 cyclin-dependent kinase 2 Bcl-xL B-cell lymphoma-extra large c-FLIP cellular FLICE-like inhibitory protein CDDP cisplatin COX-2 cyclooxygenase-2 cyt c cytochrome c DNA-PKcs DNA-dependent protein kinase EGFR epidermal growth factor receptor EMT epithelial-mesenchymal transition ERK extracellular signal-regulated kinase ES Ewing`s sarcoma ETS2 erythroblastosis virus transcription factor 2 GBM glioblastoma multiforme HCC hepatocellular carcinoma HNSCC head and neck squamous cell carcinoma IAP inhibitor of apoptosis protein IkappaBalpha inhibitor of kappaB alpha IKK inhibitor of kappaB kinase IR ionizing radiation lncRNA long non-coding RNA luc luciferase Mcl-1 myeloid cell leukemia-1 MDR1 multidrug resistance protein 1 miR microRNA MMP-9 matrix metalloproteinase-9 mTOR mammalian target of rapamycin NB neuroblastoma NF-kappaB nuclear factor-kappaB NPC nasopharyngeal carcinoma NSCLC non-small cell lung cancer OSCC oral squamous cell carcinoma PARP poly-(ADP-ribose)-polymerase pH2AX phosphorylated histone 2AX-immunoreactive PI3K phosphatidylinositol 3-kinase Prp4K Pre-mRNA processing factor 4 kinase RCC renal cell carcinoma ROS reactive oxygen species SCC squamous cell carcinoma SLN solid lipid nanoparticle SOD2 superoxide dismutase 2 TERT telomerase reverse transcriptase TNF-alpha tumor necrosis factor-alpha TxnRd1 thioredoxin reductase-1 VEGF vascular endothelial growth factor XIAP X-linked inhibitor of apoptosis protein DeltaPsim mitochondrial membrane potential.	Oxygen	293-299	superoxide dismutase 2	Homo sapiens	1381-1385
31648572-7	2020	Abbreviations AKT protein kinase B ARMS alveolar rhabdomyosarcoma ATM ataxia telangiectasia mutated Bax Bcl-2-associated X protein Bcl-2 B-cell lymphoma 2 CDC2 cyclin-dependent kinase 2 Bcl-xL B-cell lymphoma-extra large c-FLIP cellular FLICE-like inhibitory protein CDDP cisplatin COX-2 cyclooxygenase-2 cyt c cytochrome c DNA-PKcs DNA-dependent protein kinase EGFR epidermal growth factor receptor EMT epithelial-mesenchymal transition ERK extracellular signal-regulated kinase ES Ewing`s sarcoma ETS2 erythroblastosis virus transcription factor 2 GBM glioblastoma multiforme HCC hepatocellular carcinoma HNSCC head and neck squamous cell carcinoma IAP inhibitor of apoptosis protein IkappaBalpha inhibitor of kappaB alpha IKK inhibitor of kappaB kinase IR ionizing radiation lncRNA long non-coding RNA luc luciferase Mcl-1 myeloid cell leukemia-1 MDR1 multidrug resistance protein 1 miR microRNA MMP-9 matrix metalloproteinase-9 mTOR mammalian target of rapamycin NB neuroblastoma NF-kappaB nuclear factor-kappaB NPC nasopharyngeal carcinoma NSCLC non-small cell lung cancer OSCC oral squamous cell carcinoma PARP poly-(ADP-ribose)-polymerase pH2AX phosphorylated histone 2AX-immunoreactive PI3K phosphatidylinositol 3-kinase Prp4K Pre-mRNA processing factor 4 kinase RCC renal cell carcinoma ROS reactive oxygen species SCC squamous cell carcinoma SLN solid lipid nanoparticle SOD2 superoxide dismutase 2 TERT telomerase reverse transcriptase TNF-alpha tumor necrosis factor-alpha TxnRd1 thioredoxin reductase-1 VEGF vascular endothelial growth factor XIAP X-linked inhibitor of apoptosis protein DeltaPsim mitochondrial membrane potential.	Superoxides	1386-1396	superoxide dismutase 2	Homo sapiens	1381-1385
31991717-4	2020	In our experimental model, main carnosine beneficial effects were: (1) the modulation of nitric oxide production and metabolism; (2) the amelioration of the macrophage energy state; (3) the decrease of the expressions of pro-oxidant enzymes (Nox-2, Cox-2) and of the lipid peroxidation product malondialdehyde; (4) the restoration and/or increase of the expressions of antioxidant enzymes (Gpx1, SOD-2 and Cat); (5) the increase of the transforming growth factor-beta1 (TGF-beta1) and the down-regulation of the expressions of interleukins 1beta and 6 (IL-1beta and IL-6) and 6) the increase of the expressions of Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase-1 (HO-1).	Carnosine	32-41	superoxide dismutase 2	Homo sapiens	396-401
31812668-4	2020	We demonstrate that mutant p53 induces MnSOD expression, which is recovered by the ROS scavenger N-acetyl-l-cysteine.	Acetylcysteine	97-116	superoxide dismutase 2	Homo sapiens	39-44
31812668-6	2020	We also demonstrate that mutant p53 induces the expression of Sirtuin3 (SIRT3), a major mitochondrial NAD+-dependent deacetylase, stimulating MnSOD deacetylation and enzymatic activity.	NAD	102-105	superoxide dismutase 2	Homo sapiens	142-147
31630030-2	2020	Here, a 3D multiple self-cleaning electrochemical ratiometric microfluidic paper-based analytical device (SER-muPAD) has been constructed for manganese super oxide dismutase (MnSOD) gene detection on the basis of the inner reference probe and exonuclease SH (Exo SH)-assisted analytes recycling amplification method.	(2,2'-L-serine)-gramicidin S	106-109	superoxide dismutase 2	Homo sapiens	142-173
31630030-2	2020	Here, a 3D multiple self-cleaning electrochemical ratiometric microfluidic paper-based analytical device (SER-muPAD) has been constructed for manganese super oxide dismutase (MnSOD) gene detection on the basis of the inner reference probe and exonuclease SH (Exo SH)-assisted analytes recycling amplification method.	(2,2'-L-serine)-gramicidin S	106-109	superoxide dismutase 2	Homo sapiens	175-180
31630030-4	2020	For achieving sensitive detection of MnSOD gene, the methylene blue (MB)-modified capture probe (CP) as the inner reference element was first self-assembled on triangular Au nanosheets modified paper working electrode to provide a built-in correction and improve the detection accuracy.	Methylene Chloride	53-62	superoxide dismutase 2	Homo sapiens	37-42
31630030-4	2020	For achieving sensitive detection of MnSOD gene, the methylene blue (MB)-modified capture probe (CP) as the inner reference element was first self-assembled on triangular Au nanosheets modified paper working electrode to provide a built-in correction and improve the detection accuracy.	Gold	171-173	superoxide dismutase 2	Homo sapiens	37-42
31630030-5	2020	When MnSOD gene existed, it hybridized with the hairpin-structured signal probe, triggering the cyclic amplification with the assistance of Exo SH selective digestion to engender numerous residual DNA labeled with ferrocene (Fc) that could be captured on electrode surface by CPs.	ferrocene	214-223	superoxide dismutase 2	Homo sapiens	5-10
31630030-5	2020	When MnSOD gene existed, it hybridized with the hairpin-structured signal probe, triggering the cyclic amplification with the assistance of Exo SH selective digestion to engender numerous residual DNA labeled with ferrocene (Fc) that could be captured on electrode surface by CPs.	ferrocene	225-227	superoxide dismutase 2	Homo sapiens	5-10
33585836-0	2020	Succinate Accumulation Links Mitochondrial MnSOD Depletion to Aberrant Nuclear DNA Methylation and Altered Cell Fate.	Succinic Acid	0-9	superoxide dismutase 2	Homo sapiens	43-48
33585836-5	2020	Furthermore, SOD2 -/- cells exhibited significantly reduced TET enzyme activity concomitant with decreases in genomic 5-hmC and corresponding increases in 5-mC.	tetramethylenedisulfotetramine	60-63	superoxide dismutase 2	Homo sapiens	13-17
33585836-6	2020	Finally, when stimulated with delta-aminolevulonic acid (delta-ALA), SOD2 -/- HEL cells failed to properly differentiate toward an erythroid phenotype, likely due to failure to complete the necessary global DNA demethylation program required for erythroid maturation.	delta-aminolevulonic acid	30-55	superoxide dismutase 2	Homo sapiens	69-73
33585836-6	2020	Finally, when stimulated with delta-aminolevulonic acid (delta-ALA), SOD2 -/- HEL cells failed to properly differentiate toward an erythroid phenotype, likely due to failure to complete the necessary global DNA demethylation program required for erythroid maturation.	Aminolevulinic Acid	57-66	superoxide dismutase 2	Homo sapiens	69-73
33585836-7	2020	Together, our findings support the model of an SDH/succinate/TET axis and a role for succinate as a retrograde signaling molecule of mitochondrial origin that significantly perturbs nuclear epigenetic reprogramming and introduce MnSOD as a governor of the SDH/succinate/TET axis.	Succinic Acid	85-94	superoxide dismutase 2	Homo sapiens	229-234
33585836-7	2020	Together, our findings support the model of an SDH/succinate/TET axis and a role for succinate as a retrograde signaling molecule of mitochondrial origin that significantly perturbs nuclear epigenetic reprogramming and introduce MnSOD as a governor of the SDH/succinate/TET axis.	Succinic Acid	85-94	superoxide dismutase 2	Homo sapiens	229-234
33585836-7	2020	Together, our findings support the model of an SDH/succinate/TET axis and a role for succinate as a retrograde signaling molecule of mitochondrial origin that significantly perturbs nuclear epigenetic reprogramming and introduce MnSOD as a governor of the SDH/succinate/TET axis.	tetramethylenedisulfotetramine	270-273	superoxide dismutase 2	Homo sapiens	229-234
31526949-5	2020	Importantly, we reveal that melatonin supplementation reverses the defective phenotypes in aged oocytes through a Sirt1/Sod2-dependent mechanism.	Melatonin	28-37	superoxide dismutase 2	Homo sapiens	120-124
31385236-1	2019	The purpose of this study was to investigate the effect of a superoxide-hydrogen peroxide (S-HP) imbalance of the superoxide dismutase manganese dependent (SOD2) gene, generated by paraquat and porphyrin exposure, on the keratinocytes cell line (HaCaT) oxidative metabolism.	superoxide-hydrogen peroxide	61-89	superoxide dismutase 2	Homo sapiens	156-160
31556759-10	2019	AX-SLN exhibited the protective effect against the LPO, enzymic (SOD, CuZnSOD, MnSOD, GPx, and CAT), and nonenzymic (GSH) in the serum, mammary gland, renal, and hepatic tissues.	Amoxicillin	0-2	superoxide dismutase 2	Homo sapiens	79-84
31690112-7	2019	The mRNA expression levels of catalase and manganese superoxide dismutase, which are well-known targets of YAP, were increased by H2O2 treatment but down-regulated by NEDD4 silencing using a specific small interfering RNA targeting NEDD4 (siNEDD4).	Hydrogen Peroxide	130-134	superoxide dismutase 2	Homo sapiens	43-73
31385236-1	2019	The purpose of this study was to investigate the effect of a superoxide-hydrogen peroxide (S-HP) imbalance of the superoxide dismutase manganese dependent (SOD2) gene, generated by paraquat and porphyrin exposure, on the keratinocytes cell line (HaCaT) oxidative metabolism.	s-hp	91-95	superoxide dismutase 2	Homo sapiens	156-160
31385236-2	2019	Paraquat acts increasing superoxide (O 2  - ) levels, while porphyrin increases hydrogen peroxide (H2O2) levels, acting as VV-SOD2-like and AA-SOD2-like molecules, respectively.	Porphyrins	60-69	superoxide dismutase 2	Homo sapiens	126-130
31385236-2	2019	Paraquat acts increasing superoxide (O 2  - ) levels, while porphyrin increases hydrogen peroxide (H2O2) levels, acting as VV-SOD2-like and AA-SOD2-like molecules, respectively.	Porphyrins	60-69	superoxide dismutase 2	Homo sapiens	143-147
31512047-6	2019	We also found a marked correlation between TC and CC genotypes of MnSOD rs4880 polymorphism and a 1.9- to 2.3-fold increase risk of PE (OR = 1.9, 95%CI 1.2-2.9; P = 0.005 and OR = 2.3, 95%CI 1-5.1; P = 0.04, respectively).	Technetium	43-45	superoxide dismutase 2	Homo sapiens	66-71
31026089-3	2019	In addition, the effect of L and OXL for the activation of AMPK that triggers the downstream regulator peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha), TFAM expression, mitochondrial DNA (mtDNA), mitochondrial biogenesis and superoxide dismutase 2 (SOD2) in high glucose treated HepG2 cells were investigated by quantitative polymerase chain reaction and Western blot analysis.	Lutein	27-28	superoxide dismutase 2	Homo sapiens	258-280
31622021-4	2019	Naringenin enhances the viability of the PA-treated HUVECs and, additionally, effectively decreases oxidative stress by scavenging ROS, and increasing the SOD2 level and GPx activity.	naringenin	0-10	superoxide dismutase 2	Homo sapiens	155-159
31819369-5	2019	The mRNA and protein expression levels of redox transcription factor Nrf2 and the downstream effector SOD-1, SOD-2, NQO-1 and HO-1 were assayed to explore the detailed mechanism by which ICA alleviates ECM degradation.	icariin	187-190	superoxide dismutase 2	Homo sapiens	109-114
31591207-0	2019	SOD2 acetylation on lysine 68 promotes stem cell reprogramming in breast cancer.	tyrosyl-lysine	20-26	superoxide dismutase 2	Homo sapiens	0-4
31591207-1	2019	Mitochondrial superoxide dismutase (SOD2) suppresses tumor initiation but promotes invasion and dissemination of tumor cells at later stages of the disease.	Superoxides	14-24	superoxide dismutase 2	Homo sapiens	36-40
31591207-3	2019	Our results indicate that as SOD2 expression increases acetylation of lysine 68 ensues.	tyrosyl-lysine	70-76	superoxide dismutase 2	Homo sapiens	29-33
31591207-4	2019	Acetylated SOD2 promotes hypoxic signaling via increased mitochondrial reactive oxygen species (mtROS).	Oxygen	80-86	superoxide dismutase 2	Homo sapiens	11-15
31228093-0	2019	Superoxide Dismutases SOD1 and SOD2 Rescue the Toxic Effect of Dopamine-Derived Products in Human SH-SY5Y Neuroblastoma Cells.	Dopamine	63-71	superoxide dismutase 2	Homo sapiens	31-35
31228093-5	2019	Then, we tested and demonstrated the capability of the antioxidant enzymes SOD1 and SOD2 to protect cells from the noxious effects induced by DA treatment.	Dopamine	142-144	superoxide dismutase 2	Homo sapiens	84-88
31652453-12	2019	Meanwhile, the changes of Catalase and MnSOD showed that ROS was enhanced by ketamine, however, such an effect was ameliorated by down-regulation of TXNIP in SV-HUC-1 cells.	Ketamine	77-85	superoxide dismutase 2	Homo sapiens	39-44
31624381-11	2019	The overexpression of circ-SOD2 in Caco2 cells resulted in a decrease of transepithelial electrical resistance (TEER), an increase of the FITC-dextran permeability and the downregulation of epithelial barrier related molecule CLDN-8 (P<0.05).	fluorescein isothiocyanate dextran	138-150	superoxide dismutase 2	Homo sapiens	27-31
31629402-0	2019	Enrichment of superoxide dismutase 2 in glioblastoma confers to acquisition of temozolomide resistance that is associated with tumor-initiating cell subsets.	temozolomide	79-91	superoxide dismutase 2	Homo sapiens	14-36
31629402-7	2019	SOD2 in the resistant cells functionally determined the cell fate by limiting TMZ-stimulated superoxide reaction and cleavage of caspase-3.	temozolomide	78-81	superoxide dismutase 2	Homo sapiens	0-4
31629402-7	2019	SOD2 in the resistant cells functionally determined the cell fate by limiting TMZ-stimulated superoxide reaction and cleavage of caspase-3.	Superoxides	93-103	superoxide dismutase 2	Homo sapiens	0-4
31629402-13	2019	CONCLUSION: SOD2 plays crucial roles in the tumor-initiating features that are related to TMZ resistance.	temozolomide	90-93	superoxide dismutase 2	Homo sapiens	12-16
31220783-5	2019	In maternal peripheral blood, the SOD2 promoter methylation levels were positively associated with the exposure concentrations of PM10 (during the entire pregnancy and the second trimester) and nitrogen dioxide (NO2) (during the first trimester of pregnancy), whereas the levels were negatively associated with the exposure concentrations of NO2 during the third trimester of pregnancy.	Nitrogen Dioxide	194-210	superoxide dismutase 2	Homo sapiens	34-38
31220783-5	2019	In maternal peripheral blood, the SOD2 promoter methylation levels were positively associated with the exposure concentrations of PM10 (during the entire pregnancy and the second trimester) and nitrogen dioxide (NO2) (during the first trimester of pregnancy), whereas the levels were negatively associated with the exposure concentrations of NO2 during the third trimester of pregnancy.	Nitrogen Dioxide	212-215	superoxide dismutase 2	Homo sapiens	34-38
31220783-5	2019	In maternal peripheral blood, the SOD2 promoter methylation levels were positively associated with the exposure concentrations of PM10 (during the entire pregnancy and the second trimester) and nitrogen dioxide (NO2) (during the first trimester of pregnancy), whereas the levels were negatively associated with the exposure concentrations of NO2 during the third trimester of pregnancy.	Nitrogen Dioxide	342-345	superoxide dismutase 2	Homo sapiens	34-38
31220783-6	2019	Additionally, interaction analyses revealed that the maternal SOD2 promoter methylation level and sulfur dioxide (SO2) exposure (during the entire pregnancy and the third trimester), as well as NO2 exposure (during the third trimester of pregnancy), had an interaction effect on the SOD2 promoter methylation level in umbilical cord blood.	Sulfur Dioxide	98-112	superoxide dismutase 2	Homo sapiens	62-66
31220783-6	2019	Additionally, interaction analyses revealed that the maternal SOD2 promoter methylation level and sulfur dioxide (SO2) exposure (during the entire pregnancy and the third trimester), as well as NO2 exposure (during the third trimester of pregnancy), had an interaction effect on the SOD2 promoter methylation level in umbilical cord blood.	Sulfur Dioxide	114-117	superoxide dismutase 2	Homo sapiens	62-66
31423616-8	2019	Tert-butylhydroquinone enhanced Nrf2 and SOD2 expression, and partially reversed ATO-induced cytotoxicity, ROS accumulation, MMP reduction, ATP depletion and mitochondria-dependent apoptosis.	2-tert-butylhydroquinone	0-22	superoxide dismutase 2	Homo sapiens	41-45
31364751-0	2019	TNF-alpha-mediated upregulation of SOD-2 contributes to cell proliferation and cisplatin resistance in esophageal squamous cell carcinoma.	Cisplatin	79-88	superoxide dismutase 2	Homo sapiens	35-40
31364751-3	2019	Super dismutase [Mn], mitochondrial (SOD-2), an important primary antioxidant enzyme located in mitochondria, could regulate ROS production.	Reactive Oxygen Species	125-128	superoxide dismutase 2	Homo sapiens	37-42
31364751-5	2019	Therefore, the present study aimed to identify if TNF-alpha mediated SOD-2 upregulation is involved in cisplatin resistance in ESCC.	Cisplatin	103-112	superoxide dismutase 2	Homo sapiens	69-74
31364751-10	2019	Furthermore, it was observed that TNF-alpha could induce cisplatin resistance in Eca109 cells, while transfection with SOD-2 siRNA could significantly increase the chemosensitivity of ESCC to cisplatin.	Cisplatin	192-201	superoxide dismutase 2	Homo sapiens	119-124
31364751-11	2019	Therefore, the present results suggested that SOD-2 may serve as an oncogene, and the upregulation of SOD-2 by TNF-alpha/NF-kappaB may contribute to cisplatin resistance in ESCC.	Cisplatin	149-158	superoxide dismutase 2	Homo sapiens	102-107
30819616-3	2019	Loss of MnSOD led to specific increases in mitochondrial O2- with no evident changes in hydrogen peroxide (H2O2), peroxynitrite (ONOO-), or copper/zinc superoxide dismutase (CuZnSOD) levels.	Oxygen	57-60	superoxide dismutase 2	Homo sapiens	8-13
31695757-19	2019	ALDH1A1-induced upregulation of SOD2 and GPX4, as well as ALDH1A1 itself, mitigated erlotinib-induced oxidative and carbonyl stress, and imparted the TKI resistance.	erlotinib	84-93	superoxide dismutase 2	Homo sapiens	32-36
31695757-19	2019	ALDH1A1-induced upregulation of SOD2 and GPX4, as well as ALDH1A1 itself, mitigated erlotinib-induced oxidative and carbonyl stress, and imparted the TKI resistance.	carbonyl fluoride	116-124	superoxide dismutase 2	Homo sapiens	32-36
31506286-5	2019	Superoxide dismutase 2 (SOD2) is a mitochondrial-specific antioxidant enzyme that dismutates superoxide to hydrogen peroxide, which is then converted to water by catalase and glutathione peroxidase.	Superoxides	93-103	superoxide dismutase 2	Homo sapiens	0-22
31506286-5	2019	Superoxide dismutase 2 (SOD2) is a mitochondrial-specific antioxidant enzyme that dismutates superoxide to hydrogen peroxide, which is then converted to water by catalase and glutathione peroxidase.	Superoxides	93-103	superoxide dismutase 2	Homo sapiens	24-28
31506286-5	2019	Superoxide dismutase 2 (SOD2) is a mitochondrial-specific antioxidant enzyme that dismutates superoxide to hydrogen peroxide, which is then converted to water by catalase and glutathione peroxidase.	Hydrogen Peroxide	107-124	superoxide dismutase 2	Homo sapiens	0-22
31506286-5	2019	Superoxide dismutase 2 (SOD2) is a mitochondrial-specific antioxidant enzyme that dismutates superoxide to hydrogen peroxide, which is then converted to water by catalase and glutathione peroxidase.	Hydrogen Peroxide	107-124	superoxide dismutase 2	Homo sapiens	24-28
31506286-5	2019	Superoxide dismutase 2 (SOD2) is a mitochondrial-specific antioxidant enzyme that dismutates superoxide to hydrogen peroxide, which is then converted to water by catalase and glutathione peroxidase.	Water	153-158	superoxide dismutase 2	Homo sapiens	0-22
31506286-5	2019	Superoxide dismutase 2 (SOD2) is a mitochondrial-specific antioxidant enzyme that dismutates superoxide to hydrogen peroxide, which is then converted to water by catalase and glutathione peroxidase.	Water	153-158	superoxide dismutase 2	Homo sapiens	24-28
30565018-0	2019	Vitamin C Attenuates Sodium Fluoride-Induced Mitochondrial Oxidative Stress and Apoptosis via Sirt1-SOD2 Pathway in F9 Cells.	Ascorbic Acid	0-9	superoxide dismutase 2	Homo sapiens	100-104
30565018-0	2019	Vitamin C Attenuates Sodium Fluoride-Induced Mitochondrial Oxidative Stress and Apoptosis via Sirt1-SOD2 Pathway in F9 Cells.	Sodium Fluoride	21-36	superoxide dismutase 2	Homo sapiens	100-104
30565018-6	2019	However, all NaF-induced mitochondrial oxidative injuries were efficiently ameliorated by overexpression of Sirt1 or incubation with Mito-TEMPO (a SOD2 mimetic).	MitoTEMPO	133-143	superoxide dismutase 2	Homo sapiens	147-151
30565018-8	2019	Knockdown of Sirt1 blocked the vitamin C-mediated reduction in mROS and apoptosis via inhibiting Sirt1-SOD2 signaling.	Ascorbic Acid	31-40	superoxide dismutase 2	Homo sapiens	103-107
30565018-9	2019	Importantly, sodium-dependent vitamin C transporter 2 (SVCT-2) siRNA was found to partially block the ability of vitamin C to promote Sirt1/SOD2 signaling.	Ascorbic Acid	30-39	superoxide dismutase 2	Homo sapiens	140-144
30565018-10	2019	In summary, our data indicate that Sirt1 plays a pivotal role in the ability of vitamin C to stimulate SOD2 activity and attenuate mitochondrial oxidative stress, which partially through vitamin C receptor in NaF-induced F9 cells injury.	Ascorbic Acid	80-89	superoxide dismutase 2	Homo sapiens	103-107
31218727-3	2019	To our knowledge, this study is the first to screen systematically the mechanism of TP-induced toxicity through a global cytotoxicity profile high-content analysis using three independent cytotoxic assay panels with multiple endpoints of cytotoxicity, including cell loss, mitochondrial membrane potential, nuclear membrane permeability, manganese superoxide dismutase, phosphorylated gamma-H2AX, light chain 3B, lysosome, reactive oxygen species and glutathione.	triptolide	84-86	superoxide dismutase 2	Homo sapiens	338-368
31416388-10	2019	Importantly, exosomal miR-146a secreted by oxLDL-treated macrophages promoted ROS and NETs release via targeting SOD2.	Reactive Oxygen Species	78-81	superoxide dismutase 2	Homo sapiens	113-117
31476900-7	2019	Disruptions of the SOD2 gene reproduced PPHN phenotypes, manifested by elevated right ventricular systolic pressure, PA-endothelial cells apoptosis, and PA-smooth muscle cells proliferation.	Protactinium	117-119	superoxide dismutase 2	Homo sapiens	19-23
31273612-0	2019	Expression and molecular characterization of stress-responsive genes (hsp70 and Mn-sod) and evaluation of antioxidant enzymes (CAT and GPx) in heavy metal exposed freshwater ciliate, Tetmemena sp.	Metals	149-154	superoxide dismutase 2	Homo sapiens	80-86
31273612-4	2019	Quantitative real time PCR (qRT-PCR) was employed to evaluate the effects of Cd and Cu on the expression of cytosolic hsp70 and Mn-sod genes.	Cadmium	77-79	superoxide dismutase 2	Homo sapiens	128-134
31273612-4	2019	Quantitative real time PCR (qRT-PCR) was employed to evaluate the effects of Cd and Cu on the expression of cytosolic hsp70 and Mn-sod genes.	Copper	84-86	superoxide dismutase 2	Homo sapiens	128-134
31175926-0	2019	The Val16Ala-SOD2 polymorphism affects cyto-genotoxicity of pyridostigmine bromide on human peripheral blood mononuclear cells.	Pyridostigmine Bromide	60-82	superoxide dismutase 2	Homo sapiens	13-17
31601079-7	2019	Further, TC or CC genotype carriers in SOD2 had a much higher risk of Parkinson"s disease compared with corresponding TT genotypes, and the C carriers had an increased risk over allele T carriers in the single nucleotide polymorphism (rs4880 T/C) in SOD2.	Technetium	9-11	superoxide dismutase 2	Homo sapiens	39-43
31601079-7	2019	Further, TC or CC genotype carriers in SOD2 had a much higher risk of Parkinson"s disease compared with corresponding TT genotypes, and the C carriers had an increased risk over allele T carriers in the single nucleotide polymorphism (rs4880 T/C) in SOD2.	Technetium	9-11	superoxide dismutase 2	Homo sapiens	250-254
31026089-3	2019	In addition, the effect of L and OXL for the activation of AMPK that triggers the downstream regulator peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha), TFAM expression, mitochondrial DNA (mtDNA), mitochondrial biogenesis and superoxide dismutase 2 (SOD2) in high glucose treated HepG2 cells were investigated by quantitative polymerase chain reaction and Western blot analysis.	Lutein	27-28	superoxide dismutase 2	Homo sapiens	282-286
31026089-3	2019	In addition, the effect of L and OXL for the activation of AMPK that triggers the downstream regulator peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha), TFAM expression, mitochondrial DNA (mtDNA), mitochondrial biogenesis and superoxide dismutase 2 (SOD2) in high glucose treated HepG2 cells were investigated by quantitative polymerase chain reaction and Western blot analysis.	oxl	33-36	superoxide dismutase 2	Homo sapiens	258-280
31026089-3	2019	In addition, the effect of L and OXL for the activation of AMPK that triggers the downstream regulator peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha), TFAM expression, mitochondrial DNA (mtDNA), mitochondrial biogenesis and superoxide dismutase 2 (SOD2) in high glucose treated HepG2 cells were investigated by quantitative polymerase chain reaction and Western blot analysis.	oxl	33-36	superoxide dismutase 2	Homo sapiens	282-286
31464618-13	2019	CONCLUSIONS: Resveratrol can activate p38 MAPK and repress FOXO3a, thereby causing repression of SOD2, catalase, and increase of ROS accumulation, leading to apoptosis in BPH-1 cells.	Resveratrol	13-24	superoxide dismutase 2	Homo sapiens	97-101
31177508-4	2019	Further, GSK650394, a specific inhibitor of SGK1 reduces monensin-induced increase of mitochondrial protein abundance of Tom20 and MnSOD.	2-cyclopentyl-4-(5-phenyl-1H-pyrrolo(2,3-b)pyridin-3-yl)-benzoic acid	9-18	superoxide dismutase 2	Homo sapiens	131-136
31177508-7	2019	In conclusion, in HEK293 cells, mitochondrial reactive oxygen species increase protein abundance of mitochondrial SGK1, which leads to a rise of mitochondrial Tom20, resulting in importing MnSOD protein into the mitochondria.	Reactive Oxygen Species	46-69	superoxide dismutase 2	Homo sapiens	189-194
31470840-8	2019	The MnSOD genotype had a significant effect on the percentage of PDs of 4~9 mm (p = 0.02), and salivary DeltaMnSOD had a significant effect on the PlI (p = 0.03).	Palladium	65-68	superoxide dismutase 2	Homo sapiens	4-9
31470840-10	2019	There was a significant interaction between the MnSOD genotype and salivary DeltaMnSOD on PDs of 4~9 mm.	Palladium	90-93	superoxide dismutase 2	Homo sapiens	48-53
30957724-13	2019	Stronger staining for MnSOD in MDAH-2774 vs. SK-OV-3 cells after co-treatment with cisplatin and valspodar may determine the resistance of MDAH-2774 cell line to cisplatin.	Cisplatin	83-92	superoxide dismutase 2	Homo sapiens	22-27
30957724-13	2019	Stronger staining for MnSOD in MDAH-2774 vs. SK-OV-3 cells after co-treatment with cisplatin and valspodar may determine the resistance of MDAH-2774 cell line to cisplatin.	Cisplatin	162-171	superoxide dismutase 2	Homo sapiens	22-27
31405216-8	2019	Pre-incubation with BAY-11-7082 counteracted visfatin-induced expression of miRNA, BCL2, SOD-2, CAT and NRF2.	3-(4-methylphenylsulfonyl)-2-propenenitrile	20-31	superoxide dismutase 2	Homo sapiens	89-94
31194992-14	2019	Furthermore, ASP treatment inhibited H2O2-induced ROS generation and apoptosis via the activated ERK1/2-SOD2 pathway.	Hydrogen Peroxide	37-41	superoxide dismutase 2	Homo sapiens	104-108
31382611-1	2019	Background: Experimental data show that superoxide dismutase 2 (SOD2) is involved in ochratoxin (OTA)-induced nephrotoxicity, whereas clinical data indicate the role of SOD2 rs4880 or glutathione peroxidase 1 (GPX1) rs1050450 polymorphisms in end-stage renal disease and urothelial carcinoma risk, known to be the major complications of Balkan endemic nephropathy (BEN).	Ochratoxins	85-95	superoxide dismutase 2	Homo sapiens	40-62
31382611-1	2019	Background: Experimental data show that superoxide dismutase 2 (SOD2) is involved in ochratoxin (OTA)-induced nephrotoxicity, whereas clinical data indicate the role of SOD2 rs4880 or glutathione peroxidase 1 (GPX1) rs1050450 polymorphisms in end-stage renal disease and urothelial carcinoma risk, known to be the major complications of Balkan endemic nephropathy (BEN).	Ochratoxins	85-95	superoxide dismutase 2	Homo sapiens	64-68
31343981-7	2019	Treatment of cells with EAE or EA showed upregulation of mRNA expression of the antioxidative gene superoxide dismutase (SOD)-2 and downregulated the expression of inducible nitric oxide synthase (iNOS), soluble cell adhesion molecule (sICAM), and cyclooxygenase (COX)-2.	EAE	24-27	superoxide dismutase 2	Homo sapiens	99-127
31189433-9	2019	SIRT3 physically interacted with SOD2 and eliminated excess mitochondrial reactive oxygen species, restored mitochondrial function through enhancing SOD2 activity by deacetylation of K68.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	183-186	superoxide dismutase 2	Homo sapiens	33-37
31189433-9	2019	SIRT3 physically interacted with SOD2 and eliminated excess mitochondrial reactive oxygen species, restored mitochondrial function through enhancing SOD2 activity by deacetylation of K68.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	183-186	superoxide dismutase 2	Homo sapiens	149-153
31695757-11	2019	Metabolomic analysis demonstrated lower ROS-RCS levels in ALDH1A1-addicted, erlotinib-resistant cells; in line with this, key enzymes for metabolizing ROS and RCS, SOD2 and GPX4, respectively, were upregulated in these cells.	erlotinib	76-85	superoxide dismutase 2	Homo sapiens	164-168
31695757-12	2019	Knockdown of SOD2 or GPX4 re-sensitized the resistant cells to erlotinib and the effect was abrogated by ROS-RCS scavenging and mimicked by ROS-RCS induction.	erlotinib	63-72	superoxide dismutase 2	Homo sapiens	13-17
30811038-12	2019	AURKA interference can reverse the reactive oxygen species elevation caused by SOD2 overexpression or lysine-48 (K48) mutation, respectively, leading to mitochondrial dysfunction.	Reactive Oxygen Species	35-58	superoxide dismutase 2	Homo sapiens	79-83
31343981-7	2019	Treatment of cells with EAE or EA showed upregulation of mRNA expression of the antioxidative gene superoxide dismutase (SOD)-2 and downregulated the expression of inducible nitric oxide synthase (iNOS), soluble cell adhesion molecule (sICAM), and cyclooxygenase (COX)-2.	Ellagic Acid	24-26	superoxide dismutase 2	Homo sapiens	99-127
30906548-0	2019	Role of SOD2 Ala16Val polymorphism in primary brain tumors.	ala16val	13-21	superoxide dismutase 2	Homo sapiens	8-12
31098737-6	2019	Consequently, SOD2 expression emerges as a potential biomarker of PH in SCD being a link among hemolysis, inflammation, iron overload, oxidative stress, and SCD cardiopathy.	Iron	120-124	superoxide dismutase 2	Homo sapiens	14-18
30411306-2	2019	Sirtuin3 (Sirt3) plays an important role in maintaining appropriate ROS levels by regulating manganese superoxide dismutase (MnSOD), which scavenges ROS in mitochondria.	Reactive Oxygen Species	68-71	superoxide dismutase 2	Homo sapiens	93-123
30411306-2	2019	Sirtuin3 (Sirt3) plays an important role in maintaining appropriate ROS levels by regulating manganese superoxide dismutase (MnSOD), which scavenges ROS in mitochondria.	Reactive Oxygen Species	68-71	superoxide dismutase 2	Homo sapiens	125-130
30411306-2	2019	Sirtuin3 (Sirt3) plays an important role in maintaining appropriate ROS levels by regulating manganese superoxide dismutase (MnSOD), which scavenges ROS in mitochondria.	Reactive Oxygen Species	149-152	superoxide dismutase 2	Homo sapiens	93-123
30411306-2	2019	Sirtuin3 (Sirt3) plays an important role in maintaining appropriate ROS levels by regulating manganese superoxide dismutase (MnSOD), which scavenges ROS in mitochondria.	Reactive Oxygen Species	149-152	superoxide dismutase 2	Homo sapiens	125-130
30411306-3	2019	Using a SE model, we demonstrated that Sirt3 directly regulated MnSOD activity by deacetylation, which protects hippocampal cells against damage from ROS.	Reactive Oxygen Species	150-153	superoxide dismutase 2	Homo sapiens	64-69
30411306-6	2019	Our data indicate that Sirt3 has an important function in regulating MnSOD, which results in decreased ROS in hippocampal cells.	Reactive Oxygen Species	103-106	superoxide dismutase 2	Homo sapiens	69-74
31195721-0	2019	Cannabidiol Overcomes Oxaliplatin Resistance by Enhancing NOS3- and SOD2-Induced Autophagy in Human Colorectal Cancer Cells.	Cannabidiol	0-11	superoxide dismutase 2	Homo sapiens	68-72
31018749-4	2019	Methods and Results Cord-blood-derived CD 34+ stem cells exposed to high glucose displayed increased reactive oxygen species production, overexpression of p66shc gene, and downregulation of antioxidant genes catalase and manganese superoxide dismutase when compared with normoglycemic cells.	Glucose	73-80	superoxide dismutase 2	Homo sapiens	221-251
30896828-7	2019	The knockdown of MnSOD increased H2O2 levels, enzyme activity, the mRNA levels of matrix metalloproteinase-1, -2 and -9, and the migratory and invasive abilities of the cells.	Hydrogen Peroxide	33-37	superoxide dismutase 2	Homo sapiens	17-22
30896828-8	2019	Inducing a reduction in H2O2 using diphenyleneiodonium (DPI) and N-acetyl-l-cysteine decreased the migratory abilities of the cell lines, and DPI attenuated the migratory ability that had been increased by MnSOD small interfering RNA knockdown.	Hydrogen Peroxide	24-28	superoxide dismutase 2	Homo sapiens	206-211
30896828-8	2019	Inducing a reduction in H2O2 using diphenyleneiodonium (DPI) and N-acetyl-l-cysteine decreased the migratory abilities of the cell lines, and DPI attenuated the migratory ability that had been increased by MnSOD small interfering RNA knockdown.	diphenyleneiodonium	35-54	superoxide dismutase 2	Homo sapiens	206-211
30896828-8	2019	Inducing a reduction in H2O2 using diphenyleneiodonium (DPI) and N-acetyl-l-cysteine decreased the migratory abilities of the cell lines, and DPI attenuated the migratory ability that had been increased by MnSOD small interfering RNA knockdown.	diphenyleneiodonium	56-59	superoxide dismutase 2	Homo sapiens	206-211
30896828-8	2019	Inducing a reduction in H2O2 using diphenyleneiodonium (DPI) and N-acetyl-l-cysteine decreased the migratory abilities of the cell lines, and DPI attenuated the migratory ability that had been increased by MnSOD small interfering RNA knockdown.	diphenyleneiodonium	142-145	superoxide dismutase 2	Homo sapiens	206-211
30896828-10	2019	Taken together, these data suggest that reduced MnSOD may induce ROS imbalance in cells and promote the metastatic ability of cancer cells.	Reactive Oxygen Species	65-68	superoxide dismutase 2	Homo sapiens	48-53
30858178-0	2019	UVB-induced inactivation of manganese-containing superoxide dismutase promotes mitophagy via ROS-mediated mTORC2 pathway activation.	Reactive Oxygen Species	93-96	superoxide dismutase 2	Homo sapiens	28-69
30829051-9	2019	Moreover, PGC-1alpha increased superoxide dismutase 1 (SOD1) and SOD2 contents in vivo and in vitro, whereas SOD2 deletion eliminated PGC-1alpha-mediated mtROS change and promoted calcium deposition.	Calcium	180-187	superoxide dismutase 2	Homo sapiens	109-113
30932749-11	2019	Concomitantly, it enhances the scavenger of reactive oxygen species (SOD-2) to maintain moderate levels of oxidative stress.	Oxygen	53-59	superoxide dismutase 2	Homo sapiens	69-74
31537245-12	2019	Results Palmitate increased the triglycerides level, induced the oxidative stress in both the cells and the mitochondria, decreased the gene expression and protein levels of SIRT1, PGC1alpha, SOD2 and CAT, increased the levels of TNF-alpha and IL-6, decreased the mitochondrial membrane potential, and impaired the mitochondrial function.	Palmitates	8-17	superoxide dismutase 2	Homo sapiens	192-196
31086870-0	2019	Manganese influx and expression of ZIP8 is essential in primary myoblasts and contributes to activation of SOD2.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	107-111
30536754-5	2019	Moreover, the redox gene encoding the manganese-dependent mitochondrial enzyme, superoxide dismutase (SOD)2, was strongly induced at the mRNA and protein levels by multiple signaling pathways downstream of TLR2, namely JAK-STAT3, JNK MAPK and NF-kappaB.	Manganese	38-47	superoxide dismutase 2	Homo sapiens	80-107
31002860-6	2019	Overexpression of antioxidants (SOD1/SOD2) mitigates Cd-induced ROS that results in inhibition of ER stress and autophagy in prostate epithelial cells.	Cadmium	53-55	superoxide dismutase 2	Homo sapiens	37-41
31002860-6	2019	Overexpression of antioxidants (SOD1/SOD2) mitigates Cd-induced ROS that results in inhibition of ER stress and autophagy in prostate epithelial cells.	Reactive Oxygen Species	64-67	superoxide dismutase 2	Homo sapiens	37-41
31160585-0	2019	Lysine 68 acetylation directs MnSOD as a tetrameric detoxification complex versus a monomeric tumor promoter.	Lysine	0-6	superoxide dismutase 2	Homo sapiens	30-35
31160585-5	2019	MnSODK68Q expressing cells exhibit resistance to tamoxifen (Tam) and cells selected for Tam resistance exhibited increased K68-Ac and monomeric MnSOD.	Tamoxifen	49-58	superoxide dismutase 2	Homo sapiens	0-5
31160585-5	2019	MnSODK68Q expressing cells exhibit resistance to tamoxifen (Tam) and cells selected for Tam resistance exhibited increased K68-Ac and monomeric MnSOD.	Tamoxifen	60-63	superoxide dismutase 2	Homo sapiens	0-5
31160585-6	2019	These results suggest a MnSOD-K68-Ac metabolic pathway for Tam resistance, carcinogenesis and tumor progression.	Tamoxifen	59-62	superoxide dismutase 2	Homo sapiens	24-29
31106605-7	2019	CA alleviated ROS production and prevented the reduction of antioxidant capacity in cells exposed to PQ by increasing NF-E2-related factor 2 (Nrf2), superoxide dismutase 2 (SOD2) and glutathione levels.	Paraquat	101-103	superoxide dismutase 2	Homo sapiens	149-171
31106605-7	2019	CA alleviated ROS production and prevented the reduction of antioxidant capacity in cells exposed to PQ by increasing NF-E2-related factor 2 (Nrf2), superoxide dismutase 2 (SOD2) and glutathione levels.	Paraquat	101-103	superoxide dismutase 2	Homo sapiens	173-177
31205586-7	2019	The increase of oxidative stress in lung cancer cells treated with BA6 was accompanied by a decrease in the expression of antioxidant enzymes Cu/Zn SOD, MnSOD, and catalase.	(2S)-heptane-1,2,7-triol	67-70	superoxide dismutase 2	Homo sapiens	153-158
30807827-10	2019	iHAEs showed relatively high resistance to ROS stimulation, which can be attributed to the high SOD2 expression and up-regulation of Nrf2, HO-1 after x-rays exposure.	Reactive Oxygen Species	43-46	superoxide dismutase 2	Homo sapiens	96-100
30284207-0	2019	A Study of the Activity of Recombinant Mn-Superoxide Dismutase in the Presence of Gold and Silver Nanoparticles.	Silver	91-97	superoxide dismutase 2	Homo sapiens	39-62
30684560-9	2019	The mtsERbeta afforded a resistance to oxidative insult-induced apoptosis through the induction of the ROS scavenger enzyme Mn-superoxide dismutase and anti-apoptotic protein Bcl-2.	mtserbeta	4-13	superoxide dismutase 2	Homo sapiens	124-147
30684560-9	2019	The mtsERbeta afforded a resistance to oxidative insult-induced apoptosis through the induction of the ROS scavenger enzyme Mn-superoxide dismutase and anti-apoptotic protein Bcl-2.	Reactive Oxygen Species	103-106	superoxide dismutase 2	Homo sapiens	124-147
30906548-1	2019	The present study aimed to investigate the possible association between the genetic polymorphism of the enzyme superoxide dismutase 2 (SOD2, also known as manganese-dependent SOD), Ala16Val (rs4880), and primary brain tumor risk in the Turkish population.	ala16val	181-189	superoxide dismutase 2	Homo sapiens	111-133
30906548-1	2019	The present study aimed to investigate the possible association between the genetic polymorphism of the enzyme superoxide dismutase 2 (SOD2, also known as manganese-dependent SOD), Ala16Val (rs4880), and primary brain tumor risk in the Turkish population.	ala16val	181-189	superoxide dismutase 2	Homo sapiens	135-139
30906548-1	2019	The present study aimed to investigate the possible association between the genetic polymorphism of the enzyme superoxide dismutase 2 (SOD2, also known as manganese-dependent SOD), Ala16Val (rs4880), and primary brain tumor risk in the Turkish population.	ala16val	181-189	superoxide dismutase 2	Homo sapiens	135-138
30906548-8	2019	In summary, the results of the present study indicated that the Ala16Val polymorphism of the SOD2 gene was not associated with primary brain tumor risk in the Turkish population studied.	ala16val	64-72	superoxide dismutase 2	Homo sapiens	93-97
30813936-12	2019	CONCLUSIONS: The delay in DSB repair and lower sensitivity to daunorubicin seen in the B lymphocyte derived SUP-B15 cells could be due to loss of function of p53 that may be correlated to increased expression of SOD2 and lower ROS production.	Daunorubicin	62-74	superoxide dismutase 2	Homo sapiens	212-216
30137220-2	2019	In this study, we first examined whether rosiglitazone, an agonist of the peroxisome proliferator-activated receptor-gamma (PPARgamma), protects the human trophoblast from oxidative injury by regulating key antioxidant proteins, catalase (CAT) and the superoxide dismutases (SOD1 and SOD2).	Rosiglitazone	41-54	superoxide dismutase 2	Homo sapiens	284-288
30685970-8	2019	The results showed that Arg promoted the protein expression of Nrf2, up-regulated expression of the phase II metabolizing enzymes (NQO1 and HO-1), as well as antioxidative enzymes (GPx1, CAT, and SOD2) for alleviating oxidative injury and protected IOECs from LPS-induced apoptosis.	Arginine	24-27	superoxide dismutase 2	Homo sapiens	196-200
30736780-5	2019	The protein expression of SOD2 and lipid peroxidation (thiobarbituric acid reactive substances) was measured by the TBARS Assay kit and enzyme-linked immunosorbent assay (ELISA) respectively.	Thiobarbituric Acid Reactive Substances	116-121	superoxide dismutase 2	Homo sapiens	26-30
30137220-5	2019	Treatment with rosiglitazone dose-dependently upregulated anti-oxidative CAT and SOD2, and rescued hypoxic injury in first trimester villous explants and JEG-3 cells, strongly suggesting the involvement of the PPARgamma in regulating their expressions.	Rosiglitazone	15-28	superoxide dismutase 2	Homo sapiens	81-85
30698880-6	2019	Interestingly, the amount of manganese-dependent superoxide dismutase (MnSOD), a mitochondrial-resident antioxidant enzyme, was increased when melanin synthesis was decreased by the whole placental extract.	Melanins	143-150	superoxide dismutase 2	Homo sapiens	29-69
30226809-7	2019	Knockdown of MnSOD in huc-MSCs decreased the level of MnSOD in huc-MSC-EVs and attenuated the antiapoptotic and antioxidant capacities of huc-MSC-EVs, which could be partially rescued by MnSOD mimetic manganese (III) 5,10,15,20-tetrakis (4-benzoic acid) porphyrin (MnTBAP).	manganese (iii) 5,10,15,20-tetrakis (4-benzoic acid) porphyrin	201-263	superoxide dismutase 2	Homo sapiens	13-18
30529301-9	2019	Deficiency of LSD1 activity and maintenance of PARP1 at the SOD2 promoter substantially upregulated SOD2 level, thereby further increasing resistance of M1 macrophages to hydrogen peroxide.	Hydrogen Peroxide	171-188	superoxide dismutase 2	Homo sapiens	60-64
30698880-6	2019	Interestingly, the amount of manganese-dependent superoxide dismutase (MnSOD), a mitochondrial-resident antioxidant enzyme, was increased when melanin synthesis was decreased by the whole placental extract.	Melanins	143-150	superoxide dismutase 2	Homo sapiens	71-76
30628023-10	2019	High-glucose treatment for 24 h down-regulated the protein expression of redox-specific transcription factors Nrf-2, XBP-1 and NF-kappaB, and subsequently decreased the expression of HO-1, catalase, and SOD-2.	Glucose	5-12	superoxide dismutase 2	Homo sapiens	203-208
30477822-10	2019	The positive association between PM2.5 in and homocysteine was (borderline) statistically significantly modified by genetic variants in MnSOD (p interaction = 0.02), GSTP1 (p interaction = 0.07) and the sum score of the 3 studied SNPs in the CAT gene (p interaction=0.09), suggesting oxidative stress as an underlying mechanism of action.	Homocysteine	46-58	superoxide dismutase 2	Homo sapiens	136-141
30471001-0	2019	Differentiation-Dependent Effects of a New Recombinant Manganese Superoxide Dismutase on Human SK-N-BE Neuron-Like Cells.	sk-n	95-99	superoxide dismutase 2	Homo sapiens	55-85
30471001-3	2019	Among endogenous antioxidants, SOD constitutes the first line of natural defence against pathological effects induced by an excess of free radicals.	Free Radicals	134-147	superoxide dismutase 2	Homo sapiens	31-34
30719005-6	2018	The supplementation of saturated palmitic acid with the monounsaturated oleic acid reversed the negative effects of palmitic acid alone regulating insulin secretion from pancreatic beta cells through ROS, MMP-2, ATF6, XBP1u, IL8 reduction and SOD2, PTP-1B activation.	saturated palmitic acid	23-46	superoxide dismutase 2	Homo sapiens	243-247
30719005-6	2018	The supplementation of saturated palmitic acid with the monounsaturated oleic acid reversed the negative effects of palmitic acid alone regulating insulin secretion from pancreatic beta cells through ROS, MMP-2, ATF6, XBP1u, IL8 reduction and SOD2, PTP-1B activation.	monounsaturated oleic acid	56-82	superoxide dismutase 2	Homo sapiens	243-247
30719005-6	2018	The supplementation of saturated palmitic acid with the monounsaturated oleic acid reversed the negative effects of palmitic acid alone regulating insulin secretion from pancreatic beta cells through ROS, MMP-2, ATF6, XBP1u, IL8 reduction and SOD2, PTP-1B activation.	Palmitic Acid	33-46	superoxide dismutase 2	Homo sapiens	243-247
30422963-1	2019	BACKGROUND: Individual susceptibility to valproic acid (VPA)-caused hepatotoxicity might result from genetic deficiencies in the detoxification and antioxidant enzymes including glutathione S-transferases (GSTs), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx).	Valproic Acid	41-54	superoxide dismutase 2	Homo sapiens	251-254
30422963-1	2019	BACKGROUND: Individual susceptibility to valproic acid (VPA)-caused hepatotoxicity might result from genetic deficiencies in the detoxification and antioxidant enzymes including glutathione S-transferases (GSTs), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx).	Valproic Acid	56-59	superoxide dismutase 2	Homo sapiens	251-254
30719005-5	2018	Oleic acid alone had opposite effects due to its different capacity of controlling these metabolic pathways, in particular by reduction of the ROS levels and MMP-2 activity, down-regulation of BiP, eIF2alpha, ATF6, XBP1u, CHOP, IL6, IL8 and by SOD2 and PTP-1B overexpression.	Oleic Acid	0-10	superoxide dismutase 2	Homo sapiens	244-248
29766814-1	2019	OBJECTIVE: This research aimed to study the anti-aging and anti-inflammatory effects of low and high doses of the beta-D-mannuronic (M2000) on gene expression of enzymes involved in oxidative stress (including SOD2, GST, GPX1, CAT, iNOS, and MPO) in peripheral blood mononuclear cells (PBMCs) of healthy donors under in vitro conditions.	beta-d-mannuronic	114-131	superoxide dismutase 2	Homo sapiens	210-214
30486606-4	2018	Low antioxidant MnSOD level in breast cancer cell line MCF-7 leads to low concentration of hydrogenperoxide, because antioxidant MnSOD will convert radical superoxide to hydrogen peroxide.	Hydrogen Peroxide	91-107	superoxide dismutase 2	Homo sapiens	16-21
30414534-7	2019	First, we prevented the exercise-induced increase in diaphragmatic SOD2 via delivery of an antisense oligonucleotide targeted against SOD2 post-exercise.	Oligonucleotides	101-116	superoxide dismutase 2	Homo sapiens	67-71
30414534-7	2019	First, we prevented the exercise-induced increase in diaphragmatic SOD2 via delivery of an antisense oligonucleotide targeted against SOD2 post-exercise.	Oligonucleotides	101-116	superoxide dismutase 2	Homo sapiens	134-138
30193891-7	2018	MnSOD then converts superoxide into hydrogen peroxide, which activates ERK1/2 to promote tumor cell migration and activates FAK to promote tumor cell adhesion.	Superoxides	20-30	superoxide dismutase 2	Homo sapiens	0-5
30193891-7	2018	MnSOD then converts superoxide into hydrogen peroxide, which activates ERK1/2 to promote tumor cell migration and activates FAK to promote tumor cell adhesion.	Hydrogen Peroxide	36-53	superoxide dismutase 2	Homo sapiens	0-5
30259659-6	2018	Subsequently, we confirmed miR-382-5p/SOD2 interaction by luciferase assay and we showed that miR-382-5p overexpression in CD34+ cells causes the decrease in SOD2 activity leading to reactive oxygen species (ROS) accumulation and oxidative DNA damage.	Reactive Oxygen Species	183-206	superoxide dismutase 2	Homo sapiens	38-42
30259659-6	2018	Subsequently, we confirmed miR-382-5p/SOD2 interaction by luciferase assay and we showed that miR-382-5p overexpression in CD34+ cells causes the decrease in SOD2 activity leading to reactive oxygen species (ROS) accumulation and oxidative DNA damage.	Reactive Oxygen Species	183-206	superoxide dismutase 2	Homo sapiens	158-162
30259659-6	2018	Subsequently, we confirmed miR-382-5p/SOD2 interaction by luciferase assay and we showed that miR-382-5p overexpression in CD34+ cells causes the decrease in SOD2 activity leading to reactive oxygen species (ROS) accumulation and oxidative DNA damage.	Reactive Oxygen Species	208-211	superoxide dismutase 2	Homo sapiens	38-42
30368039-0	2019	Efficacy of 5-aminolevulinic acid-based photodynamic therapy against keloid compromised by downregulation of SIRT1-SIRT3-SOD2-mROS dependent autophagy pathway.	5-amino levulinic acid	12-33	superoxide dismutase 2	Homo sapiens	121-125
30368039-6	2019	Interestingly, 5-ALA-PDT promoted the SIRT3 protein expression and the activity of mitochondrial superoxide dismutase 2 (SOD2), but SIRT1 protein expression level was decreased.	5-amino levulinic acid	15-20	superoxide dismutase 2	Homo sapiens	121-125
30368039-7	2019	SOD2 as a key enzyme can decrease mitochondrial ROS (mROS) level, Deacetylation of SOD2 by SIRT3 regulates SOD2 enzymatic activity has been identified.	ros	48-51	superoxide dismutase 2	Homo sapiens	0-4
30368039-7	2019	SOD2 as a key enzyme can decrease mitochondrial ROS (mROS) level, Deacetylation of SOD2 by SIRT3 regulates SOD2 enzymatic activity has been identified.	ros	48-51	superoxide dismutase 2	Homo sapiens	83-87
30368039-7	2019	SOD2 as a key enzyme can decrease mitochondrial ROS (mROS) level, Deacetylation of SOD2 by SIRT3 regulates SOD2 enzymatic activity has been identified.	ros	48-51	superoxide dismutase 2	Homo sapiens	83-87
30368039-8	2019	Then we explored SOD2 acetylation level with immunoprecipitation, found that 5-ALA-PDT significantly increased the acetylation levels of SOD2.	5-amino levulinic acid	77-82	superoxide dismutase 2	Homo sapiens	17-21
30368039-8	2019	Then we explored SOD2 acetylation level with immunoprecipitation, found that 5-ALA-PDT significantly increased the acetylation levels of SOD2.	5-amino levulinic acid	77-82	superoxide dismutase 2	Homo sapiens	137-141
30368039-10	2019	Found that inhibition of SIRT3 by 3-TYP significantly increased the level of SOD2 acetylation level compared with control group or 5-ALA-PDT group.	5-amino levulinic acid	131-136	superoxide dismutase 2	Homo sapiens	77-81
30368039-13	2019	These results may demonstrate that 5-ALA-PDT induced SIRT1 protein level decreased, which promoted the effect of SIRT3 increased activity of SOD2 that can reduce mROS level, and then compromised 5-ALA-PDT induced autophagic cell death.	5-amino levulinic acid	35-40	superoxide dismutase 2	Homo sapiens	141-145
30368039-13	2019	These results may demonstrate that 5-ALA-PDT induced SIRT1 protein level decreased, which promoted the effect of SIRT3 increased activity of SOD2 that can reduce mROS level, and then compromised 5-ALA-PDT induced autophagic cell death.	5-amino levulinic acid	195-200	superoxide dismutase 2	Homo sapiens	141-145
30259659-6	2018	Subsequently, we confirmed miR-382-5p/SOD2 interaction by luciferase assay and we showed that miR-382-5p overexpression in CD34+ cells causes the decrease in SOD2 activity leading to reactive oxygen species (ROS) accumulation and oxidative DNA damage.	Reactive Oxygen Species	208-211	superoxide dismutase 2	Homo sapiens	158-162
30259659-9	2018	Our data showed that TGF-beta1 treatment enhances miR-382-5p expression and reduces SOD2 activity leading to ROS accumulation.	Reactive Oxygen Species	109-112	superoxide dismutase 2	Homo sapiens	84-88
30259659-10	2018	Finally, inhibition of TGF-beta1 signaling in PMF CD34+ cells by galunisertib significantly reduced miR-382-5p expression and ROS accumulation and restored SOD2 activity.	LY-2157299	65-77	superoxide dismutase 2	Homo sapiens	156-160
30259659-11	2018	As a whole, this study reports that TGF-beta1/miR-382-5p/SOD2 axis deregulation in PMF cells is linked to ROS overproduction that may contribute to enhanced oxidative stress and inflammation.	Reactive Oxygen Species	106-109	superoxide dismutase 2	Homo sapiens	57-61
30301388-12	2018	The increase in ROS was associated with a 54% decrease in MnSOD and 47% increase in NOX2 protein compared to the other groups.	Reactive Oxygen Species	16-19	superoxide dismutase 2	Homo sapiens	58-63
30486606-4	2018	Low antioxidant MnSOD level in breast cancer cell line MCF-7 leads to low concentration of hydrogenperoxide, because antioxidant MnSOD will convert radical superoxide to hydrogen peroxide.	Hydrogen Peroxide	91-107	superoxide dismutase 2	Homo sapiens	129-134
30486606-4	2018	Low antioxidant MnSOD level in breast cancer cell line MCF-7 leads to low concentration of hydrogenperoxide, because antioxidant MnSOD will convert radical superoxide to hydrogen peroxide.	Superoxides	156-166	superoxide dismutase 2	Homo sapiens	16-21
30486606-4	2018	Low antioxidant MnSOD level in breast cancer cell line MCF-7 leads to low concentration of hydrogenperoxide, because antioxidant MnSOD will convert radical superoxide to hydrogen peroxide.	Superoxides	156-166	superoxide dismutase 2	Homo sapiens	129-134
30486606-4	2018	Low antioxidant MnSOD level in breast cancer cell line MCF-7 leads to low concentration of hydrogenperoxide, because antioxidant MnSOD will convert radical superoxide to hydrogen peroxide.	Hydrogen Peroxide	170-187	superoxide dismutase 2	Homo sapiens	16-21
30486606-4	2018	Low antioxidant MnSOD level in breast cancer cell line MCF-7 leads to low concentration of hydrogenperoxide, because antioxidant MnSOD will convert radical superoxide to hydrogen peroxide.	Hydrogen Peroxide	170-187	superoxide dismutase 2	Homo sapiens	129-134
30588251-9	2018	Furthermore, we observed that resistant cells had increased levels of the mitochondrial enzymes SOD2 and PRDX1, which function to reduce ROS levels in the mitochondria.	Reactive Oxygen Species	137-140	superoxide dismutase 2	Homo sapiens	96-100
30485823-6	2018	We demonstrate that Akt1 binds to and phosphorylates the C terminus of Hsp70 on Serine631, which inhibits CHIP-mediated SOD2 degradation thereby stabilizing and promoting SOD2 import.	serine631	80-89	superoxide dismutase 2	Homo sapiens	120-124
30485823-6	2018	We demonstrate that Akt1 binds to and phosphorylates the C terminus of Hsp70 on Serine631, which inhibits CHIP-mediated SOD2 degradation thereby stabilizing and promoting SOD2 import.	serine631	80-89	superoxide dismutase 2	Homo sapiens	171-175
30439336-3	2018	(2018) show that in macrophages, mitochondrial-derived vesicles deliver the superoxide dismutase Sod2 to bacteria-containing phagosomes to produce hydrogen peroxide and kill invading bacteria.	Hydrogen Peroxide	147-164	superoxide dismutase 2	Homo sapiens	97-101
30538800-0	2018	SIRT3 a Major Player in Attenuation of Hepatic Ischemia-Reperfusion Injury by Reducing ROS via Its Downstream Mediators: SOD2, CYP-D, and HIF-1alpha.	Reactive Oxygen Species	87-90	superoxide dismutase 2	Homo sapiens	121-125
30538800-3	2018	SIRT3 plays a major role in the mechanism of IRI, and its activation has been shown to attenuate the deleterious effect of ROS during IRI via SOD2-, CYP-D-, and HIF-1alpha-mediated pathways.	Reactive Oxygen Species	123-126	superoxide dismutase 2	Homo sapiens	142-146
30464607-15	2018	Both PRL-3 and RAP1 could regulate the expression of manganese superoxide dismutase 2 (SOD2) and the uncoupling protein 2 (UCP2), which may be related to PRL-3 suppression induced mitochondria superoxide anion.	Superoxides	193-209	superoxide dismutase 2	Homo sapiens	87-91
30190170-11	2018	A hypo-methylation of H3K4 at SOD2 promoter by LSD-1 increased ROS causing diabetic retinopathy.	ros	63-66	superoxide dismutase 2	Homo sapiens	30-34
29972711-4	2018	In this study, we investigated roles of SOD2, the main antioxidant enzyme maintaining reactive oxygen species (ROS) homeostasis, under inflammatory conditions.	Reactive Oxygen Species	86-109	superoxide dismutase 2	Homo sapiens	40-44
29972711-4	2018	In this study, we investigated roles of SOD2, the main antioxidant enzyme maintaining reactive oxygen species (ROS) homeostasis, under inflammatory conditions.	Reactive Oxygen Species	111-114	superoxide dismutase 2	Homo sapiens	40-44
30279321-0	2018	Redox manipulation of the manganese metal in human manganese superoxide dismutase for neutron diffraction.	Manganese	26-35	superoxide dismutase 2	Homo sapiens	51-81
30279365-0	2018	Exogenous C8-Ceramide Induces Apoptosis by Overproduction of ROS and the Switch of Superoxide Dismutases SOD1 to SOD2 in Human Lung Cancer Cells.	2,3-N-octanoylsphingosine	10-21	superoxide dismutase 2	Homo sapiens	113-117
30279365-5	2018	Interestingly, the ratio of superoxide dismutases (SODs) SOD1 and SOD2 seem to be regulated by C8-ceramide treatment.	2,3-N-octanoylsphingosine	95-106	superoxide dismutase 2	Homo sapiens	66-70
30279365-8	2018	These results suggest that C8-ceramide acts as a potent chemotherapeutic agent and may increase the endogenous ROS level by regulating the switch of SOD1 and SOD2, causing the anti-proliferation, and consequently triggering the apoptosis of NSCLC H1299 cells.	2,3-N-octanoylsphingosine	27-38	superoxide dismutase 2	Homo sapiens	158-162
30279365-8	2018	These results suggest that C8-ceramide acts as a potent chemotherapeutic agent and may increase the endogenous ROS level by regulating the switch of SOD1 and SOD2, causing the anti-proliferation, and consequently triggering the apoptosis of NSCLC H1299 cells.	Reactive Oxygen Species	111-114	superoxide dismutase 2	Homo sapiens	158-162
30279321-0	2018	Redox manipulation of the manganese metal in human manganese superoxide dismutase for neutron diffraction.	Metals	36-41	superoxide dismutase 2	Homo sapiens	51-81
30279321-1	2018	Human manganese superoxide dismutase (MnSOD) is one of the most significant enzymes in preventing mitochondrial dysfunction and related diseases by combating reactive oxygen species (ROS) in the mitochondrial matrix.	Reactive Oxygen Species	158-181	superoxide dismutase 2	Homo sapiens	6-36
30279321-1	2018	Human manganese superoxide dismutase (MnSOD) is one of the most significant enzymes in preventing mitochondrial dysfunction and related diseases by combating reactive oxygen species (ROS) in the mitochondrial matrix.	Reactive Oxygen Species	158-181	superoxide dismutase 2	Homo sapiens	38-43
30279321-1	2018	Human manganese superoxide dismutase (MnSOD) is one of the most significant enzymes in preventing mitochondrial dysfunction and related diseases by combating reactive oxygen species (ROS) in the mitochondrial matrix.	Reactive Oxygen Species	183-186	superoxide dismutase 2	Homo sapiens	6-36
30279321-1	2018	Human manganese superoxide dismutase (MnSOD) is one of the most significant enzymes in preventing mitochondrial dysfunction and related diseases by combating reactive oxygen species (ROS) in the mitochondrial matrix.	Reactive Oxygen Species	183-186	superoxide dismutase 2	Homo sapiens	38-43
30279321-2	2018	Mitochondria are the source of up to 90% of cellular ROS generation, and MnSOD performs its necessary bioprotective role by converting superoxide into oxygen and hydrogen peroxide.	Superoxides	135-145	superoxide dismutase 2	Homo sapiens	73-78
30279321-2	2018	Mitochondria are the source of up to 90% of cellular ROS generation, and MnSOD performs its necessary bioprotective role by converting superoxide into oxygen and hydrogen peroxide.	Oxygen	151-157	superoxide dismutase 2	Homo sapiens	73-78
30279321-2	2018	Mitochondria are the source of up to 90% of cellular ROS generation, and MnSOD performs its necessary bioprotective role by converting superoxide into oxygen and hydrogen peroxide.	Hydrogen Peroxide	162-179	superoxide dismutase 2	Homo sapiens	73-78
30217947-9	2018	Mechanism study revealed that HDAC2 bound to the promoter of MnSOD and repressed the expression of MnSOD by regulating the level of acetylated H3K9 and H3K27, which led to the promotion of oxidative stress and contributed to the function of HDAC2 in ECs under high glucose condition.	Glucose	265-272	superoxide dismutase 2	Homo sapiens	61-66
30119201-9	2018	While ROS increased, certain ROS-related proteins (catalase and SOD2) clearly decreased in cells treated with a combination of GEM plus TPL.	triptolide	136-139	superoxide dismutase 2	Homo sapiens	64-68
30402861-10	2018	However, the effects of Hcy on MDA level and expressions of SOD2, eNOS, and ICAM-1 were attenuated by folic acid (Fc) and vitamin B12 (B12) treatment.	Homocysteine	24-27	superoxide dismutase 2	Homo sapiens	60-64
30402861-10	2018	However, the effects of Hcy on MDA level and expressions of SOD2, eNOS, and ICAM-1 were attenuated by folic acid (Fc) and vitamin B12 (B12) treatment.	Folic Acid	102-112	superoxide dismutase 2	Homo sapiens	60-64
30402861-10	2018	However, the effects of Hcy on MDA level and expressions of SOD2, eNOS, and ICAM-1 were attenuated by folic acid (Fc) and vitamin B12 (B12) treatment.	Vitamin B 12	122-133	superoxide dismutase 2	Homo sapiens	60-64
30138712-7	2018	We suggest that SOD2 and catalase could provide specific targets to improve the detoxification of reactive oxygen species that affects muscle proteins in these patients.	Reactive Oxygen Species	98-121	superoxide dismutase 2	Homo sapiens	16-20
30217947-9	2018	Mechanism study revealed that HDAC2 bound to the promoter of MnSOD and repressed the expression of MnSOD by regulating the level of acetylated H3K9 and H3K27, which led to the promotion of oxidative stress and contributed to the function of HDAC2 in ECs under high glucose condition.	Glucose	265-272	superoxide dismutase 2	Homo sapiens	99-104
30217947-10	2018	Altogether, our evidence demonstrated that HDAC2-MnSOD signaling was critical in oxidative stress and proliferation as well as the survival of ECs under high glucose condition.	Glucose	158-165	superoxide dismutase 2	Homo sapiens	49-54
30223548-0	2018	PCB11 Metabolite, 3,3"-Dichlorobiphenyl-4-ol, Exposure Alters the Expression of Genes Governing Fatty Acid Metabolism in the Absence of Functional Sirtuin 3: Examining the Contribution of MnSOD.	Fatty Acids	96-106	superoxide dismutase 2	Homo sapiens	188-193
30223548-5	2018	Only wild-type cells demonstrated an increase in Manganese superoxide dismutase (MnSOD) activity in response to 4OH-PCB11-induced oxidative injury.	4oh-pcb11	112-121	superoxide dismutase 2	Homo sapiens	49-79
30223548-5	2018	Only wild-type cells demonstrated an increase in Manganese superoxide dismutase (MnSOD) activity in response to 4OH-PCB11-induced oxidative injury.	4oh-pcb11	112-121	superoxide dismutase 2	Homo sapiens	81-86
30225256-2	2018	Manganese superoxide dismutase (MnSOD), catalase (CAT), and glutathione peroxidase-1 (GPx1) have evolved to address primary defense against free radical mediated damage in mitochondria.	Free Radicals	140-152	superoxide dismutase 2	Homo sapiens	0-30
30077371-6	2018	Leflunomide decreased hydrogen peroxide (H2O2) levels and increased the mRNA and protein levels of catalase, NQO1, and SOD2 in HPAECs at basal conditions.	Leflunomide	0-11	superoxide dismutase 2	Homo sapiens	119-123
30077371-7	2018	Further, leflunomide-treated cells continued to have decreased H2O2 and increased SOD2 levels upon hyperoxia exposure.	Leflunomide	9-20	superoxide dismutase 2	Homo sapiens	82-86
30077371-10	2018	Collectively, the results support the hypothesis that leflunomide decreases oxidative stress in HPAECs via SOD2-and catalase-dependent, but AhR- and NQO1-independent mechanisms.	Leflunomide	54-65	superoxide dismutase 2	Homo sapiens	107-111
30245752-1	2018	Manganese superoxide dismutase (MnSOD) plays a critical role in the defense against reactive oxygen species.	Reactive Oxygen Species	84-107	superoxide dismutase 2	Homo sapiens	0-30
30245752-1	2018	Manganese superoxide dismutase (MnSOD) plays a critical role in the defense against reactive oxygen species.	Reactive Oxygen Species	84-107	superoxide dismutase 2	Homo sapiens	32-37
29648877-11	2018	In vivo observations revealed that SOD2 immunostaining was increased in ALF patients and mice models, and in vitro experiments demonstrated that LPS/ROS promoted inflammation via inhibiting mitophagy.	Reactive Oxygen Species	149-152	superoxide dismutase 2	Homo sapiens	35-39
29936984-0	2018	Exposure to bile acids alters the intracellular location and function of MnSOD in Barrett"s esophagus.	Bile Acids and Salts	12-22	superoxide dismutase 2	Homo sapiens	73-78
29936984-2	2018	We previously reported that the macromolecular response of BE cells to this stress was largely regulated by the expression of manganese-dependent mitochondrial superoxide dismutase (MnSOD).	Manganese	126-135	superoxide dismutase 2	Homo sapiens	182-187
29936984-7	2018	Expression of MnSOD was significantly increased in the cells exposed to a mixture of bile acids and Tau versus control.	Bile Acids and Salts	85-95	superoxide dismutase 2	Homo sapiens	14-19
29936984-11	2018	Mitochondrial MnSOD contributes to resistance of BAR-T cells to the bile-salt insults.	Bile Acids and Salts	68-77	superoxide dismutase 2	Homo sapiens	14-19
30225256-2	2018	Manganese superoxide dismutase (MnSOD), catalase (CAT), and glutathione peroxidase-1 (GPx1) have evolved to address primary defense against free radical mediated damage in mitochondria.	Free Radicals	140-152	superoxide dismutase 2	Homo sapiens	32-37
30225256-9	2018	Results: The MnSOD Val/Ala+Ala/Ala genotype was significantly associated with an increased risk of CAD compared to the Val/Val genotype (OR = 1.86, 95% CI = 1.15-3.01).	Valine	19-22	superoxide dismutase 2	Homo sapiens	13-18
30225256-9	2018	Results: The MnSOD Val/Ala+Ala/Ala genotype was significantly associated with an increased risk of CAD compared to the Val/Val genotype (OR = 1.86, 95% CI = 1.15-3.01).	Alanine	23-26	superoxide dismutase 2	Homo sapiens	13-18
30225256-9	2018	Results: The MnSOD Val/Ala+Ala/Ala genotype was significantly associated with an increased risk of CAD compared to the Val/Val genotype (OR = 1.86, 95% CI = 1.15-3.01).	Alanine	27-30	superoxide dismutase 2	Homo sapiens	13-18
30225256-9	2018	Results: The MnSOD Val/Ala+Ala/Ala genotype was significantly associated with an increased risk of CAD compared to the Val/Val genotype (OR = 1.86, 95% CI = 1.15-3.01).	Alanine	27-30	superoxide dismutase 2	Homo sapiens	13-18
30225256-9	2018	Results: The MnSOD Val/Ala+Ala/Ala genotype was significantly associated with an increased risk of CAD compared to the Val/Val genotype (OR = 1.86, 95% CI = 1.15-3.01).	Valine	119-122	superoxide dismutase 2	Homo sapiens	13-18
30225256-9	2018	Results: The MnSOD Val/Ala+Ala/Ala genotype was significantly associated with an increased risk of CAD compared to the Val/Val genotype (OR = 1.86, 95% CI = 1.15-3.01).	Valine	119-122	superoxide dismutase 2	Homo sapiens	13-18
30225256-12	2018	Among cigarette smokers, the harmful genetic effect of MnSOD Ala allele on CAD risk was much higher (OR = 2.23, 95% CI = 1.02-4.88).	Alanine	61-64	superoxide dismutase 2	Homo sapiens	55-60
30815314-7	2019	The mRNA and protein expressions of antioxidant enzymes, such as copper-zinc superoxide dismutase and manganese superoxide dismutase increased in cells treated with the 70% alcohol extract.	Alcohols	173-180	superoxide dismutase 2	Homo sapiens	102-132
30103475-0	2018	4-Acetyl-Antroquinonol B Suppresses SOD2-Enhanced Cancer Stem Cell-Like Phenotypes and Chemoresistance of Colorectal Cancer Cells by Inducing hsa-miR-324 re-Expression.	4-acetylantroquinonol B	0-24	superoxide dismutase 2	Homo sapiens	36-40
30103475-5	2018	RESULTS: This converse hsa-miR-324-5p/SOD2 relationship is associated with enhanced oncogenicity, which is effectively inhibited by 4-acetylantroquinonol B (4-AAQB), as evidenced by inhibited cell viability and proliferation, as well as attenuated migration, invasion, and clonogenicity in 4-AAQB-treated DLD1 and HCT116 cells.	4-acetylantroquinonol B	132-155	superoxide dismutase 2	Homo sapiens	38-42
30103475-5	2018	RESULTS: This converse hsa-miR-324-5p/SOD2 relationship is associated with enhanced oncogenicity, which is effectively inhibited by 4-acetylantroquinonol B (4-AAQB), as evidenced by inhibited cell viability and proliferation, as well as attenuated migration, invasion, and clonogenicity in 4-AAQB-treated DLD1 and HCT116 cells.	4-acetylantroquinonol B	157-163	superoxide dismutase 2	Homo sapiens	38-42
30103475-5	2018	RESULTS: This converse hsa-miR-324-5p/SOD2 relationship is associated with enhanced oncogenicity, which is effectively inhibited by 4-acetylantroquinonol B (4-AAQB), as evidenced by inhibited cell viability and proliferation, as well as attenuated migration, invasion, and clonogenicity in 4-AAQB-treated DLD1 and HCT116 cells.	4-acetylantroquinonol B	290-296	superoxide dismutase 2	Homo sapiens	38-42
30103475-7	2018	We also showed that 4-AAQB-induced re-expression of hsa-miR-324-5p, akin to short-interfering RNA, reduced SOD2 expression, correlates with the concurrent down-regulation of SOD2, N-cadherin, vimentin, c-Myc, and BcL-xL2, with concomitant up-regulation of E-cadherin and BAX2 proteins.	4-acetylantroquinonol B	20-26	superoxide dismutase 2	Homo sapiens	107-111
30103475-7	2018	We also showed that 4-AAQB-induced re-expression of hsa-miR-324-5p, akin to short-interfering RNA, reduced SOD2 expression, correlates with the concurrent down-regulation of SOD2, N-cadherin, vimentin, c-Myc, and BcL-xL2, with concomitant up-regulation of E-cadherin and BAX2 proteins.	4-acetylantroquinonol B	20-26	superoxide dismutase 2	Homo sapiens	174-178
30103475-9	2018	Additionally, 4-AAQB synergistically potentiates the FOLFOX (folinate (leucovorin), fluorouracil (5FU), and oxaliplatin) anticancer effect by eliciting the re-expression of SOD2-suppressed hsa-miR-324, and inhibiting SOD2-mediated tumorigenicity.	4-acetylantroquinonol B	14-20	superoxide dismutase 2	Homo sapiens	173-177
29940201-4	2018	EGCG markedly decreased the levels of inflammatory and oxidative stress factors including nuclear factor kappaB (NF-kappaB), tumor necrosis factor-alpha, interleukin-6, reactive oxygen species, malondialdehyde and p53 protein, and markedly increased superoxide dismutases (SOD), glutathione peroxidase and SOD2 protein.	epigallocatechin gallate	0-4	superoxide dismutase 2	Homo sapiens	273-276
30103475-9	2018	Additionally, 4-AAQB synergistically potentiates the FOLFOX (folinate (leucovorin), fluorouracil (5FU), and oxaliplatin) anticancer effect by eliciting the re-expression of SOD2-suppressed hsa-miR-324, and inhibiting SOD2-mediated tumorigenicity.	4-acetylantroquinonol B	14-20	superoxide dismutase 2	Homo sapiens	217-221
30103475-9	2018	Additionally, 4-AAQB synergistically potentiates the FOLFOX (folinate (leucovorin), fluorouracil (5FU), and oxaliplatin) anticancer effect by eliciting the re-expression of SOD2-suppressed hsa-miR-324, and inhibiting SOD2-mediated tumorigenicity.	Folfox protocol	53-59	superoxide dismutase 2	Homo sapiens	173-177
30103475-9	2018	Additionally, 4-AAQB synergistically potentiates the FOLFOX (folinate (leucovorin), fluorouracil (5FU), and oxaliplatin) anticancer effect by eliciting the re-expression of SOD2-suppressed hsa-miR-324, and inhibiting SOD2-mediated tumorigenicity.	Folfox protocol	53-59	superoxide dismutase 2	Homo sapiens	217-221
29940201-4	2018	EGCG markedly decreased the levels of inflammatory and oxidative stress factors including nuclear factor kappaB (NF-kappaB), tumor necrosis factor-alpha, interleukin-6, reactive oxygen species, malondialdehyde and p53 protein, and markedly increased superoxide dismutases (SOD), glutathione peroxidase and SOD2 protein.	epigallocatechin gallate	0-4	superoxide dismutase 2	Homo sapiens	306-310
29909234-6	2018	Additionally, the Puerarin treatment also significantly enhanced (P &lt; 0.001) the mRNA expressions levels of the anti-oxidant enzymes such as Nrf2, HO-1 and SOD2.	puerarin	18-26	superoxide dismutase 2	Homo sapiens	159-163
29784452-9	2018	RESULTS: CoQ did not affect oxygen consumption but reduced the level of O2- and H2O2 while shifted to a pro-oxidant cell status mainly due to a decrease in catalase activity and SOD2 level.	coenzyme Q10	9-12	superoxide dismutase 2	Homo sapiens	178-182
29745991-0	2018	Association of pre-eclampsia with SOD2 Ala16Val polymorphism among mother-father-infant triads.	ala16val	39-47	superoxide dismutase 2	Homo sapiens	34-38
29745991-6	2018	RESULTS: Dual presence of the SOD2 Ala16Val TT variant among mother-father pairs (n=657) was associated with an increased risk of pre-eclampsia when compared with the absence of the TT variant among the mother-father pairs (7/48 [14.6%] vs 11/339 [3.2%]; adjusted odds ratio 6.80, 95% confidence interval 2.32-19.95; P&lt;0.001).	ala16val	35-43	superoxide dismutase 2	Homo sapiens	30-34
29323702-0	2018	Sirtuin 3 silencing improves oxaliplatin efficacy through acetylation of MnSOD in colon cancer.	Oxaliplatin	29-40	superoxide dismutase 2	Homo sapiens	73-78
30053873-0	2018	HZ08 suppresses RelB-activated MnSOD expression and enhances Radiosensitivity of prostate Cancer cells.	hz08	0-4	superoxide dismutase 2	Homo sapiens	31-36
29953407-9	2018	Also, a positive correlation was observed between the gene expression of Mn-SOD and CAT and body mass index (BMI), fasting blood sugar, insulin resistance, low density lipoprotein-cholesterol (LDL-C) cholesterol, triglycerides (TG) and systolic blood pressure (SBP).	Sugars	129-134	superoxide dismutase 2	Homo sapiens	73-79
29953407-9	2018	Also, a positive correlation was observed between the gene expression of Mn-SOD and CAT and body mass index (BMI), fasting blood sugar, insulin resistance, low density lipoprotein-cholesterol (LDL-C) cholesterol, triglycerides (TG) and systolic blood pressure (SBP).	Cholesterol	180-191	superoxide dismutase 2	Homo sapiens	73-79
29953407-9	2018	Also, a positive correlation was observed between the gene expression of Mn-SOD and CAT and body mass index (BMI), fasting blood sugar, insulin resistance, low density lipoprotein-cholesterol (LDL-C) cholesterol, triglycerides (TG) and systolic blood pressure (SBP).	Triglycerides	213-226	superoxide dismutase 2	Homo sapiens	73-79
29953407-9	2018	Also, a positive correlation was observed between the gene expression of Mn-SOD and CAT and body mass index (BMI), fasting blood sugar, insulin resistance, low density lipoprotein-cholesterol (LDL-C) cholesterol, triglycerides (TG) and systolic blood pressure (SBP).	Triglycerides	228-230	superoxide dismutase 2	Homo sapiens	73-79
30037352-10	2018	We also found that exogenous mimic-microRNA-21 targeted putative microRNA-21 ROS-homeostatic target genes, e.g., KRIT1, NRF2 and SOD2, which were significantly downregulated.	Reactive Oxygen Species	77-80	superoxide dismutase 2	Homo sapiens	129-133
30116486-4	2018	The results revealed that resveratrol-treated THJ-16T rather than THJ-11T cells showed remarkable growth arrest and extensive apoptosis accompanied with the elevated ROS generation and the attenuated superoxide dismutase 2 (SOD2) and catalase (CAT) levels.	Resveratrol	26-37	superoxide dismutase 2	Homo sapiens	200-222
30116486-4	2018	The results revealed that resveratrol-treated THJ-16T rather than THJ-11T cells showed remarkable growth arrest and extensive apoptosis accompanied with the elevated ROS generation and the attenuated superoxide dismutase 2 (SOD2) and catalase (CAT) levels.	Resveratrol	26-37	superoxide dismutase 2	Homo sapiens	224-228
30116486-4	2018	The results revealed that resveratrol-treated THJ-16T rather than THJ-11T cells showed remarkable growth arrest and extensive apoptosis accompanied with the elevated ROS generation and the attenuated superoxide dismutase 2 (SOD2) and catalase (CAT) levels.	thj	46-49	superoxide dismutase 2	Homo sapiens	200-222
30116486-4	2018	The results revealed that resveratrol-treated THJ-16T rather than THJ-11T cells showed remarkable growth arrest and extensive apoptosis accompanied with the elevated ROS generation and the attenuated superoxide dismutase 2 (SOD2) and catalase (CAT) levels.	thj	46-49	superoxide dismutase 2	Homo sapiens	224-228
29620149-5	2018	SQ29548 was utilized as a TXA2R antagonist, and relevant assays were performed to detect the cell viability, cellular reactive oxygen species (ROS) level, cell apoptosis, expression levels of superoxide dismutase-2 (SOD2), catalase and caspases, and activation of mitogen-activated protein kinase (MAPK) pathways.	SQ 29548	0-7	superoxide dismutase 2	Homo sapiens	216-220
29620149-7	2018	In addition, H2O2 raised the level of ROS in cells, inhibited the expression levels of SOD2 and catalase, and potentially enhanced cell apoptosis and the expression of caspases via activating the MAPK pathways.	Hydrogen Peroxide	13-17	superoxide dismutase 2	Homo sapiens	87-91
29620149-8	2018	Pretreatment with SQ29548 not only rescued the viability of SH-SY5Y cells, but also ameliorated the intracellular ROS level and the expression levels of SOD2 and catalase.	SQ 29548	18-25	superoxide dismutase 2	Homo sapiens	153-157
30025556-8	2018	Stratified analyses showed that the protective effects of lutein/zeaxanthin and total carotenoids on skeletal fluorosis were more evident for individuals with the AG+AA genotypes of SOD2 (rs11968525).	Carotenoids	86-97	superoxide dismutase 2	Homo sapiens	182-186
30025556-10	2018	SOD2 (rs11968525) polymorphisms might modify the inverse associations between dietary carotenoids and skeletal fluorosis.	Carotenoids	86-97	superoxide dismutase 2	Homo sapiens	0-4
29164820-3	2018	METHODS &amp; RESULTS: HepG2 cells treated with palmitic acid (PA;0.75 mM) showed decreased expression of various antioxidant biomarkers (SOD1, SOD2, glutathione peroxidase and catalase) and increased expression of inflammatory markers (TNFalpha, IL1beta and IL6).	Palmitic Acid	48-61	superoxide dismutase 2	Homo sapiens	144-148
29164820-3	2018	METHODS &amp; RESULTS: HepG2 cells treated with palmitic acid (PA;0.75 mM) showed decreased expression of various antioxidant biomarkers (SOD1, SOD2, glutathione peroxidase and catalase) and increased expression of inflammatory markers (TNFalpha, IL1beta and IL6).	Protactinium	63-65	superoxide dismutase 2	Homo sapiens	144-148
29466765-3	2018	Previous investigations described association between a genetic superoxide-hydrogen (S-HP) imbalance caused by a superoxide dismutase manganese dependent gene polymorphism (Val16Ala-SOD2 SNP, rs4880) and differential anti-inflammatory response of some drugs and bioactive molecules.	Superoxides	64-74	superoxide dismutase 2	Homo sapiens	182-186
29466765-3	2018	Previous investigations described association between a genetic superoxide-hydrogen (S-HP) imbalance caused by a superoxide dismutase manganese dependent gene polymorphism (Val16Ala-SOD2 SNP, rs4880) and differential anti-inflammatory response of some drugs and bioactive molecules.	Hydrogen	75-83	superoxide dismutase 2	Homo sapiens	182-186
30223548-0	2018	PCB11 Metabolite, 3,3"-Dichlorobiphenyl-4-ol, Exposure Alters the Expression of Genes Governing Fatty Acid Metabolism in the Absence of Functional Sirtuin 3: Examining the Contribution of MnSOD.	3,3'-dichlorobiphenyl	0-5	superoxide dismutase 2	Homo sapiens	188-193
30053873-9	2018	RESULTS: HZ08 enhanced radiosensitivity of PCa cells through increasing ROS and declining mitochondrial respiration due to suppression of mitochondrial antioxidant enzyme MnSOD.	hz08	9-13	superoxide dismutase 2	Homo sapiens	171-176
30053873-10	2018	Mechanistically, HZ08 appeared to inhibit PI3K/Akt/IKKalpha signaling axis, resulting in transcriptional repression of MnSOD expression by preventing RelB nuclear translocation.	hz08	17-21	superoxide dismutase 2	Homo sapiens	119-124
30037352-2	2018	Although mitochondrial superoxide dismutase (SOD2) is the principal defence against the toxicity of superoxide anions, the mechanism of its inactivation in diabetic subjects is still poorly understood.	Superoxides	100-117	superoxide dismutase 2	Homo sapiens	45-49
30037352-4	2018	We sought to explore the mechanism underlying defective SOD2 antioxidant response in HUVECs during exposures to constant high glucose and oscillating glucose (as glucose variability model, GV) and the role of miR-21 in increasing the susceptibility to oxidative stress by disrupting reactive oxygen species (ROS) homeostasis.	Glucose	150-157	superoxide dismutase 2	Homo sapiens	56-60
30037352-4	2018	We sought to explore the mechanism underlying defective SOD2 antioxidant response in HUVECs during exposures to constant high glucose and oscillating glucose (as glucose variability model, GV) and the role of miR-21 in increasing the susceptibility to oxidative stress by disrupting reactive oxygen species (ROS) homeostasis.	Glucose	150-157	superoxide dismutase 2	Homo sapiens	56-60
30358222-4	2018	Therefore, we aimed to determine the potential prognostic role of single nucleotide polymorphism (SNP) of the two antioxidant enzymes glutathione peroxidase 1 (GPX1) and superoxide dismutase 2 (SOD2) in metastatic UBC patients treated with cisplatin-based chemotherapy.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	214-217	superoxide dismutase 2	Homo sapiens	194-198
30358222-4	2018	Therefore, we aimed to determine the potential prognostic role of single nucleotide polymorphism (SNP) of the two antioxidant enzymes glutathione peroxidase 1 (GPX1) and superoxide dismutase 2 (SOD2) in metastatic UBC patients treated with cisplatin-based chemotherapy.	Cisplatin	240-249	superoxide dismutase 2	Homo sapiens	194-198
29945545-8	2018	Interestingly, pre-irradiation treatment of cells with mannan activates NFkappaB, p38 and JNK, alters mitochondrial physiology, increases expression of Cu/ZnSOD and MnSOD, minimizes oxidation of mitochondrial phospholipids and offers survival advantage in comparison to irradiated group, in TLR expressing normal cells.	Mannans	55-61	superoxide dismutase 2	Homo sapiens	165-170
29800573-9	2018	In addition, vosaroxin stimulated mitochondrial enzyme activities and superoxide dismutase 2 (SOD2) deacetylation via activating (Sir2 like protein 3) Sirt3.	vosaroxin	13-22	superoxide dismutase 2	Homo sapiens	70-92
29800573-9	2018	In addition, vosaroxin stimulated mitochondrial enzyme activities and superoxide dismutase 2 (SOD2) deacetylation via activating (Sir2 like protein 3) Sirt3.	vosaroxin	13-22	superoxide dismutase 2	Homo sapiens	94-98
29903860-7	2018	GSK2586881 infusion was associated with reduced plasma markers of inflammation within 2-4 h and increased SOD2 plasma protein at 2 weeks.PAH is characterised by reduced ACE2 activity.	gsk2586881	0-10	superoxide dismutase 2	Homo sapiens	106-110
29733381-7	2018	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair.	ros	147-150	superoxide dismutase 2	Homo sapiens	68-72
29737331-0	2018	Human Mn-superoxide dismutase inactivation by peroxynitrite: a paradigm of metal-catalyzed tyrosine nitration in vitro and in vivo.	Peroxynitrous Acid	46-59	superoxide dismutase 2	Homo sapiens	6-29
29737331-0	2018	Human Mn-superoxide dismutase inactivation by peroxynitrite: a paradigm of metal-catalyzed tyrosine nitration in vitro and in vivo.	Metals	75-80	superoxide dismutase 2	Homo sapiens	6-29
29737331-0	2018	Human Mn-superoxide dismutase inactivation by peroxynitrite: a paradigm of metal-catalyzed tyrosine nitration in vitro and in vivo.	Tyrosine	91-99	superoxide dismutase 2	Homo sapiens	6-29
29737331-1	2018	Human MnSOD is a homotetramer and represents an essential mitochondrial antioxidant enzyme, which catalyzes the dismutation of superoxide radicals (O2 -) at near diffusion-controlled rates.	Superoxides	127-137	superoxide dismutase 2	Homo sapiens	6-11
29737331-1	2018	Human MnSOD is a homotetramer and represents an essential mitochondrial antioxidant enzyme, which catalyzes the dismutation of superoxide radicals (O2 -) at near diffusion-controlled rates.	Superoxides	148-150	superoxide dismutase 2	Homo sapiens	6-11
29737331-2	2018	Under a variety of disease conditions and in the process of aging, nitric oxide ( NO) can outcompete MnSOD and react with O2 - to yield the potent oxidant peroxynitrite (ONOO-).	Nitric Oxide	67-79	superoxide dismutase 2	Homo sapiens	101-106
29737331-3	2018	Then, peroxynitrite can promote the regio-specific nitration of MnSOD at active site tyrosine 34, which turns the enzyme inactive.	Peroxynitrous Acid	6-19	superoxide dismutase 2	Homo sapiens	64-69
29737331-3	2018	Then, peroxynitrite can promote the regio-specific nitration of MnSOD at active site tyrosine 34, which turns the enzyme inactive.	Tyrosine	85-93	superoxide dismutase 2	Homo sapiens	64-69
29737331-4	2018	In this review we assess the kinetic aspects of the formation of peroxynitrite in the presence of MnSOD and the biochemical mechanisms of peroxynitrite-mediated MnSOD nitration.	Peroxynitrous Acid	65-78	superoxide dismutase 2	Homo sapiens	98-103
29737331-4	2018	In this review we assess the kinetic aspects of the formation of peroxynitrite in the presence of MnSOD and the biochemical mechanisms of peroxynitrite-mediated MnSOD nitration.	Peroxynitrous Acid	138-151	superoxide dismutase 2	Homo sapiens	161-166
29737331-7	2018	Herein, kinetic, molecular, structural biology and computational studies are integrated to rationalize the specificity and impact of peroxynitrite-dependent MnSOD tyrosine nitration in vitro and in vivo from both functional and structural perspectives.	Peroxynitrous Acid	133-146	superoxide dismutase 2	Homo sapiens	157-162
29737331-7	2018	Herein, kinetic, molecular, structural biology and computational studies are integrated to rationalize the specificity and impact of peroxynitrite-dependent MnSOD tyrosine nitration in vitro and in vivo from both functional and structural perspectives.	Tyrosine	163-171	superoxide dismutase 2	Homo sapiens	157-162
29510157-0	2018	Demethoxycurcumin mediated targeting of MnSOD leading to activation of apoptotic pathway and inhibition of Akt/NF-kappaB survival signalling in human glioma U87 MG cells.	demethoxycurcumin	0-17	superoxide dismutase 2	Homo sapiens	40-45
29695725-4	2018	Consistent with this observation, ROS scavenging enzymes, including superoxide dismutase (Sod2), Catalase (Cat), and glutathine peroxidase (Gpx1), are down-regulated by miR-9.	Reactive Oxygen Species	34-37	superoxide dismutase 2	Homo sapiens	90-94
29550484-7	2018	Gene set enrichment analysis performed between the two SOD2-dependent classes of CML patients revealed a significant enrichment of Reactive Oxygen Species (ROS) Pathway.	Reactive Oxygen Species	131-154	superoxide dismutase 2	Homo sapiens	55-59
29550484-7	2018	Gene set enrichment analysis performed between the two SOD2-dependent classes of CML patients revealed a significant enrichment of Reactive Oxygen Species (ROS) Pathway.	Reactive Oxygen Species	156-159	superoxide dismutase 2	Homo sapiens	55-59
29510157-6	2018	In silico molecular docking analysis showed that, the amino acid residues His30, Tyr34, Asn37, Ala63, Asn67, His74, Trp123, and Asp159 in the active site of mitochondrial SOD (MnSOD) interacted with DMC.	demethoxycurcumin	199-202	superoxide dismutase 2	Homo sapiens	171-174
29510157-6	2018	In silico molecular docking analysis showed that, the amino acid residues His30, Tyr34, Asn37, Ala63, Asn67, His74, Trp123, and Asp159 in the active site of mitochondrial SOD (MnSOD) interacted with DMC.	demethoxycurcumin	199-202	superoxide dismutase 2	Homo sapiens	176-181
29459008-0	2018	Association of the SOD2 (rs2758339 and rs5746136) polymorphisms with the risk of heroin dependency and the SOD2 expression levels.	Heroin	81-87	superoxide dismutase 2	Homo sapiens	19-23
29510157-7	2018	Furthermore, the complex MnSOD-DMC was found to be more stable as compared to native MnSOD in the MD simulations.	demethoxycurcumin	31-34	superoxide dismutase 2	Homo sapiens	25-30
29510157-7	2018	Furthermore, the complex MnSOD-DMC was found to be more stable as compared to native MnSOD in the MD simulations.	demethoxycurcumin	31-34	superoxide dismutase 2	Homo sapiens	85-90
29681991-5	2018	MnSOD val16Ala (rs4880) SNP was genotyped by the Tetra-Primer ARMS-polymerase chain reaction analysis.	val16ala	6-14	superoxide dismutase 2	Homo sapiens	0-5
29681991-8	2018	Results: The Ala allele of the MnSOD Val16Ala polymorphism was associated with a lower risk of CKD (odds ratio (OR), 0.55; 95% confidence interval (CI), 0.36-0.84; P = 0.006).	Alanine	13-16	superoxide dismutase 2	Homo sapiens	31-36
29131419-4	2018	Classes that have been developed as SOD mimetics include the Mn-metalloporphyrins, Mn-cyclic polyamines, Mn-salen complexes, MnPLED derivatives as well as the nitroxides.	mn-metalloporphyrins	61-81	superoxide dismutase 2	Homo sapiens	36-39
29131419-4	2018	Classes that have been developed as SOD mimetics include the Mn-metalloporphyrins, Mn-cyclic polyamines, Mn-salen complexes, MnPLED derivatives as well as the nitroxides.	mn-cyclic polyamines	83-103	superoxide dismutase 2	Homo sapiens	36-39
29131419-4	2018	Classes that have been developed as SOD mimetics include the Mn-metalloporphyrins, Mn-cyclic polyamines, Mn-salen complexes, MnPLED derivatives as well as the nitroxides.	Mn-salen	105-113	superoxide dismutase 2	Homo sapiens	36-39
29131419-4	2018	Classes that have been developed as SOD mimetics include the Mn-metalloporphyrins, Mn-cyclic polyamines, Mn-salen complexes, MnPLED derivatives as well as the nitroxides.	Hydroxylamine	159-169	superoxide dismutase 2	Homo sapiens	36-39
29459008-1	2018	BACKGROUND: Superoxide dismutase-2 (SOD2, OMIM: 147460) is involved in the detoxification of superoxide anions.	Superoxides	93-110	superoxide dismutase 2	Homo sapiens	12-34
29459008-1	2018	BACKGROUND: Superoxide dismutase-2 (SOD2, OMIM: 147460) is involved in the detoxification of superoxide anions.	Superoxides	93-110	superoxide dismutase 2	Homo sapiens	36-40
29459008-2	2018	The SOD2 mRNA level is down-regulated in cells exposed to morphine.	Morphine	58-66	superoxide dismutase 2	Homo sapiens	4-8
29849912-2	2018	In addition, Mn is one of the required components for Mn superoxide dismutase (MnSOD) that is mainly responsible for scavenging reactive oxygen species (ROS) in mitochondrial oxidative stress.	Reactive Oxygen Species	128-151	superoxide dismutase 2	Homo sapiens	54-77
29357430-7	2018	Administration of the SOD2 mimic manganese (III) tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP) significantly attenuated AQP2 downregulation in line with complete blockade of thiobarbituric acid-reactive substances elevation, whereas the reduction of AQP1, AQP3, and AQP4 was not affected.	manganese (iii) tetrakis(4-benzoic acid)porphyrin chloride	33-91	superoxide dismutase 2	Homo sapiens	22-26
29849912-2	2018	In addition, Mn is one of the required components for Mn superoxide dismutase (MnSOD) that is mainly responsible for scavenging reactive oxygen species (ROS) in mitochondrial oxidative stress.	Reactive Oxygen Species	128-151	superoxide dismutase 2	Homo sapiens	79-84
29849912-2	2018	In addition, Mn is one of the required components for Mn superoxide dismutase (MnSOD) that is mainly responsible for scavenging reactive oxygen species (ROS) in mitochondrial oxidative stress.	Reactive Oxygen Species	153-156	superoxide dismutase 2	Homo sapiens	54-77
29849912-2	2018	In addition, Mn is one of the required components for Mn superoxide dismutase (MnSOD) that is mainly responsible for scavenging reactive oxygen species (ROS) in mitochondrial oxidative stress.	Reactive Oxygen Species	153-156	superoxide dismutase 2	Homo sapiens	79-84
29357430-7	2018	Administration of the SOD2 mimic manganese (III) tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP) significantly attenuated AQP2 downregulation in line with complete blockade of thiobarbituric acid-reactive substances elevation, whereas the reduction of AQP1, AQP3, and AQP4 was not affected.	thiobarbituric acid	180-199	superoxide dismutase 2	Homo sapiens	22-26
29357430-7	2018	Administration of the SOD2 mimic manganese (III) tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP) significantly attenuated AQP2 downregulation in line with complete blockade of thiobarbituric acid-reactive substances elevation, whereas the reduction of AQP1, AQP3, and AQP4 was not affected.	reactive substances	200-219	superoxide dismutase 2	Homo sapiens	22-26
29455070-3	2018	Although the cause of this inflammatory disorder is still unknown, a large amount of evidence suggests that ulcerative colitis is associated with increased activity of reactive oxygen species (ROS), manganese superoxide dismutase (MnSOD) is a kind of superoxide dismutase (SOD) has been demonstrated to play a key role in the pathophysiology of colitis.	Reactive Oxygen Species	168-191	superoxide dismutase 2	Homo sapiens	231-236
29455070-3	2018	Although the cause of this inflammatory disorder is still unknown, a large amount of evidence suggests that ulcerative colitis is associated with increased activity of reactive oxygen species (ROS), manganese superoxide dismutase (MnSOD) is a kind of superoxide dismutase (SOD) has been demonstrated to play a key role in the pathophysiology of colitis.	Reactive Oxygen Species	168-191	superoxide dismutase 2	Homo sapiens	233-236
29158541-8	2018	Concurrently, in samples from children with obesity, we found decreased SOD2 activity and redox state imbalance highlighted by decreased reduced glutathione/oxidized glutathione (GSH/GSSG) ratio and significant increases in protein carbonylation.	Glutathione	145-156	superoxide dismutase 2	Homo sapiens	72-76
29158541-8	2018	Concurrently, in samples from children with obesity, we found decreased SOD2 activity and redox state imbalance highlighted by decreased reduced glutathione/oxidized glutathione (GSH/GSSG) ratio and significant increases in protein carbonylation.	Glutathione Disulfide	183-187	superoxide dismutase 2	Homo sapiens	72-76
29460119-6	2018	Our data demonstrated that Curcumin inhibited TNF-alpha-induced astrocytes migration, decreased MCP-1 expression, and up-regulated SOD2 expression in TNF-alpha-induced astrocytes in vitro.	Curcumin	27-35	superoxide dismutase 2	Homo sapiens	131-135
29750170-8	2018	After CisEP therapy, an increased immunoreactivity with SOD-2 and Casp-3 antibodies was noticed.	cisep	6-11	superoxide dismutase 2	Homo sapiens	56-61
29851012-6	2018	Superoxide dismutase (MnSOD, SOD2) from the mitochondrial matrix, as well as superoxide dismutase (Cu/ZnSOD, SOD1) present in small amounts in the mitochondrial intramembrane space, converts superoxide anion to hydrogen peroxide, which can be then converted by catalase to harmless H2O.In the chapter we describe a relation between mitochondrial membrane potential and the rate of ROS formation.	Superoxides	191-207	superoxide dismutase 2	Homo sapiens	22-27
29293455-1	2018	Manganese (Mn) is an essential nutrient for intracellular activities; it functions as a cofactor for a variety of enzymes, including arginase, glutamine synthetase (GS), pyruvate carboxylase and Mn superoxide dismutase (Mn-SOD).	Manganese	0-9	superoxide dismutase 2	Homo sapiens	195-218
29293455-1	2018	Manganese (Mn) is an essential nutrient for intracellular activities; it functions as a cofactor for a variety of enzymes, including arginase, glutamine synthetase (GS), pyruvate carboxylase and Mn superoxide dismutase (Mn-SOD).	Manganese	0-9	superoxide dismutase 2	Homo sapiens	220-226
28990726-7	2018	Moreover, DMF was able to induce an activation of manganese superoxide dismutase (MnSOD) and heme-oxygenase-1 (HO-1), decreasing the severity of oxidative stress.	Dimethyl Fumarate	10-13	superoxide dismutase 2	Homo sapiens	50-80
28990726-7	2018	Moreover, DMF was able to induce an activation of manganese superoxide dismutase (MnSOD) and heme-oxygenase-1 (HO-1), decreasing the severity of oxidative stress.	Dimethyl Fumarate	10-13	superoxide dismutase 2	Homo sapiens	82-87
29385710-7	2018	Here, we focus on human MnSOD, the most significant enzyme in protecting against ROS in the human body.	Reactive Oxygen Species	81-84	superoxide dismutase 2	Homo sapiens	24-29
29385710-8	2018	Human MnSOD resides in the mitochondrial matrix, the location of up to 90% of cellular ROS generation.	Reactive Oxygen Species	87-90	superoxide dismutase 2	Homo sapiens	6-11
29113986-7	2018	In a preplanned exploratory analysis, PSADT pre-to-post increase was significant in the 27 (26%) genotyped patients with SOD2 Alanine/Alanine genotype (rs4880 T&gt;C polymorphism) on MPX (pooled treatment arms; 6.4 months, P = 0.02), but not in control (1.8 months, P = 0.25).Conclusions: Compared with placebo, MPX did not significantly prolong PSADT in BCR patients over two different doses.	mpx	183-186	superoxide dismutase 2	Homo sapiens	121-125
29113986-7	2018	In a preplanned exploratory analysis, PSADT pre-to-post increase was significant in the 27 (26%) genotyped patients with SOD2 Alanine/Alanine genotype (rs4880 T&gt;C polymorphism) on MPX (pooled treatment arms; 6.4 months, P = 0.02), but not in control (1.8 months, P = 0.25).Conclusions: Compared with placebo, MPX did not significantly prolong PSADT in BCR patients over two different doses.	mpx	312-315	superoxide dismutase 2	Homo sapiens	121-125
29710707-5	2018	In cultured human primary hippocampal neurons, spherical aggregation of Abeta (amylospheroids) decreased PKCe and MnSOD.	amylospheroids	79-93	superoxide dismutase 2	Homo sapiens	114-119
29710707-6	2018	Treatment with t-butyl hydroperoxide (TBHP) increased superoxide, the oxidative DNA/RNA damage marker, 8-OHG, and Abeta levels, but reduced PKCe, MnSOD, BDNF, and cultured neuron density.	tert-Butylhydroperoxide	15-36	superoxide dismutase 2	Homo sapiens	146-151
29710707-6	2018	Treatment with t-butyl hydroperoxide (TBHP) increased superoxide, the oxidative DNA/RNA damage marker, 8-OHG, and Abeta levels, but reduced PKCe, MnSOD, BDNF, and cultured neuron density.	tert-Butylhydroperoxide	38-42	superoxide dismutase 2	Homo sapiens	146-151
29710707-9	2018	In cultured neurons, the increase in reactive oxygen species (ROS) associated with reduced PKCe during neurodegeneration was inhibited by the SOD mimetic MnTMPyP and the ROS scavenger NAc, indicating that strong oxidative stress suppresses PKCe level.	Reactive Oxygen Species	37-60	superoxide dismutase 2	Homo sapiens	142-145
29710707-9	2018	In cultured neurons, the increase in reactive oxygen species (ROS) associated with reduced PKCe during neurodegeneration was inhibited by the SOD mimetic MnTMPyP and the ROS scavenger NAc, indicating that strong oxidative stress suppresses PKCe level.	Reactive Oxygen Species	62-65	superoxide dismutase 2	Homo sapiens	142-145
29282552-1	2018	Superoxide dismutases (SOD) are vital enzymes for disproportionation of superoxide molecules in mammals.	Superoxides	72-82	superoxide dismutase 2	Homo sapiens	23-26
29282552-10	2018	The water pK a in Mn-SOD is higher than that in Fe-SOD by 3.5 pH units, which is similar to the shift measured experimentally.	Water	4-9	superoxide dismutase 2	Homo sapiens	18-24
29282552-10	2018	The water pK a in Mn-SOD is higher than that in Fe-SOD by 3.5 pH units, which is similar to the shift measured experimentally.	Water	4-9	superoxide dismutase 2	Homo sapiens	21-24
29197622-3	2018	In addition, dioscin markedly adjusted the levels of MDA, SOD and GSH-Px, reduced ROS level in renal tissue, and decreased the levels of TG, FFA, alpha-SMA and COL1A.	dioscin	13-20	superoxide dismutase 2	Homo sapiens	58-61
29197622-4	2018	Mechanistic study showed that dioscin significantly up-regulated the expression levels of Sirt3, SOD2, and then suppressed inflammation by decreasing the expression levels of NF-kB, HMGB1, c-Jun, c-Fos, COX2, TNF-alpha, IL-1beta and IL-6.	dioscin	30-37	superoxide dismutase 2	Homo sapiens	97-101
29197622-5	2018	Furthermore, dioscin-caused high levels of Sirt3 and SOD2 attenuated oxidative stress by regulating the expression levels of Nrf2, GST, Keap1, regulated lipid metabolism by controlling the expression levels of SREBP-1c, SCD-1, FASn, ACC, CPT1, and adjusted TGF-beta1/Smad signal to inhibit renal fibrosis.	dioscin	13-20	superoxide dismutase 2	Homo sapiens	53-57
29309894-5	2018	BaP exposure significantly increased expression of genes associated with oxidative stress, Cyp1a1, Sod1 and Sod2, while repressing Gpx1.	benzylaminopurine	0-3	superoxide dismutase 2	Homo sapiens	108-112
29127121-4	2018	Moreover, direct inhibition of SOD2 increases mitochondrial ROS and significantly impedes AML progression in vivo Furthermore, we report that PKCepsilon over-expression protects AML cells from otherwise-lethal doses of mitochondrial ROS-inducing agents.	Reactive Oxygen Species	60-63	superoxide dismutase 2	Homo sapiens	31-35
29127121-4	2018	Moreover, direct inhibition of SOD2 increases mitochondrial ROS and significantly impedes AML progression in vivo Furthermore, we report that PKCepsilon over-expression protects AML cells from otherwise-lethal doses of mitochondrial ROS-inducing agents.	Reactive Oxygen Species	233-236	superoxide dismutase 2	Homo sapiens	31-35
27849558-10	2018	RNA sequencing, mass spectrometry and siRNA interference studies demonstrate that translocase of inner mitochondrial membrane 44 (TIM44)-superoxide dismutase 2 (SOD2) pathway inhibition is responsible for the excessive ROS, autophagy and apoptosis induced by IR-58.	Reactive Oxygen Species	219-222	superoxide dismutase 2	Homo sapiens	161-165
27849558-13	2018	Additionally, TIM44 was identified for the first time as a potential oncogene, which plays an important role in autophagy through the TIM44-SOD2-ROS-mTOR pathway.	Reactive Oxygen Species	145-148	superoxide dismutase 2	Homo sapiens	140-144
29113986-7	2018	In a preplanned exploratory analysis, PSADT pre-to-post increase was significant in the 27 (26%) genotyped patients with SOD2 Alanine/Alanine genotype (rs4880 T&gt;C polymorphism) on MPX (pooled treatment arms; 6.4 months, P = 0.02), but not in control (1.8 months, P = 0.25).Conclusions: Compared with placebo, MPX did not significantly prolong PSADT in BCR patients over two different doses.	Alanine	126-133	superoxide dismutase 2	Homo sapiens	121-125
29339975-8	2018	(B) Only CR showed statistically changes (p &lt; 0.05) in several CV, BV, and AV for the SNPs - 21A&gt;T CAT (rs7943316) and 47C&gt;T SOD2 (rs4880).	Chromium	9-11	superoxide dismutase 2	Homo sapiens	134-138
29339975-9	2018	The dietary intervention effect was statistically significantly between the polymorphisms of 47C&gt;T SOD2 and BMI, SBP, TBARS, total cholesterol, and C-LCL (p &lt; 0.05) and between the polymorphisms of - 21A&gt;T CAT (rs7943316) and SBP, DBP, total cholesterol, and atherogenic index (p &lt; 0.05).	Cholesterol	251-262	superoxide dismutase 2	Homo sapiens	102-106
29851012-6	2018	Superoxide dismutase (MnSOD, SOD2) from the mitochondrial matrix, as well as superoxide dismutase (Cu/ZnSOD, SOD1) present in small amounts in the mitochondrial intramembrane space, converts superoxide anion to hydrogen peroxide, which can be then converted by catalase to harmless H2O.In the chapter we describe a relation between mitochondrial membrane potential and the rate of ROS formation.	Superoxides	191-207	superoxide dismutase 2	Homo sapiens	29-33
28776259-8	2017	In addition, we found that exogenous CUG2 overexpression reduced the formation of ROS during doxorubicin treatment by enhancing the expression of antioxidant and multidrug resistant proteins such as MnSOD, Foxo1, Foxo4, MRP2 and BCRP, whereas EGFR silencing congruently increased the levels of ROS by decreasing the expression of these proteins.	Doxorubicin	93-104	superoxide dismutase 2	Homo sapiens	199-204
29292727-7	2017	Furthermore, H2O2 significantly up-regulated the expression levels of SOD-2, CAT, GPx and NRF2, and modulated miR-146a and miR-34a gene expression.	Hydrogen Peroxide	13-17	superoxide dismutase 2	Homo sapiens	70-75
28919892-8	2017	Exposure to PS enhanced the antioxidant capacity of MSCs, notably the expression of SOD2 antioxidant gene.	ps	12-14	superoxide dismutase 2	Homo sapiens	84-88
29109056-6	2017	In ST group, post-training decrease in serum lipid hydroperoxides (p &lt; 0.05) and creatine kinase activity (p &lt; 0.05) was associated with Ala/Ala genotype of SOD2 Val16Ala polymorphism.	Hydrogen Peroxide	51-65	superoxide dismutase 2	Homo sapiens	163-167
29109056-6	2017	In ST group, post-training decrease in serum lipid hydroperoxides (p &lt; 0.05) and creatine kinase activity (p &lt; 0.05) was associated with Ala/Ala genotype of SOD2 Val16Ala polymorphism.	Alanine	143-146	superoxide dismutase 2	Homo sapiens	163-167
29109056-6	2017	In ST group, post-training decrease in serum lipid hydroperoxides (p &lt; 0.05) and creatine kinase activity (p &lt; 0.05) was associated with Ala/Ala genotype of SOD2 Val16Ala polymorphism.	Alanine	147-150	superoxide dismutase 2	Homo sapiens	163-167
30647680-2	2017	The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against reactive oxygen species (ROS) within the mitochondria.	Reactive Oxygen Species	96-119	superoxide dismutase 2	Homo sapiens	4-34
30647680-2	2017	The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against reactive oxygen species (ROS) within the mitochondria.	Reactive Oxygen Species	96-119	superoxide dismutase 2	Homo sapiens	36-41
30647680-2	2017	The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against reactive oxygen species (ROS) within the mitochondria.	Reactive Oxygen Species	121-124	superoxide dismutase 2	Homo sapiens	4-34
30647680-2	2017	The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against reactive oxygen species (ROS) within the mitochondria.	Reactive Oxygen Species	121-124	superoxide dismutase 2	Homo sapiens	36-41
28838761-6	2017	The basal formation of reactive oxygen species (ROS) was 3-fold higher in SK-LMS-1 cells than in the MES-SA cells and SK-LMS-1 cells expressed glutathione peroxidase 1 (GPx1) and more superoxide dismutase 2 (SOD2) than the MES-SA cells.	Reactive Oxygen Species	23-46	superoxide dismutase 2	Homo sapiens	184-206
28838761-6	2017	The basal formation of reactive oxygen species (ROS) was 3-fold higher in SK-LMS-1 cells than in the MES-SA cells and SK-LMS-1 cells expressed glutathione peroxidase 1 (GPx1) and more superoxide dismutase 2 (SOD2) than the MES-SA cells.	Reactive Oxygen Species	23-46	superoxide dismutase 2	Homo sapiens	208-212
28838761-6	2017	The basal formation of reactive oxygen species (ROS) was 3-fold higher in SK-LMS-1 cells than in the MES-SA cells and SK-LMS-1 cells expressed glutathione peroxidase 1 (GPx1) and more superoxide dismutase 2 (SOD2) than the MES-SA cells.	Reactive Oxygen Species	48-51	superoxide dismutase 2	Homo sapiens	184-206
28838761-6	2017	The basal formation of reactive oxygen species (ROS) was 3-fold higher in SK-LMS-1 cells than in the MES-SA cells and SK-LMS-1 cells expressed glutathione peroxidase 1 (GPx1) and more superoxide dismutase 2 (SOD2) than the MES-SA cells.	Reactive Oxygen Species	48-51	superoxide dismutase 2	Homo sapiens	208-212
29116107-8	2017	Transfection of human cardiomyocytes with miR-222-3p mimic or inhibitor induced respectively a decrease and an increase of SOD2 expression.	mir-222-3p	42-52	superoxide dismutase 2	Homo sapiens	123-127
28950658-5	2017	7,8-DHF also significantly reduced the generation of intracellular reactive oxygen species (ROS), induced the expression of anti-oxidant enzymes, such as catalase, manganese superoxide dismutase (Mn-SOD), and heme oxygenase-1 (HO-1), and scavenged DPPH free radicals.	6,7-dihydroxyflavone	0-7	superoxide dismutase 2	Homo sapiens	164-194
28950658-5	2017	7,8-DHF also significantly reduced the generation of intracellular reactive oxygen species (ROS), induced the expression of anti-oxidant enzymes, such as catalase, manganese superoxide dismutase (Mn-SOD), and heme oxygenase-1 (HO-1), and scavenged DPPH free radicals.	6,7-dihydroxyflavone	0-7	superoxide dismutase 2	Homo sapiens	196-202
28785805-4	2017	Melatonin improves the intramitochondrial antioxidative defense by enhancing reduced glutathione levels and inducing glutathione peroxidase and Mn-superoxide dismutase (Mn-SOD) in the matrix and Cu,Zn-SOD in the intermembrane space.	Melatonin	0-9	superoxide dismutase 2	Homo sapiens	144-167
28785805-4	2017	Melatonin improves the intramitochondrial antioxidative defense by enhancing reduced glutathione levels and inducing glutathione peroxidase and Mn-superoxide dismutase (Mn-SOD) in the matrix and Cu,Zn-SOD in the intermembrane space.	Melatonin	0-9	superoxide dismutase 2	Homo sapiens	169-175
28650465-0	2017	MCU-dependent mitochondrial Ca2+ inhibits NAD+/SIRT3/SOD2 pathway to promote ROS production and metastasis of HCC cells.	NAD	42-46	superoxide dismutase 2	Homo sapiens	53-57
28650465-0	2017	MCU-dependent mitochondrial Ca2+ inhibits NAD+/SIRT3/SOD2 pathway to promote ROS production and metastasis of HCC cells.	Reactive Oxygen Species	77-80	superoxide dismutase 2	Homo sapiens	53-57
28650465-4	2017	Upregulation of MCU clearly enhanced the Ca2+ uptake into mitochondria, which significantly promoted ROS production by downregulating nicotinamide adenine dinucleotide+ (NAD+)/reduced form of nicotinamide adenine dinucleotid (NADH) ratio and the NAD+-dependent deacetylase activity of sirtuin 3 to inhibit superoxide dismutase 2 (SOD2) activity.	Reactive Oxygen Species	101-104	superoxide dismutase 2	Homo sapiens	306-328
28650465-4	2017	Upregulation of MCU clearly enhanced the Ca2+ uptake into mitochondria, which significantly promoted ROS production by downregulating nicotinamide adenine dinucleotide+ (NAD+)/reduced form of nicotinamide adenine dinucleotid (NADH) ratio and the NAD+-dependent deacetylase activity of sirtuin 3 to inhibit superoxide dismutase 2 (SOD2) activity.	Reactive Oxygen Species	101-104	superoxide dismutase 2	Homo sapiens	330-334
28552711-0	2017	ALA16VAL-MnSOD gene polymorphism and stroke: Association with dyslipidemia and glucose levels.	Glucose	79-86	superoxide dismutase 2	Homo sapiens	9-14
28552711-2	2017	The ALA16VAL-MnSOD gene single nucleotide polymorphism (SNP) has shown to modulate risk factors of several metabolic and vascular diseases, such as blood glucose (GLU) and lipid levels.	Blood Glucose	148-161	superoxide dismutase 2	Homo sapiens	13-18
28552711-2	2017	The ALA16VAL-MnSOD gene single nucleotide polymorphism (SNP) has shown to modulate risk factors of several metabolic and vascular diseases, such as blood glucose (GLU) and lipid levels.	Glucose	163-166	superoxide dismutase 2	Homo sapiens	13-18
28552711-9	2017	Furthermore, we propose that the Ala16Val-MnSOD SNPs may contribute to hypercholesterolemia and higher GLU levels, increasing the risk to neurovascular events that may lead to stroke.	Glucose	103-106	superoxide dismutase 2	Homo sapiens	42-47
28042948-4	2017	Incubation of HK-2 cells with antimycin A and 2-deoxyglucose resulted in a significant decrease in intracellular adenosine triphosphate (ATP) levels; following reperfusion, ATP levels significantly increased over time in cells overexpressing sod-2.	Antimycin A	30-41	superoxide dismutase 2	Homo sapiens	242-247
28042948-4	2017	Incubation of HK-2 cells with antimycin A and 2-deoxyglucose resulted in a significant decrease in intracellular adenosine triphosphate (ATP) levels; following reperfusion, ATP levels significantly increased over time in cells overexpressing sod-2.	Deoxyglucose	46-60	superoxide dismutase 2	Homo sapiens	242-247
28042948-4	2017	Incubation of HK-2 cells with antimycin A and 2-deoxyglucose resulted in a significant decrease in intracellular adenosine triphosphate (ATP) levels; following reperfusion, ATP levels significantly increased over time in cells overexpressing sod-2.	Adenosine Triphosphate	113-135	superoxide dismutase 2	Homo sapiens	242-247
28042948-4	2017	Incubation of HK-2 cells with antimycin A and 2-deoxyglucose resulted in a significant decrease in intracellular adenosine triphosphate (ATP) levels; following reperfusion, ATP levels significantly increased over time in cells overexpressing sod-2.	Adenosine Triphosphate	173-176	superoxide dismutase 2	Homo sapiens	242-247
28493603-6	2018	Compared to the young, MitoQ in the old diminished the initially elevated mitochondria-derived O2- levels and appeared to attenuate the breakdown of MnSOD.	mitoquinone	23-28	superoxide dismutase 2	Homo sapiens	149-154
29118033-0	2017	Trimethylamine-N-Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3-SOD2-mtROS Signaling Pathway.	trimethyloxamine	0-22	superoxide dismutase 2	Homo sapiens	108-112
29099803-4	2017	SOD2 has both tumor suppressive and promoting functions, which are primarily related to its role as a mitochondrial superoxide scavenger and H2O2 regulator.	Superoxides	116-126	superoxide dismutase 2	Homo sapiens	0-4
29099803-4	2017	SOD2 has both tumor suppressive and promoting functions, which are primarily related to its role as a mitochondrial superoxide scavenger and H2O2 regulator.	Hydrogen Peroxide	141-145	superoxide dismutase 2	Homo sapiens	0-4
28950658-8	2017	7,8-DHF effectively attenuated oxidative stress by up-regulating the anti-oxidant enzymes catalase, Mn-SOD, and HO-1, and reducing activation of the Akt and MAPKs signaling pathways in aged skin cells.	6,7-dihydroxyflavone	0-7	superoxide dismutase 2	Homo sapiens	100-106
28964868-6	2017	The stimulation of mitochondrial function and anti-oxidative stress by rosiglitazone was associated with activation of the PGC1alpha pathway by up-regulation of mitochondrial (NRF-1 and Tfam) and oxidative defense (SOD1, SOD2 and Gpx1) genes.	Rosiglitazone	71-84	superoxide dismutase 2	Homo sapiens	221-225
29042516-5	2017	The fraction of cellular Mn2+ present as H-complexes (H-Mn2+), as measured by EPR of live, nonirradiated Mn-replete cells, is now the strongest known gauge of biological IR resistance between and within organisms representing all three domains of life: Antioxidant H-Mn2+ complexes, not antioxidant enzymes (e.g., Mn superoxide dismutase), govern IR survival.	Manganese(2+)	25-29	superoxide dismutase 2	Homo sapiens	314-337
29042516-5	2017	The fraction of cellular Mn2+ present as H-complexes (H-Mn2+), as measured by EPR of live, nonirradiated Mn-replete cells, is now the strongest known gauge of biological IR resistance between and within organisms representing all three domains of life: Antioxidant H-Mn2+ complexes, not antioxidant enzymes (e.g., Mn superoxide dismutase), govern IR survival.	Manganese(2+)	56-60	superoxide dismutase 2	Homo sapiens	314-337
29042516-5	2017	The fraction of cellular Mn2+ present as H-complexes (H-Mn2+), as measured by EPR of live, nonirradiated Mn-replete cells, is now the strongest known gauge of biological IR resistance between and within organisms representing all three domains of life: Antioxidant H-Mn2+ complexes, not antioxidant enzymes (e.g., Mn superoxide dismutase), govern IR survival.	h-mn2+	54-60	superoxide dismutase 2	Homo sapiens	314-337
28676971-2	2017	In the present study non-cytotoxic dose of oxidants, H2O2 (100 muM) and GO (10 muU/ml) was used to induce moderate oxidative stress via generating ROS in human glioblastoma cell line U-87 MG cells, which showed a marked increase in the antioxidant capacity as studied by measuring the modulation in expression levels and activities of superoxide dismutase (SOD1 and SOD2) and catalase (CAT) enzymes, and the GSH content.	Hydrogen Peroxide	53-57	superoxide dismutase 2	Homo sapiens	366-370
28676971-2	2017	In the present study non-cytotoxic dose of oxidants, H2O2 (100 muM) and GO (10 muU/ml) was used to induce moderate oxidative stress via generating ROS in human glioblastoma cell line U-87 MG cells, which showed a marked increase in the antioxidant capacity as studied by measuring the modulation in expression levels and activities of superoxide dismutase (SOD1 and SOD2) and catalase (CAT) enzymes, and the GSH content.	Reactive Oxygen Species	147-150	superoxide dismutase 2	Homo sapiens	366-370
28574756-0	2017	SOD2 Facilitates the Antiviral Innate Immune Response by Scavenging Reactive Oxygen Species.	Reactive Oxygen Species	68-91	superoxide dismutase 2	Homo sapiens	0-4
28574756-1	2017	Superoxide dismutase 2 (SOD2) is essential in radical scavenging, which balances the intracellular level of reactive oxygen species (ROS).	Reactive Oxygen Species	108-131	superoxide dismutase 2	Homo sapiens	0-22
28574756-1	2017	Superoxide dismutase 2 (SOD2) is essential in radical scavenging, which balances the intracellular level of reactive oxygen species (ROS).	Reactive Oxygen Species	108-131	superoxide dismutase 2	Homo sapiens	24-28
28574756-1	2017	Superoxide dismutase 2 (SOD2) is essential in radical scavenging, which balances the intracellular level of reactive oxygen species (ROS).	Reactive Oxygen Species	133-136	superoxide dismutase 2	Homo sapiens	0-22
28574756-1	2017	Superoxide dismutase 2 (SOD2) is essential in radical scavenging, which balances the intracellular level of reactive oxygen species (ROS).	Reactive Oxygen Species	133-136	superoxide dismutase 2	Homo sapiens	24-28
28574756-7	2017	SOD2 deficiency-mediated ROS accumulation potently inhibits RIG-I-like receptor (RLR)-induced innate immune responses through the regulation of nuclear factor-kappa B (NF-kappaB) and interferon regulatory factor-3 activation.	Reactive Oxygen Species	25-28	superoxide dismutase 2	Homo sapiens	0-4
28655148-4	2017	Common functional polymorphisms have been described in the MnSOD gene [rs4880, NM_000636.3:c.47 T &gt; C, alanine (ALA) to valine (Val)] and in the CAT promoter region [rs1001179, NG_013339.1:g.4760 C &gt; T].	Alanine	106-113	superoxide dismutase 2	Homo sapiens	59-64
28655148-4	2017	Common functional polymorphisms have been described in the MnSOD gene [rs4880, NM_000636.3:c.47 T &gt; C, alanine (ALA) to valine (Val)] and in the CAT promoter region [rs1001179, NG_013339.1:g.4760 C &gt; T].	Alanine	115-118	superoxide dismutase 2	Homo sapiens	59-64
28655148-4	2017	Common functional polymorphisms have been described in the MnSOD gene [rs4880, NM_000636.3:c.47 T &gt; C, alanine (ALA) to valine (Val)] and in the CAT promoter region [rs1001179, NG_013339.1:g.4760 C &gt; T].	Valine	123-129	superoxide dismutase 2	Homo sapiens	59-64
28655148-4	2017	Common functional polymorphisms have been described in the MnSOD gene [rs4880, NM_000636.3:c.47 T &gt; C, alanine (ALA) to valine (Val)] and in the CAT promoter region [rs1001179, NG_013339.1:g.4760 C &gt; T].	Valine	131-134	superoxide dismutase 2	Homo sapiens	59-64
28687409-8	2017	Furthermore, the deacetylase effect of Sirt3 enhanced the MnSOD activity by deacetylation at the lysine 68 residue and therapeutic effect of UCB-MSCs on skin-wound healing was increased by EphB2 activation.	Lysine	97-103	superoxide dismutase 2	Homo sapiens	58-63
28042948-6	2017	Ex vivo delivery of sod-2 significantly increased ATP levels in organs after 24 h of cold perfusion.	Adenosine Triphosphate	50-53	superoxide dismutase 2	Homo sapiens	20-25
28841898-1	2017	BACKGROUND: This study aims to determine the relationship between expression levels of ALDH2 and SOD2 genes and clinical parameters such as alcohol drinking, tobacco smoking, primary site of HNSCC, and human papilloma virus (HPV) state.	Alcohols	140-147	superoxide dismutase 2	Homo sapiens	97-101
28042948-7	2017	In vitro and ex vivo results suggested that BacMam transduction successfully delivered sod-2, which reduced injury associated with I/R, by improving ATP cell content and decreasing LDH release with a subsequent increase in kidney tissue viability.	bacmam	44-50	superoxide dismutase 2	Homo sapiens	87-92
28042948-7	2017	In vitro and ex vivo results suggested that BacMam transduction successfully delivered sod-2, which reduced injury associated with I/R, by improving ATP cell content and decreasing LDH release with a subsequent increase in kidney tissue viability.	Adenosine Triphosphate	149-152	superoxide dismutase 2	Homo sapiens	87-92
28411102-7	2017	In addition, ZL006 stimulated mitochondrial enzyme activities and SOD2 deacetylation in a Sirt3-dependent manner.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	13-18	superoxide dismutase 2	Homo sapiens	66-70
28814292-6	2017	RESULTS: Compared to the vehicle control, treatment with resveratrol improved intestinal morphology, decreased apoptosis of crypt cells, maintained cell regeneration, and ameliorated SOD2 expression and activity.	Resveratrol	57-68	superoxide dismutase 2	Homo sapiens	183-187
28801561-0	2017	Inflammation-mediated SOD-2 upregulation contributes to epithelial-mesenchymal transition and migration of tumor cells in aflatoxin G1-induced lung adenocarcinoma.	Aflatoxins	122-131	superoxide dismutase 2	Homo sapiens	22-27
29245915-7	2017	Curcumin and sildenafil exposure reduced the expression of MCL-1, BCL-XL, thioredoxin and superoxide dismutase 2 (SOD2) in an eIF2alpha-dependent fashion.	Curcumin	0-8	superoxide dismutase 2	Homo sapiens	90-112
28688900-3	2017	Results showed that genistein restrained reactive oxygen species (ROS) and malondialdehyde (MDA) production, and ameliorated the inhibitory effect on superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx) activity elicited by ox-LDL stimulation.	Genistein	20-29	superoxide dismutase 2	Homo sapiens	172-175
28688900-5	2017	Moreover, the antioxidation of genistein was associated with miR-34a/sirtuin-1-mediated nuclear translocation and deacetylation of foxo3a, accompanying with the enhanced expressions of MnSOD and CAT.	Genistein	31-40	superoxide dismutase 2	Homo sapiens	185-190
29245915-8	2017	Curcumin and sildenafil interacted in a greater than additive fashion to increase the levels of reactive oxygen species; knock down of thioredoxin or SOD2 enhanced killing and over-expression of thioredoxin or SOD2 suppressed killing.	Sildenafil Citrate	13-23	superoxide dismutase 2	Homo sapiens	210-214
29245915-8	2017	Curcumin and sildenafil interacted in a greater than additive fashion to increase the levels of reactive oxygen species; knock down of thioredoxin or SOD2 enhanced killing and over-expression of thioredoxin or SOD2 suppressed killing.	Reactive Oxygen Species	96-119	superoxide dismutase 2	Homo sapiens	150-154
28495429-1	2017	Superoxide-hydrogen peroxide (S-HP) imbalance genetically caused by a gene polymorphism in the human manganese superoxide dismutase enzyme (Val16Ala-MnSOD) is associated with several diseases.	superoxide-hydrogen peroxide	0-28	superoxide dismutase 2	Homo sapiens	149-154
28495429-1	2017	Superoxide-hydrogen peroxide (S-HP) imbalance genetically caused by a gene polymorphism in the human manganese superoxide dismutase enzyme (Val16Ala-MnSOD) is associated with several diseases.	s-hp	30-34	superoxide dismutase 2	Homo sapiens	149-154
28495429-2	2017	Into mitochondria, MnSOD catalyses superoxide radical producing HP and oxygen.	Superoxides	35-53	superoxide dismutase 2	Homo sapiens	19-24
28495429-2	2017	Into mitochondria, MnSOD catalyses superoxide radical producing HP and oxygen.	histidylproline	64-66	superoxide dismutase 2	Homo sapiens	19-24
28495429-2	2017	Into mitochondria, MnSOD catalyses superoxide radical producing HP and oxygen.	Oxygen	71-77	superoxide dismutase 2	Homo sapiens	19-24
28495429-5	2017	Since, synthesis and activities of selenoenzymes are selenium dependent, we hypothesized that AA-MnSOD cells could have an improvement on antioxidant status undergoing Seleno-L-methionine (SeMet) treatment.	Selenium	53-61	superoxide dismutase 2	Homo sapiens	97-102
28495429-5	2017	Since, synthesis and activities of selenoenzymes are selenium dependent, we hypothesized that AA-MnSOD cells could have an improvement on antioxidant status undergoing Seleno-L-methionine (SeMet) treatment.	Selenomethionine	168-187	superoxide dismutase 2	Homo sapiens	97-102
28495429-5	2017	Since, synthesis and activities of selenoenzymes are selenium dependent, we hypothesized that AA-MnSOD cells could have an improvement on antioxidant status undergoing Seleno-L-methionine (SeMet) treatment.	Selenomethionine	189-194	superoxide dismutase 2	Homo sapiens	97-102
28400010-9	2017	Supporting these founding, the SOD-2 gene expression of Caco-2 cells also showed a lowest pro-oxidant effect induced by the four CFS of GMG fermented by lactic acid bacteria and bifidobacteria.	glucose-mannose-glucose	136-139	superoxide dismutase 2	Homo sapiens	31-36
28400010-9	2017	Supporting these founding, the SOD-2 gene expression of Caco-2 cells also showed a lowest pro-oxidant effect induced by the four CFS of GMG fermented by lactic acid bacteria and bifidobacteria.	Lactic Acid	153-164	superoxide dismutase 2	Homo sapiens	31-36
28616679-15	2017	In addition, we will discuss how H2O2 formation in mitochondria depends on and is controlled by MnSOD.	Hydrogen Peroxide	33-37	superoxide dismutase 2	Homo sapiens	96-101
28756653-3	2017	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products.	Reactive Oxygen Species	97-100	superoxide dismutase 2	Homo sapiens	0-30
28756653-3	2017	Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products.	Reactive Oxygen Species	97-100	superoxide dismutase 2	Homo sapiens	32-37
28756653-4	2017	In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury.	Hydrogen Peroxide	64-81	superoxide dismutase 2	Homo sapiens	35-40
27389776-6	2017	We found that T-I pretreatment significantly protected mitochondria against PQ-induced redox impairment through an Nrf2-dependent mechanism involving upregulation of antioxidant enzymes, such as Mn-superoxide dismutase (Mn-SOD), glutathione peroxidase (GPx), and both catalytic and modifier subunits of gamma-glutamate-cysteine ligase (gamma-GCL).	Paraquat	76-78	superoxide dismutase 2	Homo sapiens	195-218
27389776-6	2017	We found that T-I pretreatment significantly protected mitochondria against PQ-induced redox impairment through an Nrf2-dependent mechanism involving upregulation of antioxidant enzymes, such as Mn-superoxide dismutase (Mn-SOD), glutathione peroxidase (GPx), and both catalytic and modifier subunits of gamma-glutamate-cysteine ligase (gamma-GCL).	Paraquat	76-78	superoxide dismutase 2	Homo sapiens	220-226
28214706-7	2017	Moreover, the lower pO2 was associated with lower glutathione content, the induction of p66 Shc and Mn-SOD proteins, and increased SOD activity only in HepG2.	PO-2	20-23	superoxide dismutase 2	Homo sapiens	100-106
28214706-7	2017	Moreover, the lower pO2 was associated with lower glutathione content, the induction of p66 Shc and Mn-SOD proteins, and increased SOD activity only in HepG2.	PO-2	20-23	superoxide dismutase 2	Homo sapiens	103-106
28231483-3	2017	Here, we demonstrate that, in transgenic mice expressing the human manganese superoxide dismutase (MnSOD) gene, a scavenger of ROS in mitochondria, the number and function of mouse hematopoietic stem/progenitor cells (HSPC) under physiological conditions are enhanced.	Reactive Oxygen Species	127-130	superoxide dismutase 2	Homo sapiens	67-97
28231483-3	2017	Here, we demonstrate that, in transgenic mice expressing the human manganese superoxide dismutase (MnSOD) gene, a scavenger of ROS in mitochondria, the number and function of mouse hematopoietic stem/progenitor cells (HSPC) under physiological conditions are enhanced.	Reactive Oxygen Species	127-130	superoxide dismutase 2	Homo sapiens	99-104
28869736-1	2017	Superoxide dismutase (SOD) family is necessary to protect cells from the toxicity of reactive oxygen species produced during normal metabolism.	Reactive Oxygen Species	85-108	superoxide dismutase 2	Homo sapiens	22-25
28869736-4	2017	DNA construct was then transformed into Escherichia coli BL21 (DE3) and expression was induced with IPTG at 25 C. The recombinant fusion protein GST-SOD2 (46 kDa) was purified from the bacterial lysate by GST resin column affinity chromatography.	Isopropyl Thiogalactoside	100-104	superoxide dismutase 2	Homo sapiens	149-153
28869736-5	2017	GST tag was cleaved with thrombin, and a crude SOD2 recombinant protein (25 kDa) was obtained and further purified by heparin affinity chromatography.	Heparin	118-125	superoxide dismutase 2	Homo sapiens	47-51
28720775-5	2017	Metformin alleviated NAPDH oxidase- and mitochondria-mediated ROS production with an increase in superoxide dismutase (SOD) activity and SOD2 expression.	Metformin	0-9	superoxide dismutase 2	Homo sapiens	137-141
28978113-10	2017	PKM2, a miR-138 target gene, enhances the metastatic potential of TSCC through the SOD2-H2O2 pathway.	Hydrogen Peroxide	88-92	superoxide dismutase 2	Homo sapiens	83-87
29245915-7	2017	Curcumin and sildenafil exposure reduced the expression of MCL-1, BCL-XL, thioredoxin and superoxide dismutase 2 (SOD2) in an eIF2alpha-dependent fashion.	Curcumin	0-8	superoxide dismutase 2	Homo sapiens	114-118
29245915-7	2017	Curcumin and sildenafil exposure reduced the expression of MCL-1, BCL-XL, thioredoxin and superoxide dismutase 2 (SOD2) in an eIF2alpha-dependent fashion.	Sildenafil Citrate	13-23	superoxide dismutase 2	Homo sapiens	90-112
29245915-7	2017	Curcumin and sildenafil exposure reduced the expression of MCL-1, BCL-XL, thioredoxin and superoxide dismutase 2 (SOD2) in an eIF2alpha-dependent fashion.	Sildenafil Citrate	13-23	superoxide dismutase 2	Homo sapiens	114-118
29245915-8	2017	Curcumin and sildenafil interacted in a greater than additive fashion to increase the levels of reactive oxygen species; knock down of thioredoxin or SOD2 enhanced killing and over-expression of thioredoxin or SOD2 suppressed killing.	Curcumin	0-8	superoxide dismutase 2	Homo sapiens	210-214
29245915-8	2017	Curcumin and sildenafil interacted in a greater than additive fashion to increase the levels of reactive oxygen species; knock down of thioredoxin or SOD2 enhanced killing and over-expression of thioredoxin or SOD2 suppressed killing.	Sildenafil Citrate	13-23	superoxide dismutase 2	Homo sapiens	150-154
28506746-11	2017	Next, we transfected BL-Sir2 into H2O2-induced oxidative damage of 293T cells, BL-Sir2 increased the activity of manganese superoxide dismutase (MnSOD/SOD2) and catalase (CAT) and reduced reactive oxygen species(ROS).	Hydrogen Peroxide	34-38	superoxide dismutase 2	Homo sapiens	145-150
28414098-11	2017	The essential role of mitochondrial ROS was confirmed by the protective effect of overexpression of manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	36-39	superoxide dismutase 2	Homo sapiens	100-130
28414098-11	2017	The essential role of mitochondrial ROS was confirmed by the protective effect of overexpression of manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	36-39	superoxide dismutase 2	Homo sapiens	132-137
28506746-11	2017	Next, we transfected BL-Sir2 into H2O2-induced oxidative damage of 293T cells, BL-Sir2 increased the activity of manganese superoxide dismutase (MnSOD/SOD2) and catalase (CAT) and reduced reactive oxygen species(ROS).	Hydrogen Peroxide	34-38	superoxide dismutase 2	Homo sapiens	151-155
28506746-11	2017	Next, we transfected BL-Sir2 into H2O2-induced oxidative damage of 293T cells, BL-Sir2 increased the activity of manganese superoxide dismutase (MnSOD/SOD2) and catalase (CAT) and reduced reactive oxygen species(ROS).	Reactive Oxygen Species	188-211	superoxide dismutase 2	Homo sapiens	145-150
28506746-11	2017	Next, we transfected BL-Sir2 into H2O2-induced oxidative damage of 293T cells, BL-Sir2 increased the activity of manganese superoxide dismutase (MnSOD/SOD2) and catalase (CAT) and reduced reactive oxygen species(ROS).	Reactive Oxygen Species	212-215	superoxide dismutase 2	Homo sapiens	145-150
28461152-2	2017	The azide anion is a potent competitive inhibitor that binds directly to the metal and is used as a substrate analog to superoxide in studies of SOD.	Azides	4-15	superoxide dismutase 2	Homo sapiens	145-148
28461152-2	2017	The azide anion is a potent competitive inhibitor that binds directly to the metal and is used as a substrate analog to superoxide in studies of SOD.	Superoxides	120-130	superoxide dismutase 2	Homo sapiens	145-148
28461152-3	2017	The crystal structure of human MnSOD-azide complex was solved and shows the putative binding position of superoxide, providing a model for binding to the active site.	Azides	37-42	superoxide dismutase 2	Homo sapiens	31-36
28461152-3	2017	The crystal structure of human MnSOD-azide complex was solved and shows the putative binding position of superoxide, providing a model for binding to the active site.	Superoxides	105-115	superoxide dismutase 2	Homo sapiens	31-36
28398002-3	2017	Here, we demonstrate that an increase in superoxide anion radicals due to superoxide dismutase 2 (Sod2) deficiency in stromal precursor cells suppress osteogenic and adipogenic differentiation through fundamental changes in the global metabolite landscape.	Superoxides	41-66	superoxide dismutase 2	Homo sapiens	74-96
28398002-3	2017	Here, we demonstrate that an increase in superoxide anion radicals due to superoxide dismutase 2 (Sod2) deficiency in stromal precursor cells suppress osteogenic and adipogenic differentiation through fundamental changes in the global metabolite landscape.	Superoxides	41-66	superoxide dismutase 2	Homo sapiens	98-102
28398002-4	2017	Our data identify impairment of the pyruvate and l-glutamine metabolism causing toxic accumulation of alpha-ketoglutarate in the Sod2-deficient and intrinsically aged stromal precursor cells as a major cause for their reduced lineage differentiation.	Glutamine	49-60	superoxide dismutase 2	Homo sapiens	129-133
28398002-4	2017	Our data identify impairment of the pyruvate and l-glutamine metabolism causing toxic accumulation of alpha-ketoglutarate in the Sod2-deficient and intrinsically aged stromal precursor cells as a major cause for their reduced lineage differentiation.	Ketoglutaric Acids	102-121	superoxide dismutase 2	Homo sapiens	129-133
28398002-5	2017	Alpha-ketoglutarate accumulation led to enhanced nucleocytoplasmic vacuolation and chromatin condensation-mediated cell death in Sod2-deficient stromal precursor cells as a consequence of DNA damage, Hif-1alpha instability, and reduced histone H3 (Lys27) acetylation.	Ketoglutaric Acids	0-19	superoxide dismutase 2	Homo sapiens	129-133
28977893-3	2017	In the effort to develop an efficient strategy for the removal of the EBV virus, we have shown that betulinic acid (BA) slightly suppresses EBV replication through SOD2 suppression with subsequent reactive oxygen species (ROS) generation and DNA damage in EBV-transformed LCL (lymphoblastoid cell line) cells.	betulinic acid	100-114	superoxide dismutase 2	Homo sapiens	164-168
28977893-3	2017	In the effort to develop an efficient strategy for the removal of the EBV virus, we have shown that betulinic acid (BA) slightly suppresses EBV replication through SOD2 suppression with subsequent reactive oxygen species (ROS) generation and DNA damage in EBV-transformed LCL (lymphoblastoid cell line) cells.	betulinic acid	116-118	superoxide dismutase 2	Homo sapiens	164-168
28243746-10	2017	In PC-3 tumors, combination therapy with RT plus naftopidil suppressed the upregulation of RT-induced MnSOD expression.	naftopidil	49-59	superoxide dismutase 2	Homo sapiens	102-107
28595382-0	2017	Anti-inflammatory properties of Bifidobacterium longum expressing human manganese superoxide dismutase using the TNBS-induced rats model of colitis.	Trinitrobenzenesulfonic Acid	113-117	superoxide dismutase 2	Homo sapiens	72-102
28587495-1	2017	Manganese superoxide dismutase (MnSOD) is a mitochondrial-resident enzyme that reduces superoxide to hydrogen peroxide (H2O2), which can be further reduced to water by glutathione peroxidase (GPX1).	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
28587495-1	2017	Manganese superoxide dismutase (MnSOD) is a mitochondrial-resident enzyme that reduces superoxide to hydrogen peroxide (H2O2), which can be further reduced to water by glutathione peroxidase (GPX1).	Hydrogen Peroxide	101-118	superoxide dismutase 2	Homo sapiens	0-30
28587495-1	2017	Manganese superoxide dismutase (MnSOD) is a mitochondrial-resident enzyme that reduces superoxide to hydrogen peroxide (H2O2), which can be further reduced to water by glutathione peroxidase (GPX1).	Hydrogen Peroxide	101-118	superoxide dismutase 2	Homo sapiens	32-37
28587495-1	2017	Manganese superoxide dismutase (MnSOD) is a mitochondrial-resident enzyme that reduces superoxide to hydrogen peroxide (H2O2), which can be further reduced to water by glutathione peroxidase (GPX1).	Hydrogen Peroxide	120-124	superoxide dismutase 2	Homo sapiens	0-30
28587495-1	2017	Manganese superoxide dismutase (MnSOD) is a mitochondrial-resident enzyme that reduces superoxide to hydrogen peroxide (H2O2), which can be further reduced to water by glutathione peroxidase (GPX1).	Hydrogen Peroxide	120-124	superoxide dismutase 2	Homo sapiens	32-37
28587495-1	2017	Manganese superoxide dismutase (MnSOD) is a mitochondrial-resident enzyme that reduces superoxide to hydrogen peroxide (H2O2), which can be further reduced to water by glutathione peroxidase (GPX1).	Water	159-164	superoxide dismutase 2	Homo sapiens	0-30
28587495-1	2017	Manganese superoxide dismutase (MnSOD) is a mitochondrial-resident enzyme that reduces superoxide to hydrogen peroxide (H2O2), which can be further reduced to water by glutathione peroxidase (GPX1).	Water	159-164	superoxide dismutase 2	Homo sapiens	32-37
28614802-7	2017	Elevated ROS was associated with downregulated mitochondrial SOD2.	ros	9-12	superoxide dismutase 2	Homo sapiens	61-65
28492332-1	2017	Manganese(II) pentaazamacrocyclic complexes (MnPAMs) can act as small-molecule mimics of manganese superoxide dismutase (MnSOD) with potential therapeutic application in conditions linked to oxidative stress.	manganese(ii) pentaazamacrocyclic	0-33	superoxide dismutase 2	Homo sapiens	89-119
28492332-1	2017	Manganese(II) pentaazamacrocyclic complexes (MnPAMs) can act as small-molecule mimics of manganese superoxide dismutase (MnSOD) with potential therapeutic application in conditions linked to oxidative stress.	manganese(ii) pentaazamacrocyclic	0-33	superoxide dismutase 2	Homo sapiens	121-126
28456571-4	2017	EPO was found to upregulate SIRT1 activity and protein expression to reverse DOX-induced acetylation of PGC-1alpha and suppression of a suite of PGC-1alpha-activated genes involved in mitochondrial function and biogenesis, such as nuclear respiratory factor-1 (NRF1), mitochondrial transcription factor A (TFAM), citrate synthase (CS), superoxide dismutase 2 (SOD2), cytochrome c oxidase IV (COXIV), and voltage-dependent anion channel (VDAC).	Doxorubicin	77-80	superoxide dismutase 2	Homo sapiens	336-358
28456571-4	2017	EPO was found to upregulate SIRT1 activity and protein expression to reverse DOX-induced acetylation of PGC-1alpha and suppression of a suite of PGC-1alpha-activated genes involved in mitochondrial function and biogenesis, such as nuclear respiratory factor-1 (NRF1), mitochondrial transcription factor A (TFAM), citrate synthase (CS), superoxide dismutase 2 (SOD2), cytochrome c oxidase IV (COXIV), and voltage-dependent anion channel (VDAC).	Doxorubicin	77-80	superoxide dismutase 2	Homo sapiens	360-364
28364598-3	2017	The present research intended to study the anti-aging and anti-inflammatory effects of the drug G2013 (guluronic acid) at low and high doses on the genes expression of a number of enzymes involved in oxidative stress (including SOD2, GPX1, CAT, GST, iNOS, and MPO) in peripheral blood mononuclear cells (PBMCs) of healthy individuals under in vitro conditions.	guluronic acid	103-117	superoxide dismutase 2	Homo sapiens	228-232
28675952-4	2017	The expression of three antioxidant proteins, superoxide dismutase (SOD)-2, haem oxygenase (HO)-1, and sirtuin (SIRT) 1, was reduced upon H2O2 stimulation in miR-200c-overexpressed A549 cells.	Hydrogen Peroxide	138-142	superoxide dismutase 2	Homo sapiens	46-74
28243746-12	2017	Upregulation of RT-induced MnSOD expression was markedly suppressed by combination treatment with RT plus AKT inhibitor IV or naftopidil.	naftopidil	126-136	superoxide dismutase 2	Homo sapiens	27-32
27829319-5	2017	OBJECTIVE: Evaluation of Sig1R, SOD1, and SOD2 expression in different concentrations of oxygen (1%, 10%, 21%) in colon adenocarcinoma cell lines.	Oxygen	89-95	superoxide dismutase 2	Homo sapiens	42-46
27829319-10	2017	RESULTS: We observed significant changes in expression of Sig1R, SOD1, SOD2 due to different oxygen concentrations.	Oxygen	93-99	superoxide dismutase 2	Homo sapiens	71-75
28369333-6	2017	Site directed mutagenesis of lysine 68 to glutamine (K68Q), mimicking acetylation, decreased MnSOD activity in SNc dopaminergic neurons, whereas mutagenesis of lysine 68 to arginine (K68R), mimicking deacetylation, increased activity.	k68q	53-57	superoxide dismutase 2	Homo sapiens	93-98
27019981-4	2017	Here, we sought to determine a potential association between the variant rs4880 in SOD2 gene, a key mitochondrial enzyme that protects cells against ROS, and hepatotoxicity during asparaginase-based therapy in 224 patients enrolled on CALGB-10102, a treatment trial for adults with ALL.	Reactive Oxygen Species	149-152	superoxide dismutase 2	Homo sapiens	83-87
28369333-9	2017	Lastly, K68 acetylation of MnSOD was significantly increased in the SNc of PD patients.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	8-11	superoxide dismutase 2	Homo sapiens	27-32
28131761-7	2017	KEY FINDINGS: SIRT3 overexpression enhanced the ability of superoxide dismutase 2 (SOD2) to reduce cellular reactive oxygen species (ROS), which further decreased the damage to the membranes and the organelles of the cells, especially to mitochondria.	Reactive Oxygen Species	108-131	superoxide dismutase 2	Homo sapiens	59-81
28131761-7	2017	KEY FINDINGS: SIRT3 overexpression enhanced the ability of superoxide dismutase 2 (SOD2) to reduce cellular reactive oxygen species (ROS), which further decreased the damage to the membranes and the organelles of the cells, especially to mitochondria.	Reactive Oxygen Species	108-131	superoxide dismutase 2	Homo sapiens	83-87
28315685-9	2017	ABCB10 depletion upregulated ROS and the expression of ROS-detoxifying enzymes (SOD2, GSTA1, and GSTA2), and SESN3, a protein induced by ROS to protect the cell from oxidative stress.	Reactive Oxygen Species	55-58	superoxide dismutase 2	Homo sapiens	80-84
28131761-7	2017	KEY FINDINGS: SIRT3 overexpression enhanced the ability of superoxide dismutase 2 (SOD2) to reduce cellular reactive oxygen species (ROS), which further decreased the damage to the membranes and the organelles of the cells, especially to mitochondria.	Reactive Oxygen Species	133-136	superoxide dismutase 2	Homo sapiens	59-81
28131761-7	2017	KEY FINDINGS: SIRT3 overexpression enhanced the ability of superoxide dismutase 2 (SOD2) to reduce cellular reactive oxygen species (ROS), which further decreased the damage to the membranes and the organelles of the cells, especially to mitochondria.	Reactive Oxygen Species	133-136	superoxide dismutase 2	Homo sapiens	83-87
28131761-9	2017	In contrast, SIRT3 knockdown reduced the ability of SOD2 to increase cellular ROS which was directly correlated with stress-induced oxidative damage and ageing in PFFs.	Reactive Oxygen Species	78-81	superoxide dismutase 2	Homo sapiens	52-56
28482710-8	2017	Moreover, multiple regression analysis demonstrated that SOD2 genotype was a significant predictor of pre-training whole blood GPx activity and erythrocyte SOD activity (Val/Val &gt; Ala/Val &gt; Ala/Ala).	Alanine	183-186	superoxide dismutase 2	Homo sapiens	57-61
28482710-8	2017	Moreover, multiple regression analysis demonstrated that SOD2 genotype was a significant predictor of pre-training whole blood GPx activity and erythrocyte SOD activity (Val/Val &gt; Ala/Val &gt; Ala/Ala).	Alanine	183-186	superoxide dismutase 2	Homo sapiens	57-60
28315685-9	2017	ABCB10 depletion upregulated ROS and the expression of ROS-detoxifying enzymes (SOD2, GSTA1, and GSTA2), and SESN3, a protein induced by ROS to protect the cell from oxidative stress.	Reactive Oxygen Species	55-58	superoxide dismutase 2	Homo sapiens	80-84
28274879-2	2017	Recently, we have engineered a tri-functional enzyme, 6His-MnSOD-TAT/CAT-MnSOD (M-TAT/CM), with SOD, CAT and cell-permeable activities.	6his	54-58	superoxide dismutase 2	Homo sapiens	59-64
28274879-2	2017	Recently, we have engineered a tri-functional enzyme, 6His-MnSOD-TAT/CAT-MnSOD (M-TAT/CM), with SOD, CAT and cell-permeable activities.	6his	54-58	superoxide dismutase 2	Homo sapiens	73-78
28368283-4	2017	The crystal from which the human MnSOD data set was obtained is the crystal with the largest unit-cell edge (240 A) from which data have been collected via neutron diffraction to sufficient resolution (2.30 A) where hydrogen positions can be observed.	Hydrogen	216-224	superoxide dismutase 2	Homo sapiens	33-38
28237436-6	2017	cESG-TPPS was then further evaluated as a co-delivery system with siRNA for potential combination therapy, by charge-based condensation of an siRNA directed at reducing expression of manganese superoxide dismutase (Sod2) as a proof of principle target.	cesg-tpps	0-9	superoxide dismutase 2	Homo sapiens	183-213
28118753-3	2017	Leucine supplementation increased (p &lt; 0.05) MnSOD and T-AOC activities and decreased (p &lt; 0.05) the malondialdehyde content in the jejunum of IUGR piglets.	Leucine	0-7	superoxide dismutase 2	Homo sapiens	48-53
27714837-7	2017	Instead, ATP strengthened the antioxidative defense of astrocytes by inducing Cu/ZnSOD and MnSOD activities and by increasing their glutathione content.	Adenosine Triphosphate	9-12	superoxide dismutase 2	Homo sapiens	91-96
27721400-0	2017	Physical interaction of estrogen receptor with MnSOD: implication in mitochondrial O2.- upregulation and mTORC2 potentiation in estrogen-responsive breast cancer cells.	Oxygen	83-85	superoxide dismutase 2	Homo sapiens	47-52
27721400-3	2017	Manganese superoxide dismutase (MnSOD) is the principal mitochondrial attribute governing mitochondrial O2.- homeostasis, raising the possibility that its functional alteration could be instrumental in augmenting mitochondrial O2.- levels in breast cancer cells.	Oxygen	104-106	superoxide dismutase 2	Homo sapiens	0-30
27721400-3	2017	Manganese superoxide dismutase (MnSOD) is the principal mitochondrial attribute governing mitochondrial O2.- homeostasis, raising the possibility that its functional alteration could be instrumental in augmenting mitochondrial O2.- levels in breast cancer cells.	Oxygen	104-106	superoxide dismutase 2	Homo sapiens	32-37
27721400-3	2017	Manganese superoxide dismutase (MnSOD) is the principal mitochondrial attribute governing mitochondrial O2.- homeostasis, raising the possibility that its functional alteration could be instrumental in augmenting mitochondrial O2.- levels in breast cancer cells.	Oxygen	227-229	superoxide dismutase 2	Homo sapiens	0-30
27721400-3	2017	Manganese superoxide dismutase (MnSOD) is the principal mitochondrial attribute governing mitochondrial O2.- homeostasis, raising the possibility that its functional alteration could be instrumental in augmenting mitochondrial O2.- levels in breast cancer cells.	Oxygen	227-229	superoxide dismutase 2	Homo sapiens	32-37
27721400-7	2017	Acetylation at lysine-68 (K68) inhibits MnSOD catalytic activity and thus represents an important post-translational regulatory mechanism in human cells.	Lysine	15-21	superoxide dismutase 2	Homo sapiens	40-45
27721400-7	2017	Acetylation at lysine-68 (K68) inhibits MnSOD catalytic activity and thus represents an important post-translational regulatory mechanism in human cells.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	26-29	superoxide dismutase 2	Homo sapiens	40-45
27721400-9	2017	In addition, we also observed diminished interaction of MnSOD with sirtuin-3, the key mitochondrial deacetylase that deacetylates MnSOD at critical K68 and thereby activates it for scavenging O2.-.	Oxygen	192-194	superoxide dismutase 2	Homo sapiens	56-61
27721400-10	2017	Consequently, compromised deacetylation of MnSOD at K68 leading to its inhibition and a resultant buildup of O2.- within the mitochondria culminated in the activation of mTORC2.	Oxygen	109-111	superoxide dismutase 2	Homo sapiens	43-48
27424009-6	2017	Furthermore, total and mitochondrial reactive oxygen species levels were higher under basal conditions in cells overexpressing alpha-syn (-Dox) and this increase was apparently correlated with diminished levels and activities of SOD1 and SOD2 in -Dox cells.	Doxycycline	139-142	superoxide dismutase 2	Homo sapiens	238-242
27424009-6	2017	Furthermore, total and mitochondrial reactive oxygen species levels were higher under basal conditions in cells overexpressing alpha-syn (-Dox) and this increase was apparently correlated with diminished levels and activities of SOD1 and SOD2 in -Dox cells.	Doxycycline	247-250	superoxide dismutase 2	Homo sapiens	238-242
27322098-0	2017	Species-specific differences in peroxisome proliferation, catalase, and SOD2 upregulation as well as toxicity in human, mouse, and rat hepatoma cells induced by the explosive and environmental pollutant 2,4,6-trinitrotoluene.	Trinitrotoluene	203-224	superoxide dismutase 2	Homo sapiens	72-76
27322098-9	2017	TNT treatment caused an increase in catalase and SOD2 mRNA and protein levels in human and mouse, but not in rat cells.	Trinitrotoluene	0-3	superoxide dismutase 2	Homo sapiens	49-53
28198160-10	2017	Smoking was a risk factor in the development of IS for CAT TT and MnSOD Ala/Val genotypes; we found a 3.5- to 5.5-fold higher IS risk in CAT TT and MnSOD Ala/Val genotypes.	Alanine	72-75	superoxide dismutase 2	Homo sapiens	66-71
28198160-10	2017	Smoking was a risk factor in the development of IS for CAT TT and MnSOD Ala/Val genotypes; we found a 3.5- to 5.5-fold higher IS risk in CAT TT and MnSOD Ala/Val genotypes.	Alanine	154-157	superoxide dismutase 2	Homo sapiens	66-71
28198160-10	2017	Smoking was a risk factor in the development of IS for CAT TT and MnSOD Ala/Val genotypes; we found a 3.5- to 5.5-fold higher IS risk in CAT TT and MnSOD Ala/Val genotypes.	Alanine	154-157	superoxide dismutase 2	Homo sapiens	148-153
28315997-6	2017	Ruminant TFA, including tVA, tPA and the mixture of tVA and tPA, significantly reduced the TNF-alpha-induced gene expression of TNF, VCAM-1 and SOD2 in HUVEC, as well as TNF and IL-8 in HepG2 cells.	Trans Fatty Acids	9-12	superoxide dismutase 2	Homo sapiens	144-148
28315997-6	2017	Ruminant TFA, including tVA, tPA and the mixture of tVA and tPA, significantly reduced the TNF-alpha-induced gene expression of TNF, VCAM-1 and SOD2 in HUVEC, as well as TNF and IL-8 in HepG2 cells.	11-octadecenoic acid	24-27	superoxide dismutase 2	Homo sapiens	144-148
28315997-6	2017	Ruminant TFA, including tVA, tPA and the mixture of tVA and tPA, significantly reduced the TNF-alpha-induced gene expression of TNF, VCAM-1 and SOD2 in HUVEC, as well as TNF and IL-8 in HepG2 cells.	palmitoleic acid	29-32	superoxide dismutase 2	Homo sapiens	144-148
28315997-6	2017	Ruminant TFA, including tVA, tPA and the mixture of tVA and tPA, significantly reduced the TNF-alpha-induced gene expression of TNF, VCAM-1 and SOD2 in HUVEC, as well as TNF and IL-8 in HepG2 cells.	palmitoleic acid	60-63	superoxide dismutase 2	Homo sapiens	144-148
28092181-6	2017	The endogenous antioxidative enzyme gene (Sod1, Sod2, TRXR1 and Gpx1) expressions were escalated in both MSCs in response to reactive oxygen species elevation.	Reactive Oxygen Species	125-148	superoxide dismutase 2	Homo sapiens	48-52
28237436-7	2017	Simultaneous delivery of TPPS and siRNA was achieved, reducing Sod2 protein expression to 48%, while maintaining the photodynamic properties of TPPS under light exposure and maintaining low dark toxicity.	tetraphenylporphine sulfonate	25-29	superoxide dismutase 2	Homo sapiens	63-67
28208751-9	2017	Children with the GSTP1 (rs1695) AA and SOD2 (rs5746136) TT genotypes had higher MEHHP levels as compared to GG and CC types, respectively.	mono(2-ethyl-5-hydroxyhexyl) phthalate	81-86	superoxide dismutase 2	Homo sapiens	40-44
28222320-2	2017	The antioxidant enzymes manganese superoxide dismutase (SOD2), glutathione peroxidase 1 (GPX1) and catalase (CAT) represent the primary defence mechanism against reactive oxygen species (ROS).	Reactive Oxygen Species	162-185	superoxide dismutase 2	Homo sapiens	56-60
28222320-2	2017	The antioxidant enzymes manganese superoxide dismutase (SOD2), glutathione peroxidase 1 (GPX1) and catalase (CAT) represent the primary defence mechanism against reactive oxygen species (ROS).	Reactive Oxygen Species	187-190	superoxide dismutase 2	Homo sapiens	56-60
28038454-4	2017	Furthermore, by over-expression of MnSOD and GPx in cells, we show that ROS, and especially superoxide, is the primary oxidative species induced by intense heat stress and responsible for cell death.	Reactive Oxygen Species	72-75	superoxide dismutase 2	Homo sapiens	35-40
28038454-4	2017	Furthermore, by over-expression of MnSOD and GPx in cells, we show that ROS, and especially superoxide, is the primary oxidative species induced by intense heat stress and responsible for cell death.	Superoxides	92-102	superoxide dismutase 2	Homo sapiens	35-40
28028182-0	2017	Domain Mapping of Heat Shock Protein 70 Reveals That Glutamic Acid 446 and Arginine 447 Are Critical for Regulating Superoxide Dismutase 2 Function.	Glutamic Acid	53-66	superoxide dismutase 2	Homo sapiens	116-138
28028182-0	2017	Domain Mapping of Heat Shock Protein 70 Reveals That Glutamic Acid 446 and Arginine 447 Are Critical for Regulating Superoxide Dismutase 2 Function.	Arginine	75-83	superoxide dismutase 2	Homo sapiens	116-138
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Peptides	77-85	superoxide dismutase 2	Homo sapiens	22-26
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Peptides	77-85	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Peptides	77-85	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Peptides	77-85	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	geramt	61-67	superoxide dismutase 2	Homo sapiens	22-26
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	geramt	61-67	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	geramt	61-67	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	geramt	61-67	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Alanine	334-341	superoxide dismutase 2	Homo sapiens	22-26
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Alanine	334-341	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Alanine	334-341	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Alanine	334-341	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Glutamine	373-382	superoxide dismutase 2	Homo sapiens	22-26
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Glutamine	373-382	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Glutamine	373-382	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Glutamine	373-382	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Asparagine	386-396	superoxide dismutase 2	Homo sapiens	22-26
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Asparagine	386-396	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Asparagine	386-396	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	Asparagine	386-396	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	geramt	97-103	superoxide dismutase 2	Homo sapiens	22-26
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	geramt	97-103	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	geramt	97-103	superoxide dismutase 2	Homo sapiens	130-134
28028182-7	2017	This study shows that SOD2 specifically binds to hsp70 at 445GERAMT450 Small peptides containing GERAMT inhibited the transfer of SOD2 to the mitochondria and decreased SOD2 activity in vitro and in vivo To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.	geramt	97-103	superoxide dismutase 2	Homo sapiens	130-134
28152544-10	2017	Gene expression analyses demonstrated upregulation of SOD2 and CAT (ROS-detoxifying genes), and downregulation of DCK (gemcitabine-metabolising gene) in Gem-Exo-treated cells.	(1R,2S,3S,4R)-5-METHYLENECYCLOHEXANE-1,2,3,4-TETRAOL	157-160	superoxide dismutase 2	Homo sapiens	54-58
28152544-11	2017	SOD/CAT upregulation resulted, at least in part, from exosome-mediated transfer of their transcripts and they suppressed basal and gemcitabine-induced ROS production, and partly promoted chemoresistance.	gemcitabine	131-142	superoxide dismutase 2	Homo sapiens	0-3
28152544-11	2017	SOD/CAT upregulation resulted, at least in part, from exosome-mediated transfer of their transcripts and they suppressed basal and gemcitabine-induced ROS production, and partly promoted chemoresistance.	Reactive Oxygen Species	151-154	superoxide dismutase 2	Homo sapiens	0-3
28208751-11	2017	As MEHHP concentrations were dependent on GSTP1 and SOD2, but the assessment of interaction requires independent variables, we estimated MEHHP residuals and assessed their interaction, showing that the OR for SOD2 TT was further elevated to 3.32 (1.75-6.32) when the residuals of MEHHP were high.	mono(2-ethyl-5-hydroxyhexyl) phthalate	3-8	superoxide dismutase 2	Homo sapiens	52-56
28208751-11	2017	As MEHHP concentrations were dependent on GSTP1 and SOD2, but the assessment of interaction requires independent variables, we estimated MEHHP residuals and assessed their interaction, showing that the OR for SOD2 TT was further elevated to 3.32 (1.75-6.32) when the residuals of MEHHP were high.	mono(2-ethyl-5-hydroxyhexyl) phthalate	3-8	superoxide dismutase 2	Homo sapiens	209-213
28208751-11	2017	As MEHHP concentrations were dependent on GSTP1 and SOD2, but the assessment of interaction requires independent variables, we estimated MEHHP residuals and assessed their interaction, showing that the OR for SOD2 TT was further elevated to 3.32 (1.75-6.32) when the residuals of MEHHP were high.	mono(2-ethyl-5-hydroxyhexyl) phthalate	137-142	superoxide dismutase 2	Homo sapiens	209-213
28208751-11	2017	As MEHHP concentrations were dependent on GSTP1 and SOD2, but the assessment of interaction requires independent variables, we estimated MEHHP residuals and assessed their interaction, showing that the OR for SOD2 TT was further elevated to 3.32 (1.75-6.32) when the residuals of MEHHP were high.	mono(2-ethyl-5-hydroxyhexyl) phthalate	137-142	superoxide dismutase 2	Homo sapiens	209-213
28208751-13	2017	Genetic variants of SOD2, considered to be reflect oxidative stress metabolisms, might modify the association of phthalate exposure with asthma.	phthalic acid	113-122	superoxide dismutase 2	Homo sapiens	20-24
28451559-0	2017	Effect of Sodium Arsenite on the Expression of Antioxidant Genes (SOD2 and CAT) in MCF-7 and Jurkat Cell Lines.	sodium arsenite	10-25	superoxide dismutase 2	Homo sapiens	66-70
28165386-1	2017	Manganese superoxide dismutase (MNSOD) is one of the major scavengers of reactive oxygen species (ROS) in mitochondria with pivotal regulatory role in ischemic disorders, inflammation and cancer.	Reactive Oxygen Species	73-96	superoxide dismutase 2	Homo sapiens	0-30
28165386-1	2017	Manganese superoxide dismutase (MNSOD) is one of the major scavengers of reactive oxygen species (ROS) in mitochondria with pivotal regulatory role in ischemic disorders, inflammation and cancer.	Reactive Oxygen Species	73-96	superoxide dismutase 2	Homo sapiens	32-37
28165386-1	2017	Manganese superoxide dismutase (MNSOD) is one of the major scavengers of reactive oxygen species (ROS) in mitochondria with pivotal regulatory role in ischemic disorders, inflammation and cancer.	Reactive Oxygen Species	98-101	superoxide dismutase 2	Homo sapiens	0-30
28165386-1	2017	Manganese superoxide dismutase (MNSOD) is one of the major scavengers of reactive oxygen species (ROS) in mitochondria with pivotal regulatory role in ischemic disorders, inflammation and cancer.	Reactive Oxygen Species	98-101	superoxide dismutase 2	Homo sapiens	32-37
28165386-5	2017	Markedly, oxidative modifications of MNSOD were identified at histidine (H54 and H55), tyrosine (Y58), tryptophan (W147, W149, W205 and W210) and asparagine (N206 and N209) residues additional to methionine.	Histidine	62-71	superoxide dismutase 2	Homo sapiens	37-42
28165386-5	2017	Markedly, oxidative modifications of MNSOD were identified at histidine (H54 and H55), tyrosine (Y58), tryptophan (W147, W149, W205 and W210) and asparagine (N206 and N209) residues additional to methionine.	Tyrosine	87-95	superoxide dismutase 2	Homo sapiens	37-42
28165386-5	2017	Markedly, oxidative modifications of MNSOD were identified at histidine (H54 and H55), tyrosine (Y58), tryptophan (W147, W149, W205 and W210) and asparagine (N206 and N209) residues additional to methionine.	Tryptophan	103-113	superoxide dismutase 2	Homo sapiens	37-42
28165386-5	2017	Markedly, oxidative modifications of MNSOD were identified at histidine (H54 and H55), tyrosine (Y58), tryptophan (W147, W149, W205 and W210) and asparagine (N206 and N209) residues additional to methionine.	Asparagine	146-156	superoxide dismutase 2	Homo sapiens	37-42
28165386-5	2017	Markedly, oxidative modifications of MNSOD were identified at histidine (H54 and H55), tyrosine (Y58), tryptophan (W147, W149, W205 and W210) and asparagine (N206 and N209) residues additional to methionine.	Methionine	196-206	superoxide dismutase 2	Homo sapiens	37-42
28165386-8	2017	Thus, LC-MS/MS analysis revealed multiple oxidative modifications of MNSOD at different amino acid residues that might mediate the regulation of the superoxide radicals, mitochondrial ROS scavenging and MNSOD activity in kidney cancer.	Superoxides	149-159	superoxide dismutase 2	Homo sapiens	69-74
28165386-8	2017	Thus, LC-MS/MS analysis revealed multiple oxidative modifications of MNSOD at different amino acid residues that might mediate the regulation of the superoxide radicals, mitochondrial ROS scavenging and MNSOD activity in kidney cancer.	Reactive Oxygen Species	184-187	superoxide dismutase 2	Homo sapiens	69-74
28451559-3	2017	The purpose of the present study was to evaluate the alteration of mRNA levels of catalase (CAT) and superoxide dismutase 2 (SOD2) in MCF-7 and Jurkat cells after exposure to NaAsO2.	sodium arsenite	175-181	superoxide dismutase 2	Homo sapiens	101-123
28451559-3	2017	The purpose of the present study was to evaluate the alteration of mRNA levels of catalase (CAT) and superoxide dismutase 2 (SOD2) in MCF-7 and Jurkat cells after exposure to NaAsO2.	sodium arsenite	175-181	superoxide dismutase 2	Homo sapiens	125-129
28451559-11	2017	Expression levels of SOD2 decreased in Jurkat cells and increased in MCF-7 cells after treatment with NaAsO2 (P&lt;0.05).	sodium arsenite	102-108	superoxide dismutase 2	Homo sapiens	21-25
28451559-12	2017	CONCLUSION: After cells exposure to NaAsO2, CAT mRNA level decreased in both examined cell lines but the alterations of SOD2 mRNA level is cell specific.	sodium arsenite	36-42	superoxide dismutase 2	Homo sapiens	120-124
28451559-13	2017	The NAC modulated the NaAsO2 associated alterations of CAT and SOD2 mRNA levels, therefore, the NaAsO2 might act through inducing reactive oxygen species.	Acetylcysteine	4-7	superoxide dismutase 2	Homo sapiens	63-67
28451559-13	2017	The NAC modulated the NaAsO2 associated alterations of CAT and SOD2 mRNA levels, therefore, the NaAsO2 might act through inducing reactive oxygen species.	sodium arsenite	22-28	superoxide dismutase 2	Homo sapiens	63-67
28451559-13	2017	The NAC modulated the NaAsO2 associated alterations of CAT and SOD2 mRNA levels, therefore, the NaAsO2 might act through inducing reactive oxygen species.	Reactive Oxygen Species	130-153	superoxide dismutase 2	Homo sapiens	63-67
28567457-0	2017	SIRT3-SOD2-ROS pathway is involved in linalool-induced glioma cell apoptotic death.	ros	11-14	superoxide dismutase 2	Homo sapiens	6-10
28381353-8	2017	Oppositely, caseins, a whey protein/casein mixture (1:4 w/w), and glutamine aggravated the TNF-alpha-induced TNF and SOD2 gene expression.	Glutamine	66-75	superoxide dismutase 2	Homo sapiens	117-121
27926482-0	2017	Hexokinase 2 enhances the metastatic potential of tongue squamous cell carcinoma via the SOD2-H2O2 pathway.	Hydrogen Peroxide	94-98	superoxide dismutase 2	Homo sapiens	89-93
27926482-9	2017	HK2 enhances the metastatic potential of TSCC by stimulating the SOD2-H2O2 pathway.	Hydrogen Peroxide	70-74	superoxide dismutase 2	Homo sapiens	65-69
28567457-7	2017	Linalool resulted in a concentration-dependent decrease of SOD activity but had no significant effect on mRNA and protein expression of SOD2.	linalool	0-8	superoxide dismutase 2	Homo sapiens	59-62
28567457-8	2017	Moreover, linalool resulted in a significant increase of the expression of acetylated SOD2.	linalool	10-18	superoxide dismutase 2	Homo sapiens	86-90
28567457-0	2017	SIRT3-SOD2-ROS pathway is involved in linalool-induced glioma cell apoptotic death.	linalool	38-46	superoxide dismutase 2	Homo sapiens	6-10
28567457-11	2017	Linalool treatment significantly decreased the interaction between SOD2 and SIRT3.	linalool	0-8	superoxide dismutase 2	Homo sapiens	67-71
28567457-13	2017	In summary, the data demonstrated that linalool exhibited inhibitory effect on glioma cells through regulation of SIRT3-SOD2-ROS signaling.	linalool	39-47	superoxide dismutase 2	Homo sapiens	120-124
29047081-6	2017	In parallel with these different cellular sites of superoxide production, the three SOD isoforms are also specifically localized to the cytosol (SOD1), mitochondria (SOD2) or extracellular compartment (SOD3).	Superoxides	51-61	superoxide dismutase 2	Homo sapiens	166-170
28567457-13	2017	In summary, the data demonstrated that linalool exhibited inhibitory effect on glioma cells through regulation of SIRT3-SOD2-ROS signaling.	ros	125-128	superoxide dismutase 2	Homo sapiens	120-124
27976481-5	2017	Accumulation of ROS and subsequent activation of NRF2, p53, AP-1 and NF-kappaB-dependent pathways, with downstream activation of antioxidant mechanisms (e.g., SOD2 and HMOX1 expression), is observed in the UV-treated cells.	Reactive Oxygen Species	16-19	superoxide dismutase 2	Homo sapiens	159-163
27923686-0	2017	Photoactivated hypericin increases the expression of SOD-2 and makes MCF-7 cells resistant to photodynamic therapy.	hypericin	15-24	superoxide dismutase 2	Homo sapiens	53-58
27923686-3	2017	The difference in the dynamics of reactive oxygen species after hypericin activation was related to increased activity of SOD-2 in MCF-7 cells compared to MDA-MB-231 cells.	Reactive Oxygen Species	34-57	superoxide dismutase 2	Homo sapiens	122-127
27923686-3	2017	The difference in the dynamics of reactive oxygen species after hypericin activation was related to increased activity of SOD-2 in MCF-7 cells compared to MDA-MB-231 cells.	hypericin	64-73	superoxide dismutase 2	Homo sapiens	122-127
27923686-4	2017	Indeed, photodynamic therapy with hypericin significantly increased SOD-2 activity in MCF-7 cells, but only slightly in MDA-MB-231 cells.	hypericin	34-43	superoxide dismutase 2	Homo sapiens	68-73
27923686-6	2017	The role of SOD-2 in the resistance of MCF-7 cells to photodynamic therapy with hypericin was monitored using SOD-2 inhibitor - 2-methoxyestradiol.	hypericin	80-89	superoxide dismutase 2	Homo sapiens	12-17
29234413-4	2017	In this study, we found that Sal significantly prevented MPP+-induced decrease of mRNA and protein expression of Nrf2, GCLc, SOD1, and SOD2 in SH-SY5Y cells.	rhodioloside	29-32	superoxide dismutase 2	Homo sapiens	135-139
29234413-4	2017	In this study, we found that Sal significantly prevented MPP+-induced decrease of mRNA and protein expression of Nrf2, GCLc, SOD1, and SOD2 in SH-SY5Y cells.	mangion-purified polysaccharide (Candida albicans)	57-61	superoxide dismutase 2	Homo sapiens	135-139
29234413-5	2017	Moreover, silencing of Nrf2 significantly inhibited Sal-induced increase in mRNA and protein expression of GCLc, SOD1, and SOD2.	rhodioloside	52-55	superoxide dismutase 2	Homo sapiens	123-127
29234413-9	2017	Moreover, silencing of DJ-1 significantly inhibited Sal-induced increase in mRNA and protein expression of Nrf2, GCLc, SOD1, and SOD2 in MPP+-treated SH-SY5Y cells.	rhodioloside	52-55	superoxide dismutase 2	Homo sapiens	129-133
29234413-9	2017	Moreover, silencing of DJ-1 significantly inhibited Sal-induced increase in mRNA and protein expression of Nrf2, GCLc, SOD1, and SOD2 in MPP+-treated SH-SY5Y cells.	mangion-purified polysaccharide (Candida albicans)	137-141	superoxide dismutase 2	Homo sapiens	129-133
28977782-10	2017	Moreover, EDA obviously attenuated the depolarization of  psim, reduced mitochondria-derived ROS production and increased SOD-2 activity, resulting in the suppression of NLRP3 inflammasome-mediated IL-1beta secretion in Abeta-treated microglia.	Edaravone	10-13	superoxide dismutase 2	Homo sapiens	122-127
27825800-9	2016	In addition, treatment with DHL-HisZn upregulated mRNA levels of endogenous antioxidants, such as glucose-6-phosphate dehydrogenase (G6PD), superoxide dismutase 2 (SOD2), catalase (CAT) and glutathione reductase (GR).	zinc histidine dithiooctanamide	28-37	superoxide dismutase 2	Homo sapiens	140-162
26993631-3	2017	In addition we tested also the hypothesis that CO can decrease the pre-existing condition of oxidative stress in the mouse model for the human medical condition systemic lupus erythematosus by increasing two protective enzymes heme-oxygenase-1 (HO-1), and superoxide dismutase-2 (SOD-2).	Carbon Monoxide	47-49	superoxide dismutase 2	Homo sapiens	256-278
26993631-3	2017	In addition we tested also the hypothesis that CO can decrease the pre-existing condition of oxidative stress in the mouse model for the human medical condition systemic lupus erythematosus by increasing two protective enzymes heme-oxygenase-1 (HO-1), and superoxide dismutase-2 (SOD-2).	Carbon Monoxide	47-49	superoxide dismutase 2	Homo sapiens	280-285
28100855-9	2016	Manganese, copper and zinc are a part of the group of superoxide dismutase enzymes (MnSOD, Cu/ZnSOD), which catalyse the superoxide anion dismutation into hydrogen peroxide and oxygen.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	84-89
28100855-9	2016	Manganese, copper and zinc are a part of the group of superoxide dismutase enzymes (MnSOD, Cu/ZnSOD), which catalyse the superoxide anion dismutation into hydrogen peroxide and oxygen.	Copper	11-17	superoxide dismutase 2	Homo sapiens	84-89
28100855-9	2016	Manganese, copper and zinc are a part of the group of superoxide dismutase enzymes (MnSOD, Cu/ZnSOD), which catalyse the superoxide anion dismutation into hydrogen peroxide and oxygen.	Superoxides	121-137	superoxide dismutase 2	Homo sapiens	84-89
28100855-9	2016	Manganese, copper and zinc are a part of the group of superoxide dismutase enzymes (MnSOD, Cu/ZnSOD), which catalyse the superoxide anion dismutation into hydrogen peroxide and oxygen.	Hydrogen Peroxide	155-172	superoxide dismutase 2	Homo sapiens	84-89
28100855-9	2016	Manganese, copper and zinc are a part of the group of superoxide dismutase enzymes (MnSOD, Cu/ZnSOD), which catalyse the superoxide anion dismutation into hydrogen peroxide and oxygen.	Oxygen	177-183	superoxide dismutase 2	Homo sapiens	84-89
27055786-12	2016	CONCLUSIONS: This meta-analysis indicated that the Ala allele of the MnSOD gene polymorphism increases prostate cancer susceptibility.	Alanine	51-54	superoxide dismutase 2	Homo sapiens	69-74
27737889-9	2016	In terms of redox-related resistance mechanism, our results suggest that STAT3 confers Dox resistance in ABC-DLBCLs by reinforcing an antioxidant program featuring upregulation of the SOD2 gene.	Doxorubicin	87-90	superoxide dismutase 2	Homo sapiens	184-188
27825800-9	2016	In addition, treatment with DHL-HisZn upregulated mRNA levels of endogenous antioxidants, such as glucose-6-phosphate dehydrogenase (G6PD), superoxide dismutase 2 (SOD2), catalase (CAT) and glutathione reductase (GR).	zinc histidine dithiooctanamide	28-37	superoxide dismutase 2	Homo sapiens	164-168
27258818-9	2016	Minor allele frequencies (C allele) of the MnSOD Val16Ala polymorphism (rs4880) in the normal glucose tolerance (NGT) and the T2D groups were 13.57% and 14.50%, respectively.	Glucose	94-101	superoxide dismutase 2	Homo sapiens	43-48
27435539-1	2016	Manganese superoxide dismutase (MnSOD) is a vital enzyme that protects cells from free radicals through eliminating superoxide radicals (O2-).	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
27640015-7	2016	Moreover, ganoderic acid A inhibits proliferation, viability, ROS, DPPH, and analyzed the expression of SOD1, SOD2, and SOD3 by Real time PCR in a PC-3 cell in a dose-dependent manner.	ganoderic acid A	10-26	superoxide dismutase 2	Homo sapiens	110-114
27435539-1	2016	Manganese superoxide dismutase (MnSOD) is a vital enzyme that protects cells from free radicals through eliminating superoxide radicals (O2-).	Superoxides	137-139	superoxide dismutase 2	Homo sapiens	0-30
27435539-1	2016	Manganese superoxide dismutase (MnSOD) is a vital enzyme that protects cells from free radicals through eliminating superoxide radicals (O2-).	Superoxides	137-139	superoxide dismutase 2	Homo sapiens	32-37
27694440-6	2016	Ectopic expression of superoxide dismutase 2 (SOD2) reduced ROS and preserved viability of TRPM2-depleted cells, however, failed to restore ATP levels.	Reactive Oxygen Species	60-63	superoxide dismutase 2	Homo sapiens	22-44
27694440-6	2016	Ectopic expression of superoxide dismutase 2 (SOD2) reduced ROS and preserved viability of TRPM2-depleted cells, however, failed to restore ATP levels.	Reactive Oxygen Species	60-63	superoxide dismutase 2	Homo sapiens	46-50
28175303-4	2016	Treatment with the benzamide HDAC inhibitor 109 significantly upregulated FXN expression and increased Fe-S and lipoic acid-containing protein levels, downregulated SOD2 levels, normalized LIP and ROS levels, and almost fully protected FRDA neurons from oxidative stress-mediated cell death.	benzamide	19-28	superoxide dismutase 2	Homo sapiens	165-169
27847869-8	2016	Moreover, because of impaired MnSOD activity, ULM cells are sensitive to high levels of reactive oxygen species (ROS) and superoxide-generating compounds, resulting in decreased ULM cell viability.	Reactive Oxygen Species	88-111	superoxide dismutase 2	Homo sapiens	30-35
27847869-8	2016	Moreover, because of impaired MnSOD activity, ULM cells are sensitive to high levels of reactive oxygen species (ROS) and superoxide-generating compounds, resulting in decreased ULM cell viability.	Reactive Oxygen Species	113-116	superoxide dismutase 2	Homo sapiens	30-35
27847869-8	2016	Moreover, because of impaired MnSOD activity, ULM cells are sensitive to high levels of reactive oxygen species (ROS) and superoxide-generating compounds, resulting in decreased ULM cell viability.	Superoxides	122-132	superoxide dismutase 2	Homo sapiens	30-35
27753498-2	2016	We designed a new assay based on microbead linked enzymatic generation of CdS QDs (Microbead QD-ELISA) and employed it in optical and electrochemical affinity assays for the cancer biomarker superoxide dismutase 2 (SOD2).	Cadmium	74-77	superoxide dismutase 2	Homo sapiens	191-213
27753498-2	2016	We designed a new assay based on microbead linked enzymatic generation of CdS QDs (Microbead QD-ELISA) and employed it in optical and electrochemical affinity assays for the cancer biomarker superoxide dismutase 2 (SOD2).	Cadmium	74-77	superoxide dismutase 2	Homo sapiens	215-219
27753498-3	2016	Biotinylated antibodies against SOD2 were immobilized on the surface of polyvinyl chloride microbeads bearing streptavidin.	Polyvinyl Chloride	72-90	superoxide dismutase 2	Homo sapiens	32-36
27753498-8	2016	The electrochemical assay based on the detection with square-wave voltammograms of Cd2+ ions originating from immobilized CdS QDs showed linearity up to 45 ng mL-1, and the limit of SOD2 detection equal to 0.44 ng mL-1 (1.96 x 10-11 M).	cds qds	122-129	superoxide dismutase 2	Homo sapiens	182-186
27799786-3	2016	The experiments in vitro showed that ZD55-MnSOD enhances cisplatin-induced apoptosis and causes remarkable ovarian cancer cell death.	Cisplatin	57-66	superoxide dismutase 2	Homo sapiens	42-47
26970173-10	2016	Collectively, our study demonstrated that the levels of hsp27 together with MnSOD, TXNRD2, GSH, and Gpx were significantly upregulated by H2 O2 in thyroid tumors.	Hydrogen Peroxide	138-143	superoxide dismutase 2	Homo sapiens	76-81
26882122-2	2016	Superoxide anions are metabolized by manganese-dependent superoxide dismutase (MnSOD or SOD2) in the mitochondria.	Superoxides	0-17	superoxide dismutase 2	Homo sapiens	79-84
26882122-2	2016	Superoxide anions are metabolized by manganese-dependent superoxide dismutase (MnSOD or SOD2) in the mitochondria.	Superoxides	0-17	superoxide dismutase 2	Homo sapiens	88-92
26882122-3	2016	In humans, there is a gene polymorphism where a change of alanine (Ala) to valine (Val) occurs at the 16th amino acid (Ala16Val-SOD2).	Alanine	58-65	superoxide dismutase 2	Homo sapiens	128-132
26882122-3	2016	In humans, there is a gene polymorphism where a change of alanine (Ala) to valine (Val) occurs at the 16th amino acid (Ala16Val-SOD2).	Alanine	67-70	superoxide dismutase 2	Homo sapiens	128-132
26882122-3	2016	In humans, there is a gene polymorphism where a change of alanine (Ala) to valine (Val) occurs at the 16th amino acid (Ala16Val-SOD2).	Valine	75-81	superoxide dismutase 2	Homo sapiens	128-132
26882122-3	2016	In humans, there is a gene polymorphism where a change of alanine (Ala) to valine (Val) occurs at the 16th amino acid (Ala16Val-SOD2).	Valine	83-86	superoxide dismutase 2	Homo sapiens	128-132
26882122-6	2016	The findings indicate that the VV patients who present a low-efficiency SOD2 enzyme exhibit an attenuated response to rosuvastatin compared with the A-allele patients.	Rosuvastatin Calcium	118-130	superoxide dismutase 2	Homo sapiens	72-76
27799786-5	2016	In addition, the cytotoxicity caused by ZD55-MnSOD to normal cells was examined by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay and western blot analysis.	3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide	87-152	superoxide dismutase 2	Homo sapiens	45-50
27799786-7	2016	In summary, we have demonstrated that ZD55-MnSOD can sensitize human ovarian cancer cells to cisplatin-induced cell death and apoptosis in vitro and in vivo.	Cisplatin	93-102	superoxide dismutase 2	Homo sapiens	43-48
27253232-7	2016	Streptozotocin and alloxan up-regulated transcription of genes, SOD1 and SOD2 (antioxidant enzymes).	Streptozocin	0-14	superoxide dismutase 2	Homo sapiens	73-77
27583978-6	2016	It was further demonstrated that both the penetration of cells and enzymatic activity of MnSOD are essential to its inhibitory function, because only TAT-MnSOD wt, not inactive TAT-MnSOD mutant or MnSOD could successfully inhibit cell proliferation and reduce the intra-celluar reactive oxygen species (ROS).	Reactive Oxygen Species	278-301	superoxide dismutase 2	Homo sapiens	89-94
27583978-6	2016	It was further demonstrated that both the penetration of cells and enzymatic activity of MnSOD are essential to its inhibitory function, because only TAT-MnSOD wt, not inactive TAT-MnSOD mutant or MnSOD could successfully inhibit cell proliferation and reduce the intra-celluar reactive oxygen species (ROS).	Reactive Oxygen Species	278-301	superoxide dismutase 2	Homo sapiens	154-159
27583978-6	2016	It was further demonstrated that both the penetration of cells and enzymatic activity of MnSOD are essential to its inhibitory function, because only TAT-MnSOD wt, not inactive TAT-MnSOD mutant or MnSOD could successfully inhibit cell proliferation and reduce the intra-celluar reactive oxygen species (ROS).	Reactive Oxygen Species	278-301	superoxide dismutase 2	Homo sapiens	154-159
27583978-6	2016	It was further demonstrated that both the penetration of cells and enzymatic activity of MnSOD are essential to its inhibitory function, because only TAT-MnSOD wt, not inactive TAT-MnSOD mutant or MnSOD could successfully inhibit cell proliferation and reduce the intra-celluar reactive oxygen species (ROS).	Reactive Oxygen Species	278-301	superoxide dismutase 2	Homo sapiens	154-159
27583978-6	2016	It was further demonstrated that both the penetration of cells and enzymatic activity of MnSOD are essential to its inhibitory function, because only TAT-MnSOD wt, not inactive TAT-MnSOD mutant or MnSOD could successfully inhibit cell proliferation and reduce the intra-celluar reactive oxygen species (ROS).	Reactive Oxygen Species	303-306	superoxide dismutase 2	Homo sapiens	89-94
27583978-6	2016	It was further demonstrated that both the penetration of cells and enzymatic activity of MnSOD are essential to its inhibitory function, because only TAT-MnSOD wt, not inactive TAT-MnSOD mutant or MnSOD could successfully inhibit cell proliferation and reduce the intra-celluar reactive oxygen species (ROS).	Reactive Oxygen Species	303-306	superoxide dismutase 2	Homo sapiens	154-159
27583978-6	2016	It was further demonstrated that both the penetration of cells and enzymatic activity of MnSOD are essential to its inhibitory function, because only TAT-MnSOD wt, not inactive TAT-MnSOD mutant or MnSOD could successfully inhibit cell proliferation and reduce the intra-celluar reactive oxygen species (ROS).	Reactive Oxygen Species	303-306	superoxide dismutase 2	Homo sapiens	154-159
27583978-6	2016	It was further demonstrated that both the penetration of cells and enzymatic activity of MnSOD are essential to its inhibitory function, because only TAT-MnSOD wt, not inactive TAT-MnSOD mutant or MnSOD could successfully inhibit cell proliferation and reduce the intra-celluar reactive oxygen species (ROS).	Reactive Oxygen Species	303-306	superoxide dismutase 2	Homo sapiens	154-159
27591796-6	2016	In addition, levels of the Nrf2 targets MnSOD, catalase, heme oxygenase-1, glutamate cysteine ligase and Hsp70 increased at 40 C. Levels of these Nrf2 targets were enhanced by Nrf2 activator oltipraz and decreased by shRNA targeting Nrf2.	oltipraz	191-199	superoxide dismutase 2	Homo sapiens	40-45
27253232-8	2016	Ninhydrin and hydrogen peroxide up-regulated SOD2 transcription, whereas alloxan and hydrogen peroxide increased CAT transcription.	Ninhydrin	0-9	superoxide dismutase 2	Homo sapiens	45-49
27253232-8	2016	Ninhydrin and hydrogen peroxide up-regulated SOD2 transcription, whereas alloxan and hydrogen peroxide increased CAT transcription.	Hydrogen Peroxide	14-31	superoxide dismutase 2	Homo sapiens	45-49
30034766-2	2016	Intracellular H2O2 is formed mainly via the catalytic dismutation of O2 - by SODs including SOD1, SOD2 and SOD3.	Hydrogen Peroxide	14-18	superoxide dismutase 2	Homo sapiens	98-102
27325180-4	2016	The rs4880 encodes Ala16Val in SOD2 and the Val variant has been demonstrated to be functionally less efficient than the Ala variant.	Valine	24-27	superoxide dismutase 2	Homo sapiens	31-35
27325180-4	2016	The rs4880 encodes Ala16Val in SOD2 and the Val variant has been demonstrated to be functionally less efficient than the Ala variant.	Alanine	19-22	superoxide dismutase 2	Homo sapiens	31-35
27325180-5	2016	We assessed the impact of SOD2-rs4880 variants on the time to progression (TTP) and overall survival (OS) on ADT using multivariable Cox regression.	adt	109-112	superoxide dismutase 2	Homo sapiens	26-30
27489133-6	2016	RSV (2 muM) pretreatment not only recovered the activity of MnSOD, but also improved ZEA-induced cytotoxicity evidenced by increased MMP and cell viability, and decreased ROS.	Resveratrol	0-3	superoxide dismutase 2	Homo sapiens	60-65
27722009-6	2016	Furthermore, SIRT3 deficiency in cisplatin-injured cells prevented PARP1 inhibition-induced increase in forkhead box O3a transcriptional activity, and upregulation of MnSOD and catalase.	Cisplatin	33-42	superoxide dismutase 2	Homo sapiens	167-172
27207918-0	2016	Association of Superoxide Dismutase 2 (SOD2) Genotype with Gray Matter Volume Shrinkage in Chronic Alcohol Users: Replication and Further Evaluation of an Addiction Gene Panel.	Alcohols	99-106	superoxide dismutase 2	Homo sapiens	15-37
27207918-0	2016	Association of Superoxide Dismutase 2 (SOD2) Genotype with Gray Matter Volume Shrinkage in Chronic Alcohol Users: Replication and Further Evaluation of an Addiction Gene Panel.	Alcohols	99-106	superoxide dismutase 2	Homo sapiens	39-43
27207918-2	2016	High variance in the degree of gray matter tissue shrinkage among alcohol-dependent individuals and a previous neuroimaging genetics report suggest the involvement of environmental and/or genetic factors, such as superoxide dismutase 2 (SOD2).	Alcohols	66-73	superoxide dismutase 2	Homo sapiens	213-235
27207918-2	2016	High variance in the degree of gray matter tissue shrinkage among alcohol-dependent individuals and a previous neuroimaging genetics report suggest the involvement of environmental and/or genetic factors, such as superoxide dismutase 2 (SOD2).	Alcohols	66-73	superoxide dismutase 2	Homo sapiens	237-241
27207918-6	2016	RESULTS: We replicated a significant association of a functional SOD2 single nucleotide polymorphism with normalized gray matter volume, which had been reported previously in an independent smaller sample of alcohol-dependent individuals.	Alcohols	208-215	superoxide dismutase 2	Homo sapiens	65-69
27207918-9	2016	CONCLUSION: Converging independent evidence for a SOD2 gene association with gray matter volume shrinkage in chronic alcohol users suggests that SOD2 genetic variants predict differential brain volume loss mediated by free radicals.	Alcohols	117-124	superoxide dismutase 2	Homo sapiens	50-54
27207918-9	2016	CONCLUSION: Converging independent evidence for a SOD2 gene association with gray matter volume shrinkage in chronic alcohol users suggests that SOD2 genetic variants predict differential brain volume loss mediated by free radicals.	Alcohols	117-124	superoxide dismutase 2	Homo sapiens	145-149
27722009-3	2016	Exposure to 400 microM cisplatin for 8 hours in cells decreased activity and expression of manganese superoxide dismutase (MnSOD), catalase, glutathione peroxidase (GPX), and SIRT3, while it increased their lysine acetylation.	Cisplatin	23-32	superoxide dismutase 2	Homo sapiens	91-121
27722009-3	2016	Exposure to 400 microM cisplatin for 8 hours in cells decreased activity and expression of manganese superoxide dismutase (MnSOD), catalase, glutathione peroxidase (GPX), and SIRT3, while it increased their lysine acetylation.	Cisplatin	23-32	superoxide dismutase 2	Homo sapiens	123-128
27332950-0	2016	Chikusetsu saponin V attenuates H2O2-induced oxidative stress in human neuroblastoma SH-SY5Y cells through Sirt1/PGC-1alpha/Mn-SOD signaling pathways.	Saponins	11-18	superoxide dismutase 2	Homo sapiens	124-130
27332950-0	2016	Chikusetsu saponin V attenuates H2O2-induced oxidative stress in human neuroblastoma SH-SY5Y cells through Sirt1/PGC-1alpha/Mn-SOD signaling pathways.	Hydrogen Peroxide	32-36	superoxide dismutase 2	Homo sapiens	124-130
27332950-5	2016	Our data showed that CsV attenuated H2O2-induced cytotoxicity, inhibited ROS accumulation, increased the activities of superoxide dismutase (SOD) and GSH, and increased mitochondrial membrane potential dose-dependently.	chikusetsusaponin V	21-24	superoxide dismutase 2	Homo sapiens	141-144
27332950-6	2016	Further exploration of the mechanisms showed that CsV exhibited these effects through increasing the activation of oxidative-stress-associated factors including Sirt1, PGC-1alpha, and Mn-SOD.	chikusetsusaponin V	50-53	superoxide dismutase 2	Homo sapiens	184-190
27332950-8	2016	In conclusion, our study demonstrated that CsV exhibited neuroprotective effects possibly through Sirt1/PGC-1alpha/Mn-SOD signaling pathways.	chikusetsusaponin V	43-46	superoxide dismutase 2	Homo sapiens	115-121
27302388-3	2016	The aim of this study was to investigate the impact of common functional polymorphisms in the antioxidant genes SOD2, GPX1 and CAT, associated with a decreased capacity for defending against ROS, in patients with perinatal hypoxic-ischaemic encephalopathy (HIE).	Reactive Oxygen Species	191-194	superoxide dismutase 2	Homo sapiens	112-116
26935174-4	2016	Furthermore, these tumors exhibit aberrant manganese superoxide dismutase (MnSOD) acetylation at lysine 68 and lysine 122 and have abnormally high reactive oxygen species (ROS) levels, which have been observed in many types of breast cancer.	Lysine	97-103	superoxide dismutase 2	Homo sapiens	43-73
26935174-4	2016	Furthermore, these tumors exhibit aberrant manganese superoxide dismutase (MnSOD) acetylation at lysine 68 and lysine 122 and have abnormally high reactive oxygen species (ROS) levels, which have been observed in many types of breast cancer.	Lysine	97-103	superoxide dismutase 2	Homo sapiens	75-80
27400860-7	2016	Interestingly, using phenotypically distinct breast cancer cell lines, we provide evidence that constitutively high or induced expression of MnSOD promotes the EMT-like phenotype by way of a redox milieu predominantly driven by hydrogen peroxide (H2O2).	Hydrogen Peroxide	228-245	superoxide dismutase 2	Homo sapiens	141-146
26935174-6	2016	MnSOD, a primary mitochondrial detoxification enzyme, functions by scavenging excessive ROS from the mitochondria and maintaining mitochondrial and cellular homeostasis.	Reactive Oxygen Species	88-91	superoxide dismutase 2	Homo sapiens	0-5
27400860-7	2016	Interestingly, using phenotypically distinct breast cancer cell lines, we provide evidence that constitutively high or induced expression of MnSOD promotes the EMT-like phenotype by way of a redox milieu predominantly driven by hydrogen peroxide (H2O2).	Hydrogen Peroxide	247-251	superoxide dismutase 2	Homo sapiens	141-146
27400860-8	2016	Conversely, gene knockdown of MnSOD results in the reversal of EMT to a mesenchymal-epithelial transition (MET)-like program, which appears to be a function of superoxide (O2(- ))-directed signaling.	Superoxides	160-170	superoxide dismutase 2	Homo sapiens	30-35
27400860-8	2016	Conversely, gene knockdown of MnSOD results in the reversal of EMT to a mesenchymal-epithelial transition (MET)-like program, which appears to be a function of superoxide (O2(- ))-directed signaling.	Superoxides	172-174	superoxide dismutase 2	Homo sapiens	30-35
27400860-9	2016	INNOVATION AND CONCLUSION: These data underscore the involvement of MnSOD in regulating the switch between the EMT and MET-associated phenotype by influencing cellular redox environment via its effect on the intracellular ratio between O2(- ) and H2O2.	Superoxides	236-238	superoxide dismutase 2	Homo sapiens	68-73
27400860-9	2016	INNOVATION AND CONCLUSION: These data underscore the involvement of MnSOD in regulating the switch between the EMT and MET-associated phenotype by influencing cellular redox environment via its effect on the intracellular ratio between O2(- ) and H2O2.	Hydrogen Peroxide	247-251	superoxide dismutase 2	Homo sapiens	68-73
26935174-9	2016	FUTURE DIRECTIONS: Acetylation of MnSOD and other mitochondrial proteins, due to loss of SIRT3, may explain the connection between ROS and development of luminal B breast cancer and how luminal B breast cancer becomes resistant to endocrine therapy.	Reactive Oxygen Species	131-134	superoxide dismutase 2	Homo sapiens	34-39
26846100-2	2016	Manganese-superoxide dismutase (Mn-SOD) is a major antioxidant enzyme that protects cells from ROS-mediated damage.	Reactive Oxygen Species	95-98	superoxide dismutase 2	Homo sapiens	0-30
27400860-10	2016	Strategies to manipulate MnSOD expression and/or the cellular redox milieu vis-a-vis O2(- ):H2O2 could have potential therapeutic implications.	Hydrogen Peroxide	92-96	superoxide dismutase 2	Homo sapiens	25-30
27100222-3	2016	In this study, we aimed to investigate possible associations of MnSOD Ala-9Val and GPx1 Pro198Leu polymorphisms with vitiligo with in Turkish population.	ala-9val	70-78	superoxide dismutase 2	Homo sapiens	64-69
27100222-5	2016	Genotyping is performed to identify MnSOD Ala-9Val and GPx1 Pro198Leu polymorphisms.	ala-9val	42-50	superoxide dismutase 2	Homo sapiens	36-41
27100222-8	2016	Although no significant difference was found, this is the first report investigating the possible associations between the MnSOD Ala-9Val and GPx1 Pro198Leu polymorphisms in Turkish population.	ala-9val	129-137	superoxide dismutase 2	Homo sapiens	123-128
27278553-7	2016	On the contrary, ROS damage decreased by increasing SOD2 gene and protein expression and hydrogen peroxide production with parallel NF-kappaB protein expression decrease in MDA-MB-231, a tumorigenic triple-negative breast cancer cell line.	ros	17-20	superoxide dismutase 2	Homo sapiens	52-56
27208465-9	2016	Ozone levels were significantly and inversely associated with forced expiratory flow at 25% of forced vital capacity (FEF25%) (-0.43L/s; 95% CI: -0.58,-0.28L/s) in SOD2 Ala16 variant children.	Ozone	0-5	superoxide dismutase 2	Homo sapiens	164-168
28600747-7	2016	NaBu increased mitochondrial manganese-superoxide dismutase and glutathione peroxidase activity.	sethoxydim	0-4	superoxide dismutase 2	Homo sapiens	29-59
26771767-3	2016	Here we found that 7721 hepatoma cells held a higher redox homeostasis threshold than L02 normal liver cells which caused 7721 cells to have a higher demand for ROS; MnSOD over-expression in 7721 decreased endogenous reactive oxygen species (ROS) and inhibited telomerase activity; Akt phosphorylation inhibitor and NAC both inhibited 7721 telomerase activity.	Reactive Oxygen Species	161-164	superoxide dismutase 2	Homo sapiens	166-171
26771767-3	2016	Here we found that 7721 hepatoma cells held a higher redox homeostasis threshold than L02 normal liver cells which caused 7721 cells to have a higher demand for ROS; MnSOD over-expression in 7721 decreased endogenous reactive oxygen species (ROS) and inhibited telomerase activity; Akt phosphorylation inhibitor and NAC both inhibited 7721 telomerase activity.	Reactive Oxygen Species	217-240	superoxide dismutase 2	Homo sapiens	166-171
26771767-3	2016	Here we found that 7721 hepatoma cells held a higher redox homeostasis threshold than L02 normal liver cells which caused 7721 cells to have a higher demand for ROS; MnSOD over-expression in 7721 decreased endogenous reactive oxygen species (ROS) and inhibited telomerase activity; Akt phosphorylation inhibitor and NAC both inhibited 7721 telomerase activity.	Reactive Oxygen Species	242-245	superoxide dismutase 2	Homo sapiens	166-171
26846100-2	2016	Manganese-superoxide dismutase (Mn-SOD) is a major antioxidant enzyme that protects cells from ROS-mediated damage.	Reactive Oxygen Species	95-98	superoxide dismutase 2	Homo sapiens	32-38
27411103-5	2016	Diabetic Glc also promoted beta-catenin nuclear localization and the formation of a complex with FOXO3a that localized to the promoters of Sod2, p21(cip1), and potentially p27(kip1).	Glucose	9-12	superoxide dismutase 2	Homo sapiens	139-143
27473585-14	2016	Increase in ROS coincided with reduction in SOD activity in AA TN breast cancer cells.	Reactive Oxygen Species	12-15	superoxide dismutase 2	Homo sapiens	44-47
27428996-9	2016	In an in vitro study, quercitrin suppressed the production of reactive oxygen species and enhanced expression of nuclear factor E2-related factor 2 (Nrf2), activity of antioxidant response element (ARE)-reporter gene, and protein levels of NADPH: quinone oxidoreductase 1 (NQO1), catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase 2 (SOD-2) in APAP-treated HepG2 cells.	quercitrin	22-32	superoxide dismutase 2	Homo sapiens	330-352
27428996-9	2016	In an in vitro study, quercitrin suppressed the production of reactive oxygen species and enhanced expression of nuclear factor E2-related factor 2 (Nrf2), activity of antioxidant response element (ARE)-reporter gene, and protein levels of NADPH: quinone oxidoreductase 1 (NQO1), catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase 2 (SOD-2) in APAP-treated HepG2 cells.	quercitrin	22-32	superoxide dismutase 2	Homo sapiens	354-359
27428996-12	2016	Quercitrin restored protein levels of Nrf2, NQO1 and activities and expressions of CAT, GPx, SOD-2.	quercitrin	0-10	superoxide dismutase 2	Homo sapiens	93-98
27180143-5	2016	High ROS, facilitated by enzymes such as superoxide dismutase 2 (SOD2) that enhance mitochondrial hydrogen peroxide (mtH2O2), are normally linked to dedifferentiation of somatic cells.	Reactive Oxygen Species	5-8	superoxide dismutase 2	Homo sapiens	41-63
27007876-11	2016	Compared with gene expression levels at 5 % O2, which were arbitrarily set as "1," 20 % O2 is associated with significantly higher expression of BAX (2.14 +- 0.47), G6PD (2.92 +- 1.06), MnSOD (2.87 +- 0.88), and HSP70.1 (8.68 +- 4.19).	Oxygen	88-90	superoxide dismutase 2	Homo sapiens	186-191
27216458-10	2016	We found that betaOHB induced FOXO3a, an oxidative stress resistance gene, and its target enzyme, SOD2 and catalase.	betaohb	14-21	superoxide dismutase 2	Homo sapiens	98-102
27126960-4	2016	Other beneficial effects of RSV include a decrease of total intracellular ROS and the up-regulation of the expression of mitochondrial superoxide dismutase (SOD2) protein, a key antioxidant defense enzyme.	Resveratrol	28-31	superoxide dismutase 2	Homo sapiens	157-161
27126960-5	2016	The molecular mechanisms leading to the up-regulation of SOD2 protein expression by RSV require the estrogen receptor (ER) and the estrogen-related receptor alpha (ERRalpha).	Resveratrol	84-87	superoxide dismutase 2	Homo sapiens	57-61
27126960-6	2016	Although RSV increases the level of SOD2 protein in patients" fibroblasts, the enzyme activity is not increased, in contrast to normal fibroblasts.	Resveratrol	9-12	superoxide dismutase 2	Homo sapiens	36-40
27180143-5	2016	High ROS, facilitated by enzymes such as superoxide dismutase 2 (SOD2) that enhance mitochondrial hydrogen peroxide (mtH2O2), are normally linked to dedifferentiation of somatic cells.	Reactive Oxygen Species	5-8	superoxide dismutase 2	Homo sapiens	65-69
27180143-5	2016	High ROS, facilitated by enzymes such as superoxide dismutase 2 (SOD2) that enhance mitochondrial hydrogen peroxide (mtH2O2), are normally linked to dedifferentiation of somatic cells.	Hydrogen Peroxide	98-115	superoxide dismutase 2	Homo sapiens	41-63
27180143-5	2016	High ROS, facilitated by enzymes such as superoxide dismutase 2 (SOD2) that enhance mitochondrial hydrogen peroxide (mtH2O2), are normally linked to dedifferentiation of somatic cells.	Hydrogen Peroxide	98-115	superoxide dismutase 2	Homo sapiens	65-69
27180143-5	2016	High ROS, facilitated by enzymes such as superoxide dismutase 2 (SOD2) that enhance mitochondrial hydrogen peroxide (mtH2O2), are normally linked to dedifferentiation of somatic cells.	mth2o2	117-123	superoxide dismutase 2	Homo sapiens	41-63
27180143-5	2016	High ROS, facilitated by enzymes such as superoxide dismutase 2 (SOD2) that enhance mitochondrial hydrogen peroxide (mtH2O2), are normally linked to dedifferentiation of somatic cells.	mth2o2	117-123	superoxide dismutase 2	Homo sapiens	65-69
27227512-0	2016	Mechanism of the Reaction of Human Manganese Superoxide Dismutase with Peroxynitrite: Nitration of Critical Tyrosine 34.	Peroxynitrous Acid	71-84	superoxide dismutase 2	Homo sapiens	35-65
27357008-2	2016	Herein, a novel Mn-superoxide dismutase (MnSOD) mimics, silica-manganous phosphate (SiO2-Mn3(PO4)2) nanoparticles, were designed and synthesized by surface self-assembly processes that occur on the surface of silica-phytic acid (SiO2-PA) nanoparticles.	silica-manganous phosphate	56-82	superoxide dismutase 2	Homo sapiens	16-39
27357008-2	2016	Herein, a novel Mn-superoxide dismutase (MnSOD) mimics, silica-manganous phosphate (SiO2-Mn3(PO4)2) nanoparticles, were designed and synthesized by surface self-assembly processes that occur on the surface of silica-phytic acid (SiO2-PA) nanoparticles.	silica-manganous phosphate	56-82	superoxide dismutase 2	Homo sapiens	41-46
27357008-2	2016	Herein, a novel Mn-superoxide dismutase (MnSOD) mimics, silica-manganous phosphate (SiO2-Mn3(PO4)2) nanoparticles, were designed and synthesized by surface self-assembly processes that occur on the surface of silica-phytic acid (SiO2-PA) nanoparticles.	sio2-mn3(po4)2	84-98	superoxide dismutase 2	Homo sapiens	16-39
27357008-2	2016	Herein, a novel Mn-superoxide dismutase (MnSOD) mimics, silica-manganous phosphate (SiO2-Mn3(PO4)2) nanoparticles, were designed and synthesized by surface self-assembly processes that occur on the surface of silica-phytic acid (SiO2-PA) nanoparticles.	sio2-mn3(po4)2	84-98	superoxide dismutase 2	Homo sapiens	41-46
27357008-2	2016	Herein, a novel Mn-superoxide dismutase (MnSOD) mimics, silica-manganous phosphate (SiO2-Mn3(PO4)2) nanoparticles, were designed and synthesized by surface self-assembly processes that occur on the surface of silica-phytic acid (SiO2-PA) nanoparticles.	silica-phytic acid	209-227	superoxide dismutase 2	Homo sapiens	16-39
27357008-2	2016	Herein, a novel Mn-superoxide dismutase (MnSOD) mimics, silica-manganous phosphate (SiO2-Mn3(PO4)2) nanoparticles, were designed and synthesized by surface self-assembly processes that occur on the surface of silica-phytic acid (SiO2-PA) nanoparticles.	silica-phytic acid	209-227	superoxide dismutase 2	Homo sapiens	41-46
27357008-2	2016	Herein, a novel Mn-superoxide dismutase (MnSOD) mimics, silica-manganous phosphate (SiO2-Mn3(PO4)2) nanoparticles, were designed and synthesized by surface self-assembly processes that occur on the surface of silica-phytic acid (SiO2-PA) nanoparticles.	sio2-pa	229-236	superoxide dismutase 2	Homo sapiens	16-39
27357008-2	2016	Herein, a novel Mn-superoxide dismutase (MnSOD) mimics, silica-manganous phosphate (SiO2-Mn3(PO4)2) nanoparticles, were designed and synthesized by surface self-assembly processes that occur on the surface of silica-phytic acid (SiO2-PA) nanoparticles.	sio2-pa	229-236	superoxide dismutase 2	Homo sapiens	41-46
27227512-0	2016	Mechanism of the Reaction of Human Manganese Superoxide Dismutase with Peroxynitrite: Nitration of Critical Tyrosine 34.	Tyrosine	108-116	superoxide dismutase 2	Homo sapiens	35-65
27227512-1	2016	Human Mn-containing superoxide dismutase (hMnSOD) is a mitochondrial enzyme that metabolizes superoxide radical (O2( -)).	Superoxides	93-111	superoxide dismutase 2	Homo sapiens	42-48
27227512-1	2016	Human Mn-containing superoxide dismutase (hMnSOD) is a mitochondrial enzyme that metabolizes superoxide radical (O2( -)).	Superoxides	113-116	superoxide dismutase 2	Homo sapiens	42-48
27227512-4	2016	We previously reported a k of ~1.0 x 10(5) M(-1) s(-1) for the reaction of hMnSOD with ONOO(-) by direct stopped-flow spectroscopy and the critical role of Mn in the nitration process.	onoo	87-91	superoxide dismutase 2	Homo sapiens	75-81
27227512-5	2016	In this study, we further established the mechanism of the reaction of hMnSOD with ONOO(-), including the necessary re-examination of the second-order rate constant by an independent method and the delineation of the microscopic steps that lead to the regio-specific nitration of Tyr34.	onoo	83-87	superoxide dismutase 2	Homo sapiens	71-77
27227512-10	2016	The data reported herein provide a kinetic and mechanistic basis for rationalizing how MnSOD constitutes an intramitochondrial target for ONOO(-) and the microscopic events, with atomic level resolution, that lead to selective and efficient nitration of critical Tyr34.	onoo	138-142	superoxide dismutase 2	Homo sapiens	87-92
27271305-3	2016	METHODS: We examined associations between single nucleotide polymorphisms (SNPs) in MnSOD, GSTP1, GSTM1, GPX1, GPX3, and CAT genes and thiobarbituric acid-reactive substances (TBARS), a blood biomarker of oxidative damage, in healthy white women randomly selected from Western New York (n = 1402).	thiobarbituric acid	135-154	superoxide dismutase 2	Homo sapiens	84-89
27271305-6	2016	RESULTS: For MnSOD, being heterozygous was associated with lower geometric means of TBARS (less oxidative stress), 1.28 mg/dL, compared to homozygous T-allele or homozygous C-allele,1.35 mg/dL, and 1.31 mg/dL correspondingly (p for trend = 0.01).	Thiobarbituric Acid Reactive Substances	84-89	superoxide dismutase 2	Homo sapiens	13-18
27181103-7	2016	In SACC-LM, reducing the expression of SOD2 by SiRNA inhibited the metastasis ability and reduced the SOD2 activities, intracellular H2O2 concentrations, and protein levels of pERK1/2 and Slug.	Hydrogen Peroxide	133-137	superoxide dismutase 2	Homo sapiens	39-43
27083052-5	2016	MnSOD knockdown increased the levels of ROS and diminished resistance to anoikis in S18 cells.	Reactive Oxygen Species	40-43	superoxide dismutase 2	Homo sapiens	0-5
26762997-0	2016	Role of MnSOD in propofol protection of human umbilical vein endothelial cells injured by heat stress.	Propofol	17-25	superoxide dismutase 2	Homo sapiens	8-13
26762997-7	2016	We further revealed that heat stress significantly reduced the level of manganese superoxide demutase (MnSOD) and Cu/Zn SOD, but that propofol could inhibit the reduction of MnSOD only.	Propofol	134-142	superoxide dismutase 2	Homo sapiens	174-179
26762997-9	2016	CONCLUSION: Propofol protected the heat stress-injured cells, at least partly, through upregulating MnSOD expression, effectively reducing the direct or indirect cell damage caused by oxidative stress.	Propofol	12-20	superoxide dismutase 2	Homo sapiens	100-105
27083311-5	2016	Furthermore, in HaCaT keratinocytes treated with H2O2, 1,25(OH)2D3, 21(OH)pD and calcipotriol stimulated the expression of SOD1 and CAT genes, but not SOD2, indicating a possible role of mitochondria in ROS-modulated cell death.	Hydrogen Peroxide	49-53	superoxide dismutase 2	Homo sapiens	151-155
27083311-5	2016	Furthermore, in HaCaT keratinocytes treated with H2O2, 1,25(OH)2D3, 21(OH)pD and calcipotriol stimulated the expression of SOD1 and CAT genes, but not SOD2, indicating a possible role of mitochondria in ROS-modulated cell death.	calcipotriene	81-93	superoxide dismutase 2	Homo sapiens	151-155
27074587-8	2016	Blockage of autophagy decreased LDHA, MCT4 and SOD2 protein levels in CAFs that might enhance ROS production.	Reactive Oxygen Species	94-97	superoxide dismutase 2	Homo sapiens	47-51
27181103-10	2016	We confirmed that SOD2 play an important role in the development and prognosis of SACC and SOD2-dependent production of H2O2 contributes to metastasis of SACC through the ERK-Slug signaling pathway.	Hydrogen Peroxide	120-124	superoxide dismutase 2	Homo sapiens	18-22
27181103-10	2016	We confirmed that SOD2 play an important role in the development and prognosis of SACC and SOD2-dependent production of H2O2 contributes to metastasis of SACC through the ERK-Slug signaling pathway.	Hydrogen Peroxide	120-124	superoxide dismutase 2	Homo sapiens	91-95
27015562-5	2016	Inhibition of ERBB1/2/4 blocked [pemetrexed + sorafenib] stimulated NFkappaB activation and SOD2 expression; and expression of IkappaB S32A S36A significantly enhanced [pemetrexed + sorafenib] lethality.	Pemetrexed	33-43	superoxide dismutase 2	Homo sapiens	92-96
27157976-3	2016	These higher activities were supported by the stored carbon, lipid and carbohydrate sources, and by a low level of mitochondrial reactive oxygen species (ROS) due to sustained SOD2 expression in the resistant RCC cells.	Reactive Oxygen Species	129-152	superoxide dismutase 2	Homo sapiens	176-180
27157976-3	2016	These higher activities were supported by the stored carbon, lipid and carbohydrate sources, and by a low level of mitochondrial reactive oxygen species (ROS) due to sustained SOD2 expression in the resistant RCC cells.	Reactive Oxygen Species	154-157	superoxide dismutase 2	Homo sapiens	176-180
27168957-12	2016	SOD2 was enhanced for redox balance with relatively stable ROS levels in differentiated cells.	Reactive Oxygen Species	59-62	superoxide dismutase 2	Homo sapiens	0-4
27212182-0	2016	The kinetics of the effect of manganese supplementation on SOD2 activity in senescent human fibroblasts.	Manganese	30-39	superoxide dismutase 2	Homo sapiens	59-63
27212182-1	2016	OBJECTIVE: To investigate the effect of increasing Mn+2 concentrations on superoxide dismutase 2 (SOD2) activity in pre-senescent and senescent cultured fibroblasts, and to determine the Km Mn+2 values required to achieve maximal SOD2 activities in such cells.	mn+2	51-55	superoxide dismutase 2	Homo sapiens	74-96
27212182-1	2016	OBJECTIVE: To investigate the effect of increasing Mn+2 concentrations on superoxide dismutase 2 (SOD2) activity in pre-senescent and senescent cultured fibroblasts, and to determine the Km Mn+2 values required to achieve maximal SOD2 activities in such cells.	mn+2	51-55	superoxide dismutase 2	Homo sapiens	98-102
26898144-8	2016	Interestingly, treatment with Mito-TEMPO, a mitochondrial-specific superoxide scavenger, recovered mitochondrial fission-fusion imbalance and blunted mitochondrial superoxide production, and reduced the IDH2 knockdown-induced decrease in MnSOD expression, eNOS phosphorylation and NO production in endothelial cells.	Superoxides	67-77	superoxide dismutase 2	Homo sapiens	238-243
27137793-1	2016	BACKGROUND: Intracellular antioxidant response to high glucose is mediated by Cu/Mn-superoxide dismutases (SOD-1/SOD-2), catalase (CAT) and glutathione peroxidases (GPx), particularly glutathione peroxidase-1 (GPx-1).	Glucose	55-62	superoxide dismutase 2	Homo sapiens	113-118
26922413-7	2016	Our study results suggest that genetic polymorphisms of COX2, EPHX1, CAT, and SOD2 modify the association of BPA with liver function.	bisphenol A	109-112	superoxide dismutase 2	Homo sapiens	78-82
27015562-5	2016	Inhibition of ERBB1/2/4 blocked [pemetrexed + sorafenib] stimulated NFkappaB activation and SOD2 expression; and expression of IkappaB S32A S36A significantly enhanced [pemetrexed + sorafenib] lethality.	Sorafenib	46-55	superoxide dismutase 2	Homo sapiens	92-96
27021683-3	2016	DNA methyltransferase 1 (Dnmt1) is up-regulated in PAH associated human PASMCs (HPASMCs), which promotes the development of PAH by hypermethylation of CpG islands within the promoter for superoxide dismutase 2 (SOD2) and down-regulating SOD2 expression.	pasmcs	72-78	superoxide dismutase 2	Homo sapiens	187-209
27021683-3	2016	DNA methyltransferase 1 (Dnmt1) is up-regulated in PAH associated human PASMCs (HPASMCs), which promotes the development of PAH by hypermethylation of CpG islands within the promoter for superoxide dismutase 2 (SOD2) and down-regulating SOD2 expression.	pasmcs	72-78	superoxide dismutase 2	Homo sapiens	211-215
27021683-3	2016	DNA methyltransferase 1 (Dnmt1) is up-regulated in PAH associated human PASMCs (HPASMCs), which promotes the development of PAH by hypermethylation of CpG islands within the promoter for superoxide dismutase 2 (SOD2) and down-regulating SOD2 expression.	pasmcs	72-78	superoxide dismutase 2	Homo sapiens	237-241
27197253-5	2016	Furthermore, B7-H3 promoted reactive oxygen species-dependent stabilization of HIF1alpha by suppressing the activity of the stress-activated transcription factor Nrf2 and its target genes, including the antioxidants SOD1, SOD2, and PRX3.	Reactive Oxygen Species	28-51	superoxide dismutase 2	Homo sapiens	222-226
26678800-7	2016	Finally, treatment with ATRA for 96h in the presence of MnSOD siRNA or PEG-catalase inhibited ATRA induced increases in NF-M expression.	Tretinoin	24-28	superoxide dismutase 2	Homo sapiens	56-61
26857738-0	2016	Manganese elevates manganese superoxide dismutase protein level through protein kinase C and protein tyrosine kinase.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	19-49
26690241-10	2016	DMF induced a stronger antioxidant response as evidenced by a higher expression of Mn-superoxide dismutase.	Dimethyl Fumarate	0-3	superoxide dismutase 2	Homo sapiens	83-106
26981780-0	2016	Ruxolitinib synergizes with DMF to kill via BIM+BAD-induced mitochondrial dysfunction and via reduced SOD2/TRX expression and ROS.	ruxolitinib	0-11	superoxide dismutase 2	Homo sapiens	102-106
26981780-0	2016	Ruxolitinib synergizes with DMF to kill via BIM+BAD-induced mitochondrial dysfunction and via reduced SOD2/TRX expression and ROS.	Dimethyl Fumarate	28-31	superoxide dismutase 2	Homo sapiens	102-106
26981780-4	2016	The combination of [ruxolitinib + MMF] inactivated ERK1/2, AKT, STAT3 and STAT5; reduced expression of MCL-1, BCL-XL, SOD2 and TRX; increased BIM expression; decreased BAD S112 S136 phosphorylation; and enhanced pro-caspase 3 cleavage.	ruxolitinib	20-31	superoxide dismutase 2	Homo sapiens	118-122
26981780-4	2016	The combination of [ruxolitinib + MMF] inactivated ERK1/2, AKT, STAT3 and STAT5; reduced expression of MCL-1, BCL-XL, SOD2 and TRX; increased BIM expression; decreased BAD S112 S136 phosphorylation; and enhanced pro-caspase 3 cleavage.	citraconic acid	34-37	superoxide dismutase 2	Homo sapiens	118-122
27141263-3	2016	Superoxide dismutase 2 (SOD2) is one of the major antioxidant defense systems against free radicals.	Free Radicals	86-99	superoxide dismutase 2	Homo sapiens	0-22
27141263-3	2016	Superoxide dismutase 2 (SOD2) is one of the major antioxidant defense systems against free radicals.	Free Radicals	86-99	superoxide dismutase 2	Homo sapiens	24-28
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Valine	52-58	superoxide dismutase 2	Homo sapiens	163-193
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Valine	52-58	superoxide dismutase 2	Homo sapiens	195-200
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Valine	52-58	superoxide dismutase 2	Homo sapiens	219-224
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Valine	60-63	superoxide dismutase 2	Homo sapiens	163-193
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Valine	60-63	superoxide dismutase 2	Homo sapiens	195-200
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Valine	60-63	superoxide dismutase 2	Homo sapiens	219-224
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Alanine	68-75	superoxide dismutase 2	Homo sapiens	163-193
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Alanine	68-75	superoxide dismutase 2	Homo sapiens	195-200
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Alanine	68-75	superoxide dismutase 2	Homo sapiens	219-224
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Alanine	77-80	superoxide dismutase 2	Homo sapiens	163-193
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Alanine	77-80	superoxide dismutase 2	Homo sapiens	195-200
27141263-6	2016	This SNP changes the amino acid at position 16 from valine (Val) to alanine (Ala), which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase (MnSOD) and also affects MnSOD activity in mitochondria.	Alanine	77-80	superoxide dismutase 2	Homo sapiens	219-224
26678800-4	2016	This was accompanied by an increase in MitoSOX and DCFH2 oxidation that could be indicative of increased steady-state levels of reactive oxygen species (ROS) such as O2( -) and H2O2, which correlated with increased levels of MnSOD activity and immuno-reactive protein.	Reactive Oxygen Species	128-151	superoxide dismutase 2	Homo sapiens	225-230
26678800-4	2016	This was accompanied by an increase in MitoSOX and DCFH2 oxidation that could be indicative of increased steady-state levels of reactive oxygen species (ROS) such as O2( -) and H2O2, which correlated with increased levels of MnSOD activity and immuno-reactive protein.	Reactive Oxygen Species	153-156	superoxide dismutase 2	Homo sapiens	225-230
26678800-4	2016	This was accompanied by an increase in MitoSOX and DCFH2 oxidation that could be indicative of increased steady-state levels of reactive oxygen species (ROS) such as O2( -) and H2O2, which correlated with increased levels of MnSOD activity and immuno-reactive protein.	Superoxides	166-168	superoxide dismutase 2	Homo sapiens	225-230
26678800-6	2016	In addition, ATRA-induced stimulation of NF-M at 48 and 72h was enhanced by decreasing SOD activity using siRNA directed at MnSOD.	Tretinoin	13-17	superoxide dismutase 2	Homo sapiens	87-90
26678800-6	2016	In addition, ATRA-induced stimulation of NF-M at 48 and 72h was enhanced by decreasing SOD activity using siRNA directed at MnSOD.	Tretinoin	13-17	superoxide dismutase 2	Homo sapiens	124-129
26678800-7	2016	Finally, treatment with ATRA for 96h in the presence of MnSOD siRNA or PEG-catalase inhibited ATRA induced increases in NF-M expression.	Tretinoin	94-98	superoxide dismutase 2	Homo sapiens	56-61
26781513-5	2016	Ourin vitrostudy revealed a well-defined POD concentration of DOX below which adaptive induction of proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) -mediated mitochondrial genes, including NRF-1, MnSOD, UCP2, and COX1, concurred with negligible changes in mitochondrial superoxide and cytotoxicity.	Doxorubicin	62-65	superoxide dismutase 2	Homo sapiens	218-223
26544677-0	2016	Association of the manganese superoxide dismutase gene Ala-9Val polymorphism with age of smoking initiation in male schizophrenia smokers.	ala-9val	55-63	superoxide dismutase 2	Homo sapiens	19-49
26958937-5	2016	We determined that oroxylin A induces p53 mitochondrial translocation and inhibits SOD2 activity.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	19-29	superoxide dismutase 2	Homo sapiens	83-87
26544677-3	2016	Manganese superoxide dismutase (MnSOD) is the major antioxidant in the mitochondria, catalyzing the metabolism of superoxide radicals to form hydrogen peroxide.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
26544677-3	2016	Manganese superoxide dismutase (MnSOD) is the major antioxidant in the mitochondria, catalyzing the metabolism of superoxide radicals to form hydrogen peroxide.	Hydrogen Peroxide	142-159	superoxide dismutase 2	Homo sapiens	0-30
26544677-3	2016	Manganese superoxide dismutase (MnSOD) is the major antioxidant in the mitochondria, catalyzing the metabolism of superoxide radicals to form hydrogen peroxide.	Hydrogen Peroxide	142-159	superoxide dismutase 2	Homo sapiens	32-37
26544677-5	2016	In this study, we hypothesized that the functional polymorphism of MnSOD Ala-9Val was associated with smoking in patients with schizophrenia.	ala-9val	73-81	superoxide dismutase 2	Homo sapiens	67-72
26544677-10	2016	These results suggest that the MnSOD Ala-9Val polymorphism may not influence smoking status in a Chinese male schizophrenia population, but may influence the age at which smoking is started among schizophrenia smokers.	ala-9val	37-45	superoxide dismutase 2	Homo sapiens	31-36
26707081-4	2016	By inhibiting mTOR and mitochondrial manganese superoxide dismutase (MnSOD), we confirmed that rapamycin functioned through the mTOR/MnSOD/reactive oxygen species (ROS) signaling pathway, and the existence of Akt governed the rapamycin-induced asymmetric division (AD) of stem cells in cases of radiation-treated breast cancer.	Reactive Oxygen Species	139-162	superoxide dismutase 2	Homo sapiens	37-67
26490979-7	2016	After SOD2 silencing, the IR-induced changes of ROS and the MMP were significantly enhanced.	Reactive Oxygen Species	48-51	superoxide dismutase 2	Homo sapiens	6-10
26874034-9	2016	Dau pretreatment resulted in further increases of H2O2-induced enhancement in levels of CAT and SOD2.	lyoniside	0-3	superoxide dismutase 2	Homo sapiens	96-100
26874034-9	2016	Dau pretreatment resulted in further increases of H2O2-induced enhancement in levels of CAT and SOD2.	Hydrogen Peroxide	50-54	superoxide dismutase 2	Homo sapiens	96-100
25575725-6	2016	Studies of human umbilical vein endothelial cells (HUVEC) and arterial endothelial cells (HAEC) showed that therapeutically relevant concentrations of MTX phosphorylate AMPKalpha(Thr172), and induce cytoprotective genes including manganese superoxide dismutase (MnSOD) and haem oxygenase-1 (HO-1).	Methotrexate	151-154	superoxide dismutase 2	Homo sapiens	230-260
25575725-6	2016	Studies of human umbilical vein endothelial cells (HUVEC) and arterial endothelial cells (HAEC) showed that therapeutically relevant concentrations of MTX phosphorylate AMPKalpha(Thr172), and induce cytoprotective genes including manganese superoxide dismutase (MnSOD) and haem oxygenase-1 (HO-1).	Methotrexate	151-154	superoxide dismutase 2	Homo sapiens	262-267
25575725-9	2016	Mechanistically, MTX treatment led to cyclic AMP response element-binding protein (CREB)(Ser133) phosphorylation, while AMPK depletion attenuated this response and the induction of MnSOD and HO-1.	Methotrexate	17-20	superoxide dismutase 2	Homo sapiens	181-186
25575725-10	2016	CREB siRNA inhibited upregulation of both cytoprotective genes by MTX, while chromatin immunoprecipitation demonstrated CREB binding to the MnSOD promoter in MTX-treated EC.	Methotrexate	158-161	superoxide dismutase 2	Homo sapiens	140-145
26707081-4	2016	By inhibiting mTOR and mitochondrial manganese superoxide dismutase (MnSOD), we confirmed that rapamycin functioned through the mTOR/MnSOD/reactive oxygen species (ROS) signaling pathway, and the existence of Akt governed the rapamycin-induced asymmetric division (AD) of stem cells in cases of radiation-treated breast cancer.	ros	164-167	superoxide dismutase 2	Homo sapiens	69-74
26707081-4	2016	By inhibiting mTOR and mitochondrial manganese superoxide dismutase (MnSOD), we confirmed that rapamycin functioned through the mTOR/MnSOD/reactive oxygen species (ROS) signaling pathway, and the existence of Akt governed the rapamycin-induced asymmetric division (AD) of stem cells in cases of radiation-treated breast cancer.	Sirolimus	95-104	superoxide dismutase 2	Homo sapiens	37-67
26707081-4	2016	By inhibiting mTOR and mitochondrial manganese superoxide dismutase (MnSOD), we confirmed that rapamycin functioned through the mTOR/MnSOD/reactive oxygen species (ROS) signaling pathway, and the existence of Akt governed the rapamycin-induced asymmetric division (AD) of stem cells in cases of radiation-treated breast cancer.	Sirolimus	95-104	superoxide dismutase 2	Homo sapiens	69-74
26707081-4	2016	By inhibiting mTOR and mitochondrial manganese superoxide dismutase (MnSOD), we confirmed that rapamycin functioned through the mTOR/MnSOD/reactive oxygen species (ROS) signaling pathway, and the existence of Akt governed the rapamycin-induced asymmetric division (AD) of stem cells in cases of radiation-treated breast cancer.	Sirolimus	95-104	superoxide dismutase 2	Homo sapiens	133-138
26707081-4	2016	By inhibiting mTOR and mitochondrial manganese superoxide dismutase (MnSOD), we confirmed that rapamycin functioned through the mTOR/MnSOD/reactive oxygen species (ROS) signaling pathway, and the existence of Akt governed the rapamycin-induced asymmetric division (AD) of stem cells in cases of radiation-treated breast cancer.	Reactive Oxygen Species	139-162	superoxide dismutase 2	Homo sapiens	69-74
26707081-4	2016	By inhibiting mTOR and mitochondrial manganese superoxide dismutase (MnSOD), we confirmed that rapamycin functioned through the mTOR/MnSOD/reactive oxygen species (ROS) signaling pathway, and the existence of Akt governed the rapamycin-induced asymmetric division (AD) of stem cells in cases of radiation-treated breast cancer.	Reactive Oxygen Species	139-162	superoxide dismutase 2	Homo sapiens	133-138
26443543-6	2016	Moreover, two stilbenes upregulated the activation of human MnSOD promoter luciferase reporter gene and protein level in human umbilical vein endothelial cells.	Stilbenes	14-23	superoxide dismutase 2	Homo sapiens	60-65
26443543-5	2016	METHODS AND RESULTS: Our results revealed that two stilbenes reduced mitochondrial superoxide-free radicals, and endothelial cell senescence, and increased the mRNA expression of several genes related to mitochondrial function, including MnSOD.	Stilbenes	51-60	superoxide dismutase 2	Homo sapiens	238-243
26443543-0	2016	ERK5/HDAC5-mediated, resveratrol-, and pterostilbene-induced expression of MnSOD in human endothelial cells.	Resveratrol	21-32	superoxide dismutase 2	Homo sapiens	75-80
26443543-9	2016	Furthermore, using a chromatin immunoprecipitation-PCR detection method, we found that resveratrol and pterostilbene promoted KLF2 binding to CACCC sites of the human MnSOD promoter.	Resveratrol	87-98	superoxide dismutase 2	Homo sapiens	167-172
26443543-0	2016	ERK5/HDAC5-mediated, resveratrol-, and pterostilbene-induced expression of MnSOD in human endothelial cells.	pterostilbene	39-52	superoxide dismutase 2	Homo sapiens	75-80
26443543-3	2016	Although polyphenols can induce the expression of MnSOD, their corresponding mechanisms remains unclear.	Polyphenols	9-20	superoxide dismutase 2	Homo sapiens	50-55
26443543-9	2016	Furthermore, using a chromatin immunoprecipitation-PCR detection method, we found that resveratrol and pterostilbene promoted KLF2 binding to CACCC sites of the human MnSOD promoter.	pterostilbene	103-116	superoxide dismutase 2	Homo sapiens	167-172
26443543-4	2016	In this study, we tested the hypothesis that resveratrol and pterostilbene can activate the expression of MnSOD through an AMPK-ERK5/HDAC5-KLF2 pathway.	Resveratrol	45-56	superoxide dismutase 2	Homo sapiens	106-111
26443543-10	2016	CONCLUSION: Resveratrol and pterostilbene can activate MnSOD expression through ERK5/HDAC5 pathway, thus alleviating mitochondrial oxidative stress in endothelial cells that relates to cardiovascular disease.	Resveratrol	12-23	superoxide dismutase 2	Homo sapiens	55-60
26443543-4	2016	In this study, we tested the hypothesis that resveratrol and pterostilbene can activate the expression of MnSOD through an AMPK-ERK5/HDAC5-KLF2 pathway.	pterostilbene	61-74	superoxide dismutase 2	Homo sapiens	106-111
26443543-10	2016	CONCLUSION: Resveratrol and pterostilbene can activate MnSOD expression through ERK5/HDAC5 pathway, thus alleviating mitochondrial oxidative stress in endothelial cells that relates to cardiovascular disease.	pterostilbene	28-41	superoxide dismutase 2	Homo sapiens	55-60
26679105-10	2016	KEY FINDINGS: Melatonin significantly increased activities and mRNA levels of SIRT1 and catalase in both patients and healthy subjects, whereas melatonin treatment caused a pronounced increase in MnSOD mRNA expression and activity only in patients.	Melatonin	144-153	superoxide dismutase 2	Homo sapiens	196-201
26679105-12	2016	SIGNIFICANCE: It appears that the antioxidant status is affected in PBMCs from MS patients and melatonin could improve impaired antioxidant defense in MS through upregulation of SIRT1, MnSOD and catalase, which might be important in MS management.	Melatonin	95-104	superoxide dismutase 2	Homo sapiens	185-190
26754536-7	2016	Cholesterol does not change GRX2 expression but it overexpresses SOD1, SOD2, CCS, PRDX1, GSR, GSS, CAT and PNKP.	Cholesterol	0-11	superoxide dismutase 2	Homo sapiens	71-75
28955838-9	2016	Further, mangiferin enhanced the expression of cell proliferative signaling cascade molecules, Cyclin d1, NFkappaB and antioxidant molecules HO-1, SOD2, by PI3K/Akt dependent pathway.	mangiferin	9-19	superoxide dismutase 2	Homo sapiens	147-151
26543228-9	2016	Consistently, with previous observations, MnSOD expression secondary to Nrf2 activation led to an increase in the glycolytic rate dependent on mtH2O2 production and the activation of AMPK.	mth2o2	143-149	superoxide dismutase 2	Homo sapiens	42-47
26052839-3	2016	Here, we reported that high glucose elevated the level of p-Akt to attenuate endogenous FoxO1 bioactivities in MCs, accompanied with decreases in the mRNA expressions of catalase (CAT) and superoxide dismutase 2 (SOD2).	Glucose	28-35	superoxide dismutase 2	Homo sapiens	189-211
27343087-7	2016	This review focuses on the recent discovery that decreased expression of SOD2, a putative tumor-suppressor gene and the major source of H2O2, results from hypermethylation of CpG islands.	Hydrogen Peroxide	136-140	superoxide dismutase 2	Homo sapiens	73-77
27343087-9	2016	In normal PASMC, SOD2 siRNA decreases H2O2 and activates HIF-1alpha.	pasmc	10-15	superoxide dismutase 2	Homo sapiens	17-21
27343087-9	2016	In normal PASMC, SOD2 siRNA decreases H2O2 and activates HIF-1alpha.	Hydrogen Peroxide	38-42	superoxide dismutase 2	Homo sapiens	17-21
27343087-10	2016	In PAH, reduced SOD2 expression decreases H2O2, reduces the cytosol and thereby activates HIF-1alpha.	Hydrogen Peroxide	42-46	superoxide dismutase 2	Homo sapiens	16-20
27343087-12	2016	The DNA methyltransferase inhibitor, 5-aza-2"-deoxycytidine, which restores SOD2 expression, corrects the proliferation/apoptosis imbalance in PAH and cancer cells.	Decitabine	37-59	superoxide dismutase 2	Homo sapiens	76-80
27343087-14	2016	SOD2 augmentation inactivates HIF-1alpha in PAH PASMC and therapy with the SOD mimetic, MnTBAP, regresses experimental PAH.	pasmc	48-53	superoxide dismutase 2	Homo sapiens	0-4
27343087-14	2016	SOD2 augmentation inactivates HIF-1alpha in PAH PASMC and therapy with the SOD mimetic, MnTBAP, regresses experimental PAH.	pasmc	48-53	superoxide dismutase 2	Homo sapiens	0-3
26899340-4	2016	As mitochondria are the main site of superoxide production, among SODs, mitochondrial manganese SOD (MnSOD) is the primary antioxidant enzyme that protects cells from ROS.	Superoxides	37-47	superoxide dismutase 2	Homo sapiens	86-99
26899340-4	2016	As mitochondria are the main site of superoxide production, among SODs, mitochondrial manganese SOD (MnSOD) is the primary antioxidant enzyme that protects cells from ROS.	Superoxides	37-47	superoxide dismutase 2	Homo sapiens	101-106
26899340-4	2016	As mitochondria are the main site of superoxide production, among SODs, mitochondrial manganese SOD (MnSOD) is the primary antioxidant enzyme that protects cells from ROS.	Reactive Oxygen Species	167-170	superoxide dismutase 2	Homo sapiens	86-99
26899340-4	2016	As mitochondria are the main site of superoxide production, among SODs, mitochondrial manganese SOD (MnSOD) is the primary antioxidant enzyme that protects cells from ROS.	Reactive Oxygen Species	167-170	superoxide dismutase 2	Homo sapiens	101-106
26111538-9	2016	These results suggest that upregulation of SOD-2 in Met-5A cells exposed to MWCNTs is mediated by ROS formation and ERK1/2 activation.	ros	98-101	superoxide dismutase 2	Homo sapiens	43-48
26881079-2	2016	We aimed to investigate the possible effects of melatonin on gene expressions and activities of MnSOD and catalase under conditions of oxidative stress induced by hydrogen peroxide (H2O2) in peripheral blood mononuclear cells (PBMCs).	Melatonin	48-57	superoxide dismutase 2	Homo sapiens	96-101
26881079-2	2016	We aimed to investigate the possible effects of melatonin on gene expressions and activities of MnSOD and catalase under conditions of oxidative stress induced by hydrogen peroxide (H2O2) in peripheral blood mononuclear cells (PBMCs).	Hydrogen Peroxide	163-180	superoxide dismutase 2	Homo sapiens	96-101
26881079-2	2016	We aimed to investigate the possible effects of melatonin on gene expressions and activities of MnSOD and catalase under conditions of oxidative stress induced by hydrogen peroxide (H2O2) in peripheral blood mononuclear cells (PBMCs).	Hydrogen Peroxide	182-186	superoxide dismutase 2	Homo sapiens	96-101
26881079-8	2016	Pretreatment of PBMCs with melatonin significantly augmented expression and activity of MnSOD which were diminished by H2O2.	Melatonin	27-36	superoxide dismutase 2	Homo sapiens	88-93
26881079-8	2016	Pretreatment of PBMCs with melatonin significantly augmented expression and activity of MnSOD which were diminished by H2O2.	Hydrogen Peroxide	119-123	superoxide dismutase 2	Homo sapiens	88-93
26881079-13	2016	It seems that melatonin could prevent from undesirable impacts of H2O2-induced oxidative stress on MnSOD downregulation.	Melatonin	14-23	superoxide dismutase 2	Homo sapiens	99-104
26881079-13	2016	It seems that melatonin could prevent from undesirable impacts of H2O2-induced oxidative stress on MnSOD downregulation.	Hydrogen Peroxide	66-70	superoxide dismutase 2	Homo sapiens	99-104
26111538-0	2016	MWCNTs Induce ROS Generation, ERK Phosphorylation, and SOD-2 Expression in Human Mesothelial Cells.	mwcnts	0-6	superoxide dismutase 2	Homo sapiens	55-60
26052839-3	2016	Here, we reported that high glucose elevated the level of p-Akt to attenuate endogenous FoxO1 bioactivities in MCs, accompanied with decreases in the mRNA expressions of catalase (CAT) and superoxide dismutase 2 (SOD2).	Glucose	28-35	superoxide dismutase 2	Homo sapiens	213-217
26671656-0	2016	N-acetyl-L-cysteine increases MnSOD activity and enhances the recruitment of quiescent human fibroblasts to the proliferation cycle during wound healing.	Acetylcysteine	0-19	superoxide dismutase 2	Homo sapiens	30-35
26678158-2	2016	It is generally believed that continuous generation of intracellular reactive oxygen species (ROS) during oxidative phosphorylation (OXPHOS) is a major underlying mechanism for generation of such mtDNA deletions while antioxidant systems, including Manganese superoxide dismutase (MnSOD), mitigating the deleterious effects of ROS.	Reactive Oxygen Species	69-92	superoxide dismutase 2	Homo sapiens	249-279
26678158-2	2016	It is generally believed that continuous generation of intracellular reactive oxygen species (ROS) during oxidative phosphorylation (OXPHOS) is a major underlying mechanism for generation of such mtDNA deletions while antioxidant systems, including Manganese superoxide dismutase (MnSOD), mitigating the deleterious effects of ROS.	Reactive Oxygen Species	69-92	superoxide dismutase 2	Homo sapiens	281-286
26678158-2	2016	It is generally believed that continuous generation of intracellular reactive oxygen species (ROS) during oxidative phosphorylation (OXPHOS) is a major underlying mechanism for generation of such mtDNA deletions while antioxidant systems, including Manganese superoxide dismutase (MnSOD), mitigating the deleterious effects of ROS.	Reactive Oxygen Species	94-97	superoxide dismutase 2	Homo sapiens	249-279
26678158-2	2016	It is generally believed that continuous generation of intracellular reactive oxygen species (ROS) during oxidative phosphorylation (OXPHOS) is a major underlying mechanism for generation of such mtDNA deletions while antioxidant systems, including Manganese superoxide dismutase (MnSOD), mitigating the deleterious effects of ROS.	Reactive Oxygen Species	94-97	superoxide dismutase 2	Homo sapiens	281-286
26678158-2	2016	It is generally believed that continuous generation of intracellular reactive oxygen species (ROS) during oxidative phosphorylation (OXPHOS) is a major underlying mechanism for generation of such mtDNA deletions while antioxidant systems, including Manganese superoxide dismutase (MnSOD), mitigating the deleterious effects of ROS.	Reactive Oxygen Species	327-330	superoxide dismutase 2	Homo sapiens	249-279
27525285-9	2016	The overproduction of ROS diminishes expression of the antioxidant enzymes (manganese superoxide dismutase, glutathione peroxidase, and catalase).	Reactive Oxygen Species	22-25	superoxide dismutase 2	Homo sapiens	76-106
25953833-6	2015	At each synapse, neurotransmitters trigger increased [Ca(2+)]i, HIF-1alpha:HIF-2alpha, and Nox2:Sod2 activity that generates increased ROS levels.	Reactive Oxygen Species	135-138	superoxide dismutase 2	Homo sapiens	96-100
26652025-9	2015	Next, we used AdSOD2 to upregulate SOD2 prior to HG exposure and thereby noted reduction in superoxide generation.	Superoxides	92-102	superoxide dismutase 2	Homo sapiens	16-20
26652025-16	2015	Delivery of superoxide dismutase (SOD2) using MSCs as a gene delivery vehicle reduces inflammation and improves glucose tolerance in vivo.	Glucose	112-119	superoxide dismutase 2	Homo sapiens	34-38
26482865-13	2015	However, following training, vitamin C and E supplementation significantly attenuated increased skeletal muscle superoxide dismutase (SOD) activity and protein abundance of SOD2 and TFAM.	Ascorbic Acid	29-38	superoxide dismutase 2	Homo sapiens	134-137
26482865-13	2015	However, following training, vitamin C and E supplementation significantly attenuated increased skeletal muscle superoxide dismutase (SOD) activity and protein abundance of SOD2 and TFAM.	Ascorbic Acid	29-38	superoxide dismutase 2	Homo sapiens	173-177
26436856-1	2015	Interactions of hydrogen sulfide (HS(-)/H2S), a reducing signaling species, with superoxide dimutases (SOD) are poorly understood.	Hydrogen Sulfide	16-32	superoxide dismutase 2	Homo sapiens	103-106
26436856-1	2015	Interactions of hydrogen sulfide (HS(-)/H2S), a reducing signaling species, with superoxide dimutases (SOD) are poorly understood.	Hydrogen	34-36	superoxide dismutase 2	Homo sapiens	103-106
26436856-1	2015	Interactions of hydrogen sulfide (HS(-)/H2S), a reducing signaling species, with superoxide dimutases (SOD) are poorly understood.	Hydrogen Sulfide	40-43	superoxide dismutase 2	Homo sapiens	103-106
26436856-2	2015	We applied low-T EPR spectroscopy to examine the effects of HS(-)/H2S and superoxide radical anion O2.- on metallocenters of FeSOD, MnSOD, and CuZnSOD.	superoxide radical anion o2	74-101	superoxide dismutase 2	Homo sapiens	132-137
26436856-4	2015	Cu(2+) was reduced to Cu(1+), while manganese appears to be released from MnSOD active center.	Manganese	36-45	superoxide dismutase 2	Homo sapiens	74-79
26436856-5	2015	Untreated and O2.- treated FeSOD and MnSOD predominantly show 5 d-electron systems, i.e. Fe(3+) and Mn(2+).	Superoxides	14-16	superoxide dismutase 2	Homo sapiens	37-42
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Superoxides	60-70	superoxide dismutase 2	Homo sapiens	0-4
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Superoxides	60-70	superoxide dismutase 2	Homo sapiens	156-160
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Oxygen	72-74	superoxide dismutase 2	Homo sapiens	0-4
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Oxygen	72-74	superoxide dismutase 2	Homo sapiens	156-160
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Hydrogen Peroxide	84-101	superoxide dismutase 2	Homo sapiens	0-4
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Hydrogen Peroxide	84-101	superoxide dismutase 2	Homo sapiens	156-160
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Hydrogen Peroxide	103-107	superoxide dismutase 2	Homo sapiens	0-4
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Hydrogen Peroxide	103-107	superoxide dismutase 2	Homo sapiens	156-160
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Oxygen	113-119	superoxide dismutase 2	Homo sapiens	0-4
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Oxygen	113-119	superoxide dismutase 2	Homo sapiens	156-160
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Oxygen	105-107	superoxide dismutase 2	Homo sapiens	0-4
26359457-5	2015	Sod2 is an antioxidant enzyme that converts highly reactive superoxide (O2 ( -)) to hydrogen peroxide (H2O2) and oxygen (O2), and our data demonstrate that Sod2 is protumorigenic and prometastatic in OCCC.	Oxygen	105-107	superoxide dismutase 2	Homo sapiens	156-160
26359457-9	2015	First, Sod2 maintains highly functional mitochondria, by scavenging O2 ( -), to support the high metabolic activity of OCCC.	Oxygen	68-70	superoxide dismutase 2	Homo sapiens	7-11
26359457-10	2015	Second, Sod2 alters the steady-state ROS balance to drive H2O2-mediated migration.	ros	37-40	superoxide dismutase 2	Homo sapiens	8-12
26359457-10	2015	Second, Sod2 alters the steady-state ROS balance to drive H2O2-mediated migration.	Hydrogen Peroxide	58-62	superoxide dismutase 2	Homo sapiens	8-12
27131313-12	2016	The data demonstrate that the miR-146a/SOD2/ROS pathway may serve as a novel therapeutic target and prognostic marker in patients with EOC.	Reactive Oxygen Species	44-47	superoxide dismutase 2	Homo sapiens	39-43
27630759-1	2016	Mitochondrial superoxide dismutase 2 (SOD2) converts superoxide anions to hydrogen peroxide and oxygen.	Superoxides	53-70	superoxide dismutase 2	Homo sapiens	38-42
27630759-1	2016	Mitochondrial superoxide dismutase 2 (SOD2) converts superoxide anions to hydrogen peroxide and oxygen.	Hydrogen Peroxide	74-91	superoxide dismutase 2	Homo sapiens	38-42
27630759-1	2016	Mitochondrial superoxide dismutase 2 (SOD2) converts superoxide anions to hydrogen peroxide and oxygen.	Oxygen	96-102	superoxide dismutase 2	Homo sapiens	38-42
27630759-6	2016	Elevating cellular superoxide production reduced SOD2 protein content.	Superoxides	19-29	superoxide dismutase 2	Homo sapiens	49-53
27630759-11	2016	Increased cellular superoxide anion production might affect SOD2 protein content.	Superoxides	19-35	superoxide dismutase 2	Homo sapiens	60-64
28053678-4	2016	Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H2O2).	Superoxides	31-41	superoxide dismutase 2	Homo sapiens	53-58
28053678-4	2016	Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H2O2).	Superoxides	31-41	superoxide dismutase 2	Homo sapiens	60-64
28053678-4	2016	Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H2O2).	Hydrogen Peroxide	120-137	superoxide dismutase 2	Homo sapiens	21-51
28053678-4	2016	Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H2O2).	Hydrogen Peroxide	120-137	superoxide dismutase 2	Homo sapiens	53-58
28053678-4	2016	Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H2O2).	Hydrogen Peroxide	120-137	superoxide dismutase 2	Homo sapiens	60-64
28053678-4	2016	Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H2O2).	Hydrogen Peroxide	139-143	superoxide dismutase 2	Homo sapiens	21-51
28053678-4	2016	Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H2O2).	Hydrogen Peroxide	139-143	superoxide dismutase 2	Homo sapiens	53-58
28053678-4	2016	Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H2O2).	Hydrogen Peroxide	139-143	superoxide dismutase 2	Homo sapiens	60-64
26208779-4	2015	These SOD2-null cells exhibit impaired clonogenic activity, which was rescued by either treatment with GC4419, a pharmacological small-molecule mimic of SOD, or growth in hypoxia.	imisopasem manganese	103-109	superoxide dismutase 2	Homo sapiens	6-10
26208779-4	2015	These SOD2-null cells exhibit impaired clonogenic activity, which was rescued by either treatment with GC4419, a pharmacological small-molecule mimic of SOD, or growth in hypoxia.	imisopasem manganese	103-109	superoxide dismutase 2	Homo sapiens	6-9
26208779-6	2015	The SOD2-null cells displayed perturbations in their mitochondrial ultrastructure and preferred glycolysis as opposed to oxidative phosphorylation to generate ATP.	Adenosine Triphosphate	159-162	superoxide dismutase 2	Homo sapiens	4-8
26208779-7	2015	The activities of mitochondrial complex I and II were both significantly impaired by the absence of MnSOD activity, presumably from disruption of the Fe/S centers in NADH dehydrogenase and succinate dehydrogenase subunit B by the aberrant redox state in the mitochondrial matrix of SOD2-null cells.	Iron	150-152	superoxide dismutase 2	Homo sapiens	100-105
26535076-7	2015	Moreover, lycopene significantly increased manganese superoxide dismutase (MnSOD) expression and decreased cellular ROS levels via the PI3K-Akt pathway.	Lycopene	10-18	superoxide dismutase 2	Homo sapiens	43-73
26885102-9	2015	CONCLUSIONS: This study is unique since an investigation to reveal the possible associations between the MnSOD Ala-9Val and GPx1 Pro 198 Leu polymorphisms and AA susceptibility and in Turkish population.	ala-9val	111-119	superoxide dismutase 2	Homo sapiens	105-110
26885102-3	2015	Therefore, we aimed to examine the possible associations between the MnSOD Ala-9Val and GPx1 Pro 198 Leu polymorphisms and AA susceptibility and disease progression in Turkish population.	ala-9val	75-83	superoxide dismutase 2	Homo sapiens	69-74
26885102-5	2015	Genotyping was performed to identify MnSOD Ala-9Val and GPx1 Pro 198 Leu polymorphisms by a method based on PCR amplification and detection of polymorphisms with hybridization probes labeled with fluorescent dyes.	ala-9val	43-51	superoxide dismutase 2	Homo sapiens	37-42
26535076-7	2015	Moreover, lycopene significantly increased manganese superoxide dismutase (MnSOD) expression and decreased cellular ROS levels via the PI3K-Akt pathway.	Lycopene	10-18	superoxide dismutase 2	Homo sapiens	75-80
25989110-2	2015	Antioxidant enzymes, such as Manganese Superoxide Dismutase (MnSOD or SOD2) and Glutathione Peroxidase-1 (GPx1), act coordinately to neutralize ROS.	Reactive Oxygen Species	144-147	superoxide dismutase 2	Homo sapiens	61-66
25989110-2	2015	Antioxidant enzymes, such as Manganese Superoxide Dismutase (MnSOD or SOD2) and Glutathione Peroxidase-1 (GPx1), act coordinately to neutralize ROS.	Reactive Oxygen Species	144-147	superoxide dismutase 2	Homo sapiens	70-74
26400460-0	2015	SOD2 genetic variant associated with treatment-related ototoxicity in cisplatin-treated pediatric medulloblastoma.	Cisplatin	70-79	superoxide dismutase 2	Homo sapiens	0-4
26400460-1	2015	Manganese superoxide dismutase (MnSOD), encoded by the SOD2 gene, is involved in the detoxification of superoxide anion.	Superoxides	103-119	superoxide dismutase 2	Homo sapiens	0-30
26400460-1	2015	Manganese superoxide dismutase (MnSOD), encoded by the SOD2 gene, is involved in the detoxification of superoxide anion.	Superoxides	103-119	superoxide dismutase 2	Homo sapiens	32-37
26400460-1	2015	Manganese superoxide dismutase (MnSOD), encoded by the SOD2 gene, is involved in the detoxification of superoxide anion.	Superoxides	103-119	superoxide dismutase 2	Homo sapiens	55-59
26400460-3	2015	Therefore, we examined SOD2 variants in association with ototoxicity among cisplatin-treated childhood medulloblastoma patients.	Cisplatin	75-84	superoxide dismutase 2	Homo sapiens	23-27
26400460-13	2015	The rs4880 T &gt; C substitution results in a Val &gt; Ala amino acid change at position 16 of the MnSOD mitochondrial targeting sequence.	Valine	46-49	superoxide dismutase 2	Homo sapiens	99-104
26400460-13	2015	The rs4880 T &gt; C substitution results in a Val &gt; Ala amino acid change at position 16 of the MnSOD mitochondrial targeting sequence.	ala amino acid	55-69	superoxide dismutase 2	Homo sapiens	99-104
26400460-14	2015	The Ala variant, which has been associated with increased MnSOD activity, was associated with hearing damage in this study.	Alanine	4-7	superoxide dismutase 2	Homo sapiens	58-63
26400460-15	2015	Platinum-based therapies increase the expression of MnSOD, which may result in an abundance of hydrogen peroxide, a reactive oxygen species.	Platinum	0-8	superoxide dismutase 2	Homo sapiens	52-57
26400460-15	2015	Platinum-based therapies increase the expression of MnSOD, which may result in an abundance of hydrogen peroxide, a reactive oxygen species.	Hydrogen Peroxide	95-112	superoxide dismutase 2	Homo sapiens	52-57
26400460-15	2015	Platinum-based therapies increase the expression of MnSOD, which may result in an abundance of hydrogen peroxide, a reactive oxygen species.	Reactive Oxygen Species	116-139	superoxide dismutase 2	Homo sapiens	52-57
26455407-7	2015	Although there was an up-regulation of some detoxifying enzyme expression such as superoxide dismutase (MnSOD) and sirtuin-1 (SIRT1), the cytotoxic effect caused by arecaidine treatment caused DNA damage, as demonstrated by the increase of histone gamma-H2AX positive cells, and chromosomal aberrations.	arecaidine	165-175	superoxide dismutase 2	Homo sapiens	104-109
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	Ketones	23-30	superoxide dismutase 2	Homo sapiens	153-175
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	Ketones	23-30	superoxide dismutase 2	Homo sapiens	177-181
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	NAD	70-76	superoxide dismutase 2	Homo sapiens	153-175
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	NAD	70-76	superoxide dismutase 2	Homo sapiens	177-181
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	Ketones	252-259	superoxide dismutase 2	Homo sapiens	177-181
26468117-4	2015	In the pharmacological model, paraquat was used to increase superoxide anion levels and porphyrin was the SOD2 analog.	Porphyrins	88-97	superoxide dismutase 2	Homo sapiens	106-110
26586994-4	2015	The results of antioxidant enzyme expression in real-time PCR study revealed that the H2O2 (200 muM) challenged HepG2 cells reduced the expression of enzymes such as SOD, GPx and CAT.	Hydrogen Peroxide	86-90	superoxide dismutase 2	Homo sapiens	166-169
26637092-15	2015	CONCLUSIONS: The profile of expression of SOD1 and SOD2 in cell lines SW480 and SW620 indicates differentiated response of tumor cells depending on access to oxygen.	Oxygen	158-164	superoxide dismutase 2	Homo sapiens	51-55
25659582-8	2015	SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF-beta-mediated induction of both ROS and senescence.	Reactive Oxygen Species	115-118	superoxide dismutase 2	Homo sapiens	0-4
26439801-3	2015	Here we show that hyperglycemia increases the hydrogen peroxide (H2O2) concentration through up-regulation of manganese superoxide dismutase (SOD2) expression, which further activates the ERK and p38 MAPK pathways, as well as the transcription factors NF-kappaB and AP-1, in a time-dependent manner.	Hydrogen Peroxide	46-63	superoxide dismutase 2	Homo sapiens	142-146
26439801-3	2015	Here we show that hyperglycemia increases the hydrogen peroxide (H2O2) concentration through up-regulation of manganese superoxide dismutase (SOD2) expression, which further activates the ERK and p38 MAPK pathways, as well as the transcription factors NF-kappaB and AP-1, in a time-dependent manner.	Hydrogen Peroxide	65-69	superoxide dismutase 2	Homo sapiens	142-146
26439801-4	2015	The invasion of pancreatic cancer cells resulting from the activation of the H2O2/MAPK axis under high glucose conditions is effectively inhibited by PD 98059 (ERK inhibitor), SB 203580 (p38 MAPK inhibitor), polyethylene glycol-conjugated catalase (PEG-CAT), or the siRNA specific to SOD2.	Hydrogen Peroxide	77-81	superoxide dismutase 2	Homo sapiens	284-288
26439801-7	2015	Taken together, our results demonstrate that hyperglycemia enhances cell invasive ability through the SOD2/H2O2/MAPK axis in human pancreatic cancer.	Hydrogen Peroxide	107-111	superoxide dismutase 2	Homo sapiens	102-106
26439801-8	2015	Thus, SOD2/H2O2/MAPK axis may represent a promising therapeutic target for pancreatic cancer patients combined with diabetes mellitus.	Hydrogen Peroxide	11-15	superoxide dismutase 2	Homo sapiens	6-10
26528342-4	2015	Determination of MnSOD Ala-9Val and GPX1 Pro198Leu polymorphisms was performed using real-time polymerase chain reaction amplification.	ala-9val	23-31	superoxide dismutase 2	Homo sapiens	17-22
26528342-8	2015	Furthermore, an overall protective effect of the Ala allele of the MnSOD polymorphism on PCa risk was detected.	Alanine	49-52	superoxide dismutase 2	Homo sapiens	67-72
26416516-8	2015	Terrein induced the induction of anti-oxidant molecules, copper/zinc-superoxide defence (Cu/ZnSOD), manganese superoxide dismutase (MnSOD) and heme oxygenase-1 (HO-1) in SIPS cells.	terrein	0-7	superoxide dismutase 2	Homo sapiens	100-130
25753816-3	2015	In humans, a single nucleotide polymorphism (SNP) is present in the enzyme manganese superoxide dismutase (SOD2), localized in codon 16 (rs4880), which can either be an alanine (A) or valine (V).	Alanine	169-176	superoxide dismutase 2	Homo sapiens	107-111
25753816-3	2015	In humans, a single nucleotide polymorphism (SNP) is present in the enzyme manganese superoxide dismutase (SOD2), localized in codon 16 (rs4880), which can either be an alanine (A) or valine (V).	Valine	184-190	superoxide dismutase 2	Homo sapiens	107-111
25753816-10	2015	In all SOD2 genotypes cells exposed to resveratrol resulted in an upregulation of Sirt1 levels.	Resveratrol	39-50	superoxide dismutase 2	Homo sapiens	7-11
25753816-11	2015	Together, these results suggest that the effect of resveratrol on human PBMC activation is not universal and is dependent on the Ala16Val-SOD2 SNP.	Resveratrol	51-62	superoxide dismutase 2	Homo sapiens	138-142
26384137-6	2015	To evaluate the MnSOD-miR-301a correlation in human PDAC, we have analyzed a total of 60 PDAC specimens, along with 20 normal pancreatic tissue (NPT) specimens.	pdac	52-56	superoxide dismutase 2	Homo sapiens	16-21
26416516-8	2015	Terrein induced the induction of anti-oxidant molecules, copper/zinc-superoxide defence (Cu/ZnSOD), manganese superoxide dismutase (MnSOD) and heme oxygenase-1 (HO-1) in SIPS cells.	terrein	0-7	superoxide dismutase 2	Homo sapiens	132-137
26117316-5	2015	We determined that enhanced Ce(3+)/Ce(4+) ratios improved intracellular dispersion and that the ameliorated intracellular distribution of CNPs-AL-PEG contributes to the elevated expression of SOD2, which leads to increased protection of normal cells against ROS and reduces the oxidatively generated DNA damage.	al-peg	143-149	superoxide dismutase 2	Homo sapiens	192-196
26118716-0	2015	Melatonin protects hepatocytes against bile acid-induced mitochondrial oxidative stress via the AMPK-SIRT3-SOD2 pathway.	Melatonin	0-9	superoxide dismutase 2	Homo sapiens	107-111
26118716-0	2015	Melatonin protects hepatocytes against bile acid-induced mitochondrial oxidative stress via the AMPK-SIRT3-SOD2 pathway.	Bile Acids and Salts	39-48	superoxide dismutase 2	Homo sapiens	107-111
26117316-5	2015	We determined that enhanced Ce(3+)/Ce(4+) ratios improved intracellular dispersion and that the ameliorated intracellular distribution of CNPs-AL-PEG contributes to the elevated expression of SOD2, which leads to increased protection of normal cells against ROS and reduces the oxidatively generated DNA damage.	ros	258-261	superoxide dismutase 2	Homo sapiens	192-196
26118716-6	2015	Notably, melatonin exerted its hepatoprotective effects by upregulating sirtuin 3 (SIRT3) activity and its expression level, thus regulating superoxide dismutase 2 (SOD2) acetylation and inhibiting the production of mROS induced by GCDCA.	Melatonin	9-18	superoxide dismutase 2	Homo sapiens	141-163
26118716-6	2015	Notably, melatonin exerted its hepatoprotective effects by upregulating sirtuin 3 (SIRT3) activity and its expression level, thus regulating superoxide dismutase 2 (SOD2) acetylation and inhibiting the production of mROS induced by GCDCA.	Melatonin	9-18	superoxide dismutase 2	Homo sapiens	165-169
26220658-8	2015	In mitochondria from red fruits, higher ascorbate peroxidase (APX) and Mn-SOD activities are involved in avoiding the accumulation of reactive oxygen species in these organelles during ripening.	Reactive Oxygen Species	134-157	superoxide dismutase 2	Homo sapiens	71-77
26118716-7	2015	Moreover, siRNA targeting SIRT3 blocked the melatonin-mediated elevation in mitochondrial function by inhibiting SIRT3/SOD2 signaling.	Melatonin	44-53	superoxide dismutase 2	Homo sapiens	119-123
26118716-10	2015	In summary, our findings indicate that melatonin is a novel hepatoprotective small molecule that functions by elevating SIRT3, stimulating SOD2 activity, and suppressing mitochondrial oxidative stress at least through AMPK, and that SIRT3 may be of therapeutic value in liver cell protection for GCDCA-induced hepatotoxicity.	Melatonin	39-48	superoxide dismutase 2	Homo sapiens	139-143
26436888-9	2015	Levels of Cu/Zn-SOD, catalase, and Trx were also reduced, while Mn-SOD increased with 50 muM resveratrol treatment.	Resveratrol	93-104	superoxide dismutase 2	Homo sapiens	64-70
26396584-13	2015	Furthermore, the transcription of major antioxidants enzymes (catalase, SOD1, SOD2, GSTK1), and their transcription factor, Nrf2, were reduced in monocytes obtained from HIV positive alcohol users compared to the HIV-negative alcohol user group.	Alcohols	183-190	superoxide dismutase 2	Homo sapiens	78-82
25858271-4	2015	METHOD: 278 (136M:142F) T1DM patients and 135 (72M:63F) normal, healthy controls were investigated for SOD-2 polymorphism in the mitochondrial targeting sequence with Ala/Val (C-9T) substitution.	Alanine	167-170	superoxide dismutase 2	Homo sapiens	103-108
25858271-4	2015	METHOD: 278 (136M:142F) T1DM patients and 135 (72M:63F) normal, healthy controls were investigated for SOD-2 polymorphism in the mitochondrial targeting sequence with Ala/Val (C-9T) substitution.	Valine	171-174	superoxide dismutase 2	Homo sapiens	103-108
25858271-10	2015	CONCLUSION: The SNP in SOD-2 results in a substitution of C to T, which causes an amino acid change from alanine to valine.	Alanine	105-112	superoxide dismutase 2	Homo sapiens	23-28
25858271-10	2015	CONCLUSION: The SNP in SOD-2 results in a substitution of C to T, which causes an amino acid change from alanine to valine.	Valine	116-122	superoxide dismutase 2	Homo sapiens	23-28
26356721-3	2015	Ala-9Val polymorphism, a functional polymorphism of MnSOD gene, has been reported to be related to the risk of schizophrenia and TD.	ala-9val	0-8	superoxide dismutase 2	Homo sapiens	52-57
26198315-10	2015	The levels of reactive oxygen and nitrogen species (ROS/RNS) between MDR and non-MDR cells significantly differed upon exposure to 6, accompanied by changes in the glutathione (GSH) levels and in the expression of manganese superoxide dismutase (MnSOD), glutathione-S-transferase pi (GST pi) and hypoxia-inducible factor-1alpha (HIF-1alpha).	ros	52-55	superoxide dismutase 2	Homo sapiens	214-244
26356721-5	2015	We performed meta-analyses aiming to assess the association between MnSOD activity and schizophrenia, as well as the association of MnSOD Ala-9Val polymorphism with schizophrenia and TD in schizophrenic patients.We search for the literature on MnSOD and schizophrenia in English or Chinese published up to May 1, 2015 on PubMed, EMBASE, the Cochrane Databases, Chinese National Knowledge Infrastructure, China Biology Medical and Wanfang databases.	ala-9val	138-146	superoxide dismutase 2	Homo sapiens	132-137
26356721-5	2015	We performed meta-analyses aiming to assess the association between MnSOD activity and schizophrenia, as well as the association of MnSOD Ala-9Val polymorphism with schizophrenia and TD in schizophrenic patients.We search for the literature on MnSOD and schizophrenia in English or Chinese published up to May 1, 2015 on PubMed, EMBASE, the Cochrane Databases, Chinese National Knowledge Infrastructure, China Biology Medical and Wanfang databases.	ala-9val	138-146	superoxide dismutase 2	Homo sapiens	132-137
26356721-14	2015	Longitudinal studies with larger sample sizes and different ethnicities are needed to confirm the association of the MnSOD Ala-9Val variants with schizophrenia and TD.	ala-9val	123-131	superoxide dismutase 2	Homo sapiens	117-122
25958349-9	2015	Serum total cholesterol (p&lt;0.01) and MDA (p&lt;0.001) levels were significantly higher in subjects with the VV genotype for MnSOD in the obese and non-obese groups.	Cholesterol	12-23	superoxide dismutase 2	Homo sapiens	127-132
25576182-4	2015	There is a growing consensus that the mitochondrial SOD isoform - SOD2 and GSH are critical for the cellular antioxidant defense.	Glutathione	75-78	superoxide dismutase 2	Homo sapiens	52-55
25937300-7	2015	We further showed that Nelfinavir increased mitochondrial ROS production by decreasing manganese superoxide dismutase (MnSOD) protein levels.	Nelfinavir	23-33	superoxide dismutase 2	Homo sapiens	87-117
25937300-7	2015	We further showed that Nelfinavir increased mitochondrial ROS production by decreasing manganese superoxide dismutase (MnSOD) protein levels.	Nelfinavir	23-33	superoxide dismutase 2	Homo sapiens	119-124
26059423-4	2015	Pretreatment with CA completely attenuated the inhibited expression of manganese superoxide dismutase (MnSOD) and the B-cell lymphoma-extra large (Bcl-xL), and reduced glutathione activity caused by H2O2, whereas it reversed reactive oxygen species accumulation and the increase in cleaved caspase-3.	Hydrogen Peroxide	199-203	superoxide dismutase 2	Homo sapiens	71-101
26059423-4	2015	Pretreatment with CA completely attenuated the inhibited expression of manganese superoxide dismutase (MnSOD) and the B-cell lymphoma-extra large (Bcl-xL), and reduced glutathione activity caused by H2O2, whereas it reversed reactive oxygen species accumulation and the increase in cleaved caspase-3.	Hydrogen Peroxide	199-203	superoxide dismutase 2	Homo sapiens	103-108
26059423-4	2015	Pretreatment with CA completely attenuated the inhibited expression of manganese superoxide dismutase (MnSOD) and the B-cell lymphoma-extra large (Bcl-xL), and reduced glutathione activity caused by H2O2, whereas it reversed reactive oxygen species accumulation and the increase in cleaved caspase-3.	Reactive Oxygen Species	225-248	superoxide dismutase 2	Homo sapiens	71-101
25937300-7	2015	We further showed that Nelfinavir increased mitochondrial ROS production by decreasing manganese superoxide dismutase (MnSOD) protein levels.	Reactive Oxygen Species	58-61	superoxide dismutase 2	Homo sapiens	87-117
25937300-7	2015	We further showed that Nelfinavir increased mitochondrial ROS production by decreasing manganese superoxide dismutase (MnSOD) protein levels.	Reactive Oxygen Species	58-61	superoxide dismutase 2	Homo sapiens	119-124
26028649-5	2015	Trx induces manganese superoxide dismutase (MnSOD) gene transcription by activating MKK4 via redox control of Cys-246 and Cys-266, as mutation of these residues abrogates MKK4 activation and MnSOD expression.	Cysteine	110-113	superoxide dismutase 2	Homo sapiens	12-42
25908444-2	2015	Manganese superoxide dismutase (SOD2) is the major enzymatic superoxide scavenger present in the mitochondrial matrix and one of the most crucial reactive oxygen species-scavenging enzymes in the cell.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-36
25908444-2	2015	Manganese superoxide dismutase (SOD2) is the major enzymatic superoxide scavenger present in the mitochondrial matrix and one of the most crucial reactive oxygen species-scavenging enzymes in the cell.	Reactive Oxygen Species	146-169	superoxide dismutase 2	Homo sapiens	32-36
25908444-3	2015	SOD2 is activated by sirtuin 3 (SIRT3) through NAD(+)-dependent deacetylation.	NAD	47-53	superoxide dismutase 2	Homo sapiens	0-4
25908444-6	2015	These SOD2 mutations affected the superoxide-scavenging activity in vitro and in HEK293T cells.	Superoxides	34-44	superoxide dismutase 2	Homo sapiens	6-10
25908444-7	2015	The lysine 68 (K68) site is the most important acetylation site contributing to SOD2 activation and plays a role in cell survival after paraquat treatment.	Lysine	4-10	superoxide dismutase 2	Homo sapiens	80-84
25908444-7	2015	The lysine 68 (K68) site is the most important acetylation site contributing to SOD2 activation and plays a role in cell survival after paraquat treatment.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	15-18	superoxide dismutase 2	Homo sapiens	80-84
25908444-7	2015	The lysine 68 (K68) site is the most important acetylation site contributing to SOD2 activation and plays a role in cell survival after paraquat treatment.	Paraquat	136-144	superoxide dismutase 2	Homo sapiens	80-84
25908444-8	2015	The molecular basis underlying the regulation of SOD2 activity by K68 was investigated in detail.	(4,5,6,7-Tetrabromo-1h-Benzimidazol-1-Yl)acetic Acid	66-69	superoxide dismutase 2	Homo sapiens	49-53
25908444-10	2015	Thus, the entry of the superoxide anion into the coordinated core of SOD2 was inhibited.	Superoxides	23-39	superoxide dismutase 2	Homo sapiens	69-73
25662905-6	2015	RESULTS: Among patients who underwent RT in the test cohort, there was a significant association between 3 of the 7 SOD2 SNPs and lethal prostate cancer: rs6917589 (overall P = .006), rs2758331 (P = .04) and the functional valine to alanine polymorphism in rs4880 (P = .04).	Valine	223-229	superoxide dismutase 2	Homo sapiens	116-120
25662905-6	2015	RESULTS: Among patients who underwent RT in the test cohort, there was a significant association between 3 of the 7 SOD2 SNPs and lethal prostate cancer: rs6917589 (overall P = .006), rs2758331 (P = .04) and the functional valine to alanine polymorphism in rs4880 (P = .04).	Alanine	233-240	superoxide dismutase 2	Homo sapiens	116-120
26028649-5	2015	Trx induces manganese superoxide dismutase (MnSOD) gene transcription by activating MKK4 via redox control of Cys-246 and Cys-266, as mutation of these residues abrogates MKK4 activation and MnSOD expression.	Cysteine	110-113	superoxide dismutase 2	Homo sapiens	44-49
26028649-5	2015	Trx induces manganese superoxide dismutase (MnSOD) gene transcription by activating MKK4 via redox control of Cys-246 and Cys-266, as mutation of these residues abrogates MKK4 activation and MnSOD expression.	Cysteine	122-125	superoxide dismutase 2	Homo sapiens	12-42
26028649-5	2015	Trx induces manganese superoxide dismutase (MnSOD) gene transcription by activating MKK4 via redox control of Cys-246 and Cys-266, as mutation of these residues abrogates MKK4 activation and MnSOD expression.	Cysteine	122-125	superoxide dismutase 2	Homo sapiens	44-49
26108578-4	2015	We herein demonstrate that mechanical loading promoted mitochondrial superoxide generation and selective Sod2 downregulation in chondrocytes in vivo and that mitochondrial superoxide inducer also downregulated Sod2 expression in chondrocytes in vitro.	Superoxides	172-182	superoxide dismutase 2	Homo sapiens	210-214
26350743-3	2015	Carnosine-induced inhibition of U-118-MG proliferation is associated with a significant: decrease in cellular reactive oxygen species levels, increase in manganese superoxide dismutase (MnSOD) and increase in cyclin B1 expression resulting in G2-block.	u-118	32-37	superoxide dismutase 2	Homo sapiens	154-184
25933618-1	2015	AIMS/HYPOTHESIS: Oxidative stress and microvascular damage have been implicated in the pathogenesis of diabetic neuropathy, with manganese superoxide dismutase 2 (SOD2) responsible for superoxide detoxification in mitochondria.	Superoxides	139-149	superoxide dismutase 2	Homo sapiens	163-167
26108578-5	2015	A genetically manipulated model revealed that Sod2 deficiency in chondrocytes also resulted in mitochondrial superoxide overproduction and dysfunction, thus leading to cartilage degeneration.	Superoxides	109-119	superoxide dismutase 2	Homo sapiens	46-50
25810259-7	2015	In contrast, the presence of a pharmacological MnSOD inhibitor, 2-methoxyestradiol, results in increased sensitivity to BNIP3-mediated cell death in adult myocytes.	2-Methoxyestradiol	64-82	superoxide dismutase 2	Homo sapiens	47-52
25810259-8	2015	Cotreatment with the mitochondria-targeted antioxidant MitoTEMPO or the MnSOD mimetic manganese (III) tetrakis (4-benzoic acid) porphyrin chloride abrogates the increased cell death by 2-methoxyestradiol.	manganese (iii) tetrakis (4-benzoic acid) porphyrin chloride	86-146	superoxide dismutase 2	Homo sapiens	72-77
25810259-8	2015	Cotreatment with the mitochondria-targeted antioxidant MitoTEMPO or the MnSOD mimetic manganese (III) tetrakis (4-benzoic acid) porphyrin chloride abrogates the increased cell death by 2-methoxyestradiol.	2-Methoxyestradiol	185-203	superoxide dismutase 2	Homo sapiens	72-77
25655385-7	2015	The 2-methoxyestradiol may bind MnSODcd to interfere with the cross-linking between the two active sites of the dimer enzyme, compromising the SOD activity.	2-Methoxyestradiol	4-22	superoxide dismutase 2	Homo sapiens	34-37
25889634-2	2015	The MTT was used to measure cytotoxicity of the MnSODm.	monooxyethylene trimethylolpropane tristearate	4-7	superoxide dismutase 2	Homo sapiens	48-54
25745980-7	2015	In addition, VPA exposure for 72 h increased levels of mitochondrial reactive oxygen species (ROS), but adversely decreased protein levels of mitochondrial superoxide dismutase SOD2, suggesting oxidative stress caused by impaired elimination of mitochondrial ROS and a novel pathomechanism related to VPA toxicity.	Valproic Acid	13-16	superoxide dismutase 2	Homo sapiens	177-181
25704631-10	2015	The expression of mitochondrium-specific antioxidant enzyme, SOD2, is reduced which may limit the ROS scavenging ability and cause imbalance of the mitochondrial ROS homeostasis.	ros	98-101	superoxide dismutase 2	Homo sapiens	61-65
25294747-1	2015	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that defends against oxidative damage due to reactive oxygen species (ROS).	Reactive Oxygen Species	110-133	superoxide dismutase 2	Homo sapiens	0-30
25294747-1	2015	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that defends against oxidative damage due to reactive oxygen species (ROS).	Reactive Oxygen Species	110-133	superoxide dismutase 2	Homo sapiens	32-37
25294747-1	2015	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that defends against oxidative damage due to reactive oxygen species (ROS).	Reactive Oxygen Species	135-138	superoxide dismutase 2	Homo sapiens	0-30
25294747-1	2015	Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that defends against oxidative damage due to reactive oxygen species (ROS).	Reactive Oxygen Species	135-138	superoxide dismutase 2	Homo sapiens	32-37
25704631-10	2015	The expression of mitochondrium-specific antioxidant enzyme, SOD2, is reduced which may limit the ROS scavenging ability and cause imbalance of the mitochondrial ROS homeostasis.	ros	162-165	superoxide dismutase 2	Homo sapiens	61-65
25855962-5	2015	Oroxylin A promotes superoxide dismutase (SOD2) gene expression through SIRT3-regulated DNA-binding activity of FOXO3a and increases the activity of SOD2 by promoting SIRT3-mediated deacetylation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	superoxide dismutase 2	Homo sapiens	42-46
25855962-5	2015	Oroxylin A promotes superoxide dismutase (SOD2) gene expression through SIRT3-regulated DNA-binding activity of FOXO3a and increases the activity of SOD2 by promoting SIRT3-mediated deacetylation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	superoxide dismutase 2	Homo sapiens	149-153
25855962-0	2015	Oroxylin A inhibits glycolysis-dependent proliferation of human breast cancer via promoting SIRT3-mediated SOD2 transcription and HIF1alpha destabilization.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	superoxide dismutase 2	Homo sapiens	107-111
25463039-2	2015	Mitochondrial manganese superoxide dismutase (MnSOD) normally keeps ROS and RNS in check.	Reactive Oxygen Species	68-71	superoxide dismutase 2	Homo sapiens	14-44
28962395-8	2015	Our present experimental data support the notion that Cr(VI) caused mitochondrial damage, apoptosis, oxidative stress, and subsequently lead to a strong induction of HO1, GCLC and SOD2 via the Nrf-2 signaling pathway in hepatocytes.	Chromium	54-56	superoxide dismutase 2	Homo sapiens	180-184
25708841-0	2015	Pre-exposure of neuroblastoma cell line to pulsed electromagnetic field prevents H2 O2 -induced ROS production by increasing MnSOD activity.	Hydrogen Peroxide	81-86	superoxide dismutase 2	Homo sapiens	125-130
25708841-0	2015	Pre-exposure of neuroblastoma cell line to pulsed electromagnetic field prevents H2 O2 -induced ROS production by increasing MnSOD activity.	Reactive Oxygen Species	96-99	superoxide dismutase 2	Homo sapiens	125-130
25463039-2	2015	Mitochondrial manganese superoxide dismutase (MnSOD) normally keeps ROS and RNS in check.	Reactive Oxygen Species	68-71	superoxide dismutase 2	Homo sapiens	46-51
25463039-2	2015	Mitochondrial manganese superoxide dismutase (MnSOD) normally keeps ROS and RNS in check.	Reactive Nitrogen Species	76-79	superoxide dismutase 2	Homo sapiens	14-44
25463039-2	2015	Mitochondrial manganese superoxide dismutase (MnSOD) normally keeps ROS and RNS in check.	Reactive Nitrogen Species	76-79	superoxide dismutase 2	Homo sapiens	46-51
24677319-2	2015	Therefore, our study investigated the effect of a butyrate treatment on catalase (CAT) and superoxide dismutase (SOD2) in matched human colon tissues of different transformation stages (n = 3-15 in each group) ex vivo.	Butyrates	50-58	superoxide dismutase 2	Homo sapiens	113-117
25578653-3	2015	Manganese superoxide dismutase (MnSOD), a primary mitochondrial antioxidant in mammals, has long been known to play a crucial role in radioadaptive protection by detoxifying O2( -) generated by mitochondrial oxidative phosphorylation.	Oxygen	174-176	superoxide dismutase 2	Homo sapiens	0-30
25578653-3	2015	Manganese superoxide dismutase (MnSOD), a primary mitochondrial antioxidant in mammals, has long been known to play a crucial role in radioadaptive protection by detoxifying O2( -) generated by mitochondrial oxidative phosphorylation.	Oxygen	174-176	superoxide dismutase 2	Homo sapiens	32-37
25578653-7	2015	The mitochondrial-localized CDK4 directly phosphorylates MnSOD at serine-106 (S106), causing enhanced MnSOD enzymatic activity and mitochondrial respiration.	Serine	66-72	superoxide dismutase 2	Homo sapiens	57-62
25578653-7	2015	The mitochondrial-localized CDK4 directly phosphorylates MnSOD at serine-106 (S106), causing enhanced MnSOD enzymatic activity and mitochondrial respiration.	Serine	66-72	superoxide dismutase 2	Homo sapiens	102-107
25524402-6	2015	The multivariate linear regression adjusting for selenium status showed that plasma Se level was significantly inversely associated only with expression of GSTP1 (beta-coef.=-0.270, p=0.009), PRDXR1 (beta-coef.=-0.245, p=0.017) and SOD2 with an inverse trend toward significance (beta-coef.=-0.186, p=0.074), but without an effect of NRF2 gene variants.	Selenium	84-86	superoxide dismutase 2	Homo sapiens	232-236
25039350-0	2015	Exposure of chronic myelogenous leukemia cells to imatinib results in the post-transcriptional induction of manganese superoxide dismutase.	Imatinib Mesylate	50-58	superoxide dismutase 2	Homo sapiens	108-138
24677319-7	2015	Despite a significantly lowered SOD2 transcript (0.51-fold, P &lt; 0.01) and, to a lesser extent, protein level (0.86-fold) after butyrate exposure of normal colon cells, the catalytic activity was significantly enhanced (1.19-fold, P &lt; 0.05), suggesting an increased protection against tissue superoxide radicals.	Butyrates	130-138	superoxide dismutase 2	Homo sapiens	32-36
26045757-13	2015	The levels of reactive oxygen species (ROS), which was an oxidative stress marker, was significantly increased in cardiomyocytes by exposure to PAL, but overexpressing Nrf1 could ameliorate ROS-induced cardiomyocyte toxicity and increase the expression of SOD1 and SOD2 in HCMs by overexpressing Nrf1.	Reactive Oxygen Species	14-37	superoxide dismutase 2	Homo sapiens	265-269
25578561-4	2015	We found that UM1 cells (TSCC cells with increased SOD2 expression, migration and invasion abilities) possessed a higher proportion of SP cells, sphere and colony formation, and expressed a higher level of stem cell markers compared to UM2 cells (reduced SOD2 expression, migration and invasion abilities).	sp	135-137	superoxide dismutase 2	Homo sapiens	51-55
26045757-13	2015	The levels of reactive oxygen species (ROS), which was an oxidative stress marker, was significantly increased in cardiomyocytes by exposure to PAL, but overexpressing Nrf1 could ameliorate ROS-induced cardiomyocyte toxicity and increase the expression of SOD1 and SOD2 in HCMs by overexpressing Nrf1.	Reactive Oxygen Species	39-42	superoxide dismutase 2	Homo sapiens	265-269
26045757-13	2015	The levels of reactive oxygen species (ROS), which was an oxidative stress marker, was significantly increased in cardiomyocytes by exposure to PAL, but overexpressing Nrf1 could ameliorate ROS-induced cardiomyocyte toxicity and increase the expression of SOD1 and SOD2 in HCMs by overexpressing Nrf1.	Reactive Oxygen Species	190-193	superoxide dismutase 2	Homo sapiens	265-269
25672499-6	2015	In PAH, acquired mitochondrial abnormalities, including epigenetic silencing of superoxide dismutase (SOD2), disrupt oxygen sensing creating a pseudo-hypoxic environment characterized by normoxic activation of hypoxia-inducible factor-1alpha (HIF-1alpha).	Oxygen	117-123	superoxide dismutase 2	Homo sapiens	102-106
25472572-5	2015	Changes of manganese superoxide dismutase, Bcl-2, and Bim were also reversed by ICA, and apoptosis was reduced.	icariin	80-83	superoxide dismutase 2	Homo sapiens	11-41
25651975-0	2015	MnSOD upregulation sustains the Warburg effect via mitochondrial ROS and AMPK-dependent signalling in cancer.	Reactive Oxygen Species	65-68	superoxide dismutase 2	Homo sapiens	0-5
25561743-6	2015	On the other hand, ectopic expression of Mn-SOD attenuated the arsenite-generated superoxide radical level, abrogated nucleolin-SUMO, and in turn inhibited arsenite-induced apoptosis by reducing GADD45alpha expression.	arsenite	63-71	superoxide dismutase 2	Homo sapiens	41-47
25561743-6	2015	On the other hand, ectopic expression of Mn-SOD attenuated the arsenite-generated superoxide radical level, abrogated nucleolin-SUMO, and in turn inhibited arsenite-induced apoptosis by reducing GADD45alpha expression.	Superoxides	82-100	superoxide dismutase 2	Homo sapiens	41-47
25561743-6	2015	On the other hand, ectopic expression of Mn-SOD attenuated the arsenite-generated superoxide radical level, abrogated nucleolin-SUMO, and in turn inhibited arsenite-induced apoptosis by reducing GADD45alpha expression.	arsenite	156-164	superoxide dismutase 2	Homo sapiens	41-47
25671321-8	2015	Further, we show that increasing mitochondrial superoxide levels through deletion of sod-2 or treatment with paraquat can still increase lifespan in clk-1;sod-1 double mutants, which live shorter than clk-1 worms.	Superoxides	47-57	superoxide dismutase 2	Homo sapiens	85-90
25901207-0	2015	SOD2 rs4880 CT/CC genotype predicts poor survival for Chinese gastric cancer patients received platinum and fluorouracil based adjuvant chemotherapy.	Platinum	95-103	superoxide dismutase 2	Homo sapiens	0-4
25901207-0	2015	SOD2 rs4880 CT/CC genotype predicts poor survival for Chinese gastric cancer patients received platinum and fluorouracil based adjuvant chemotherapy.	Fluorouracil	108-120	superoxide dismutase 2	Homo sapiens	0-4
25651975-1	2015	Manganese superoxide dismutase (MnSOD/SOD2) is a mitochondria-resident enzyme that governs the types of reactive oxygen species egressing from the organelle to affect cellular signalling.	Reactive Oxygen Species	104-127	superoxide dismutase 2	Homo sapiens	0-30
25651975-1	2015	Manganese superoxide dismutase (MnSOD/SOD2) is a mitochondria-resident enzyme that governs the types of reactive oxygen species egressing from the organelle to affect cellular signalling.	Reactive Oxygen Species	104-127	superoxide dismutase 2	Homo sapiens	32-37
25651975-1	2015	Manganese superoxide dismutase (MnSOD/SOD2) is a mitochondria-resident enzyme that governs the types of reactive oxygen species egressing from the organelle to affect cellular signalling.	Reactive Oxygen Species	104-127	superoxide dismutase 2	Homo sapiens	38-42
25651975-2	2015	Here we demonstrate that MnSOD upregulation in cancer cells establishes a steady flow of H2O2 originating from mitochondria that sustains AMP-activated kinase (AMPK) activation and the metabolic shift to glycolysis.	Hydrogen Peroxide	89-93	superoxide dismutase 2	Homo sapiens	25-30
25499851-0	2015	MnSOD overexpression confers cisplatin resistance in lung adenocarcinoma via the NF-kappaB/Snail/Bcl-2 pathway.	Cisplatin	29-38	superoxide dismutase 2	Homo sapiens	0-5
25497738-2	2015	Glutathione peroxidase (GPx) is one of the first endogenous antioxidant defense enzymes, and it works cooperatively with superoxide dismutase (SOD) and catalase (CAT) to detoxify free radicals from the cellular environment.	Free Radicals	179-192	superoxide dismutase 2	Homo sapiens	143-146
25497738-8	2015	Evaluating the subgroup of 293 ICU patients with sepsis, a pooled analysis including two genetic variants GPx1 and SOD2 (47C&gt;T SNP, rs4880; protein variant in MnSOD: Ala-9Val) showed a significant difference in relation to progression to septic shock.	Alanine	169-172	superoxide dismutase 2	Homo sapiens	115-119
25497738-8	2015	Evaluating the subgroup of 293 ICU patients with sepsis, a pooled analysis including two genetic variants GPx1 and SOD2 (47C&gt;T SNP, rs4880; protein variant in MnSOD: Ala-9Val) showed a significant difference in relation to progression to septic shock.	Alanine	169-172	superoxide dismutase 2	Homo sapiens	162-167
25499851-1	2015	Manganese superoxide dismutase (MnSOD) has been shown to be associated with doxorubicin resistance in gastric cancer cells, but the underlying mechanism of MnSOD in drug resistance remains unclear.	Doxorubicin	76-87	superoxide dismutase 2	Homo sapiens	0-30
25499851-1	2015	Manganese superoxide dismutase (MnSOD) has been shown to be associated with doxorubicin resistance in gastric cancer cells, but the underlying mechanism of MnSOD in drug resistance remains unclear.	Doxorubicin	76-87	superoxide dismutase 2	Homo sapiens	32-37
25499851-3	2015	Therefore, we hypothesized that MnSOD-mediated NF-kappaB activation might confer cisplatin resistance in lung adenocarcinoma via the NF-kappaB/Bcl-2/Snail pathway.	Cisplatin	81-90	superoxide dismutase 2	Homo sapiens	32-37
25499851-4	2015	Here, the inhibition concentration of cisplatin with 50% cell viability (IC50) was positively correlated with MnSOD expression and its activity in a panel of lung adenocarcinoma cells.	Cisplatin	38-47	superoxide dismutase 2	Homo sapiens	110-115
25499851-6	2015	Mechanistically, an increase in Bcl-2 by MnSOD-mediated NF-kappaB activation confers greater cisplatin resistance than cIAP2, Bcl-xL, Mcl-1, and Snail.	Cisplatin	93-102	superoxide dismutase 2	Homo sapiens	41-46
25499851-7	2015	MnSOD-mediated cisplatin resistance can be overcome by a Bcl-2 antagonist (ABT-199) or IKKbeta inhibitor (curcumin) in cells and xenograft tumors.	Cisplatin	15-24	superoxide dismutase 2	Homo sapiens	0-5
25499851-7	2015	MnSOD-mediated cisplatin resistance can be overcome by a Bcl-2 antagonist (ABT-199) or IKKbeta inhibitor (curcumin) in cells and xenograft tumors.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	75-78	superoxide dismutase 2	Homo sapiens	0-5
25499851-7	2015	MnSOD-mediated cisplatin resistance can be overcome by a Bcl-2 antagonist (ABT-199) or IKKbeta inhibitor (curcumin) in cells and xenograft tumors.	Curcumin	106-114	superoxide dismutase 2	Homo sapiens	0-5
25499851-9	2015	A retrospective study indicated that it was more common for MnSOD-positive, nuclear p65-positive, or high Bcl-2 mRNA tumors to have an unfavorable response to cisplatin-based chemotherapy than their counterparts.	Cisplatin	159-168	superoxide dismutase 2	Homo sapiens	60-65
25499851-10	2015	Therefore, we suggest that ABT-199 or curcumin may be potentially useful to improve tumor regression and chemotherapeutic response in patients with MnSOD/Bcl-2-positive tumors.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	27-30	superoxide dismutase 2	Homo sapiens	148-153
25499851-10	2015	Therefore, we suggest that ABT-199 or curcumin may be potentially useful to improve tumor regression and chemotherapeutic response in patients with MnSOD/Bcl-2-positive tumors.	Curcumin	38-46	superoxide dismutase 2	Homo sapiens	148-153
25499816-8	2015	In the present study, we used expressions of catalase (antioxidant against H2O2) and superoxide dismutase 2 (SOD2, antioxidant against O2(-)) to decrease ROS level and investigated their role in the process of arsenic-induced cell transformation.	Reactive Oxygen Species	154-157	superoxide dismutase 2	Homo sapiens	85-107
25434963-8	2015	The expression of PGC-1alpha and SOD-2 following chemotherapy were upregulated, but accompanied by increased ROS.	Reactive Oxygen Species	109-112	superoxide dismutase 2	Homo sapiens	33-38
25315187-8	2015	Further mass spectrometry analysis indicated that both ACAT1 and MnSOD had characterized acetylation at lysine residues, which is the first time to identify acetylation of ACAT1 and MnSOD in ccRCC.	Lysine	104-110	superoxide dismutase 2	Homo sapiens	65-70
25315187-8	2015	Further mass spectrometry analysis indicated that both ACAT1 and MnSOD had characterized acetylation at lysine residues, which is the first time to identify acetylation of ACAT1 and MnSOD in ccRCC.	Lysine	104-110	superoxide dismutase 2	Homo sapiens	182-187
25295643-8	2015	These observations lead to the hypothesis that SOD2 polymorphism may cause a defective control of the oxidative phenomena linked to cortical spreading depression, the neurophysiological hallmark of migraine aura, causing an overstimulation of trigeminal neurons and UAs triggering.	Phenindione	266-269	superoxide dismutase 2	Homo sapiens	47-51
25499816-8	2015	In the present study, we used expressions of catalase (antioxidant against H2O2) and superoxide dismutase 2 (SOD2, antioxidant against O2(-)) to decrease ROS level and investigated their role in the process of arsenic-induced cell transformation.	Reactive Oxygen Species	154-157	superoxide dismutase 2	Homo sapiens	109-113
25499816-8	2015	In the present study, we used expressions of catalase (antioxidant against H2O2) and superoxide dismutase 2 (SOD2, antioxidant against O2(-)) to decrease ROS level and investigated their role in the process of arsenic-induced cell transformation.	Arsenic	210-217	superoxide dismutase 2	Homo sapiens	85-107
25858870-5	2015	Of these, manganese-dependent SOD (MnSOD) plays a major role due to its mitochondrial location, i.e., the main site of superoxide (O(2)( -)) production.	Superoxides	119-129	superoxide dismutase 2	Homo sapiens	10-33
25445048-7	2015	Curcumin increased superoxide dimutase-2 (SOD2) transcription and activity by AMPK/PGC-1alpha axis.	Curcumin	0-8	superoxide dismutase 2	Homo sapiens	42-46
25445048-9	2015	These results demonstrated the promotion effect of curcumin on PGC-1alpha expression through AMPK pathway, which led to the increases in PPARgamma activity and in SOD-2 transcription and activity.	Curcumin	51-59	superoxide dismutase 2	Homo sapiens	163-168
25858870-5	2015	Of these, manganese-dependent SOD (MnSOD) plays a major role due to its mitochondrial location, i.e., the main site of superoxide (O(2)( -)) production.	Superoxides	119-129	superoxide dismutase 2	Homo sapiens	35-40
25858870-5	2015	Of these, manganese-dependent SOD (MnSOD) plays a major role due to its mitochondrial location, i.e., the main site of superoxide (O(2)( -)) production.	Superoxides	131-135	superoxide dismutase 2	Homo sapiens	10-33
25858870-5	2015	Of these, manganese-dependent SOD (MnSOD) plays a major role due to its mitochondrial location, i.e., the main site of superoxide (O(2)( -)) production.	Superoxides	131-135	superoxide dismutase 2	Homo sapiens	35-40
25529796-8	2015	Thus, the NAD(+)-dependent inhibition of SOD2 activity and ROS by SIRT1 provides a gatekeeper function to reduce PARK2-mediated mitophagy and aberrant cell survival.	NAD	10-16	superoxide dismutase 2	Homo sapiens	41-45
26120888-6	2015	Specifically, Cd decreased SIRT3 protein expression and activity and promoted the acetylation of SOD2, superoxide dismutase 2, mitochondrial, thus decreasing its activity, a key enzyme involved in mitochondrial ROS production, although Cd did not disrupt the interaction between SIRT3 and SOD2.	Cadmium	14-16	superoxide dismutase 2	Homo sapiens	289-293
25529796-4	2015	Genetic deletion of Sirt1 increased mitochondrial superoxide dismutase 2 (Sod2) acetylation of lysine residue 68, thereby enhancing reactive oxygen species (ROS) production and reducing SOD2 activity.	Lysine	95-101	superoxide dismutase 2	Homo sapiens	74-78
25529796-4	2015	Genetic deletion of Sirt1 increased mitochondrial superoxide dismutase 2 (Sod2) acetylation of lysine residue 68, thereby enhancing reactive oxygen species (ROS) production and reducing SOD2 activity.	Reactive Oxygen Species	132-155	superoxide dismutase 2	Homo sapiens	74-78
25529796-4	2015	Genetic deletion of Sirt1 increased mitochondrial superoxide dismutase 2 (Sod2) acetylation of lysine residue 68, thereby enhancing reactive oxygen species (ROS) production and reducing SOD2 activity.	Reactive Oxygen Species	157-160	superoxide dismutase 2	Homo sapiens	74-78
25684475-6	2015	RESULTS: The frequencies of MnSOD Ala/Ala, Ala/Val and Val/Val genotypes in healthy individuals were 24.3, 66.7 and 9%, respectively.	Alanine	34-37	superoxide dismutase 2	Homo sapiens	28-33
26120888-0	2015	SIRT3-SOD2-mROS-dependent autophagy in cadmium-induced hepatotoxicity and salvage by melatonin.	Cadmium	39-46	superoxide dismutase 2	Homo sapiens	6-10
26120888-9	2015	Notably, melatonin treatment enhanced the activity but not the expression of SIRT3, decreased the acetylation of SOD2, inhibited mitochondrial-derived O2( -) production and suppressed the autophagy induced by 10 muM Cd.	Melatonin	9-18	superoxide dismutase 2	Homo sapiens	113-117
26120888-0	2015	SIRT3-SOD2-mROS-dependent autophagy in cadmium-induced hepatotoxicity and salvage by melatonin.	Melatonin	85-94	superoxide dismutase 2	Homo sapiens	6-10
26120888-10	2015	Moreover, 3-(1H-1,2,3-triazol-4-yl)pyridine, a confirmed selective SIRT3 inhibitor, blocked the melatonin-mediated suppression of autophagy by inhibiting SIRT3-SOD2 signaling.	3-TYP	10-43	superoxide dismutase 2	Homo sapiens	160-164
26120888-6	2015	Specifically, Cd decreased SIRT3 protein expression and activity and promoted the acetylation of SOD2, superoxide dismutase 2, mitochondrial, thus decreasing its activity, a key enzyme involved in mitochondrial ROS production, although Cd did not disrupt the interaction between SIRT3 and SOD2.	Cadmium	14-16	superoxide dismutase 2	Homo sapiens	97-101
26120888-10	2015	Moreover, 3-(1H-1,2,3-triazol-4-yl)pyridine, a confirmed selective SIRT3 inhibitor, blocked the melatonin-mediated suppression of autophagy by inhibiting SIRT3-SOD2 signaling.	Melatonin	96-105	superoxide dismutase 2	Homo sapiens	160-164
26120888-12	2015	These results suggest that melatonin exerts a hepatoprotective effect on mitochondrial-derived O2( -)-stimulated autophagic cell death that is dependent on the SIRT3/SOD2 pathway.	Melatonin	27-36	superoxide dismutase 2	Homo sapiens	166-170
26120888-12	2015	These results suggest that melatonin exerts a hepatoprotective effect on mitochondrial-derived O2( -)-stimulated autophagic cell death that is dependent on the SIRT3/SOD2 pathway.	Superoxides	95-101	superoxide dismutase 2	Homo sapiens	166-170
25515622-0	2015	Trichostatin A modulates intracellular reactive oxygen species through SOD2 and FOXO1 in human bone marrow-mesenchymal stem cells.	trichostatin A	0-14	superoxide dismutase 2	Homo sapiens	71-75
25921655-5	2015	Salidroside induced the intracellular mRNA expression, protein expression, and enzymatic activities of catalase and Mn-SOD and increased the ratio of Bcl2/Bax.	rhodioloside	0-11	superoxide dismutase 2	Homo sapiens	116-122
25515622-0	2015	Trichostatin A modulates intracellular reactive oxygen species through SOD2 and FOXO1 in human bone marrow-mesenchymal stem cells.	Reactive Oxygen Species	39-62	superoxide dismutase 2	Homo sapiens	71-75
25515622-8	2015	Investigation of Forkhead box O1 (FOXO1), superoxide dismutase 2 (SOD2), and p53 levels to determine intracellular signaling by TSA in oxidative stress-induced MSCs demonstrated that expression of phosphorylated-FOXO1 and phosphorylated-SOD2 decreased in H2 O2 -treated MSCs while levels of p53 increased.	trichostatin A	128-131	superoxide dismutase 2	Homo sapiens	237-241
25515622-5	2015	Levels of the antioxidant enzyme superoxide dismutase 2 (SOD2) increased following treatment with 200 nM TSA and to a lesser level at 1-5 muM TSA.	trichostatin A	105-108	superoxide dismutase 2	Homo sapiens	33-55
25515622-10	2015	These results suggest that the main function of ROS modulation by TSA is activated through SOD2 and FOXO1.	Reactive Oxygen Species	48-51	superoxide dismutase 2	Homo sapiens	91-95
25515622-10	2015	These results suggest that the main function of ROS modulation by TSA is activated through SOD2 and FOXO1.	trichostatin A	66-69	superoxide dismutase 2	Homo sapiens	91-95
25515622-5	2015	Levels of the antioxidant enzyme superoxide dismutase 2 (SOD2) increased following treatment with 200 nM TSA and to a lesser level at 1-5 muM TSA.	trichostatin A	105-108	superoxide dismutase 2	Homo sapiens	57-61
25515622-5	2015	Levels of the antioxidant enzyme superoxide dismutase 2 (SOD2) increased following treatment with 200 nM TSA and to a lesser level at 1-5 muM TSA.	trichostatin A	142-145	superoxide dismutase 2	Homo sapiens	33-55
25515622-5	2015	Levels of the antioxidant enzyme superoxide dismutase 2 (SOD2) increased following treatment with 200 nM TSA and to a lesser level at 1-5 muM TSA.	trichostatin A	142-145	superoxide dismutase 2	Homo sapiens	57-61
25766656-0	2015	Bavachalcone-induced manganese superoxide dismutase expression through the AMP-activated protein kinase pathway in human endothelial cells.	bavachalcone	0-12	superoxide dismutase 2	Homo sapiens	21-51
26696693-2	2015	Recent evidence shows that polymorphisms in the SOD2 gene affect the elimination of the reactive oxygen species (ROS) generated in mitochondria.	Reactive Oxygen Species	88-111	superoxide dismutase 2	Homo sapiens	48-52
26696693-2	2015	Recent evidence shows that polymorphisms in the SOD2 gene affect the elimination of the reactive oxygen species (ROS) generated in mitochondria.	Reactive Oxygen Species	113-116	superoxide dismutase 2	Homo sapiens	48-52
26696693-3	2015	The aim of this study was to determine whether the functional rs4880 SNP in the SOD2 gene is a risk factor associated with aMCI and sporadic AD.	amci	123-127	superoxide dismutase 2	Homo sapiens	80-84
25755722-8	2015	Further, mechanistic study showed that SIRT3 repression results in SOD2 acetylation, leading to SOD2 inactivation, which enhanced high glucose-induced oxidative stress in endothelial cells.	Glucose	135-142	superoxide dismutase 2	Homo sapiens	67-71
25755722-8	2015	Further, mechanistic study showed that SIRT3 repression results in SOD2 acetylation, leading to SOD2 inactivation, which enhanced high glucose-induced oxidative stress in endothelial cells.	Glucose	135-142	superoxide dismutase 2	Homo sapiens	96-100
25834301-5	2015	Superoxide is considered to be a major factor in oxidant toxicity, and mitochondrial MnSOD enzymes constitute an essential defense against superoxide.	Superoxides	139-149	superoxide dismutase 2	Homo sapiens	85-90
25203678-9	2015	This suggests that VPA reduces intracellular ROS level by the modulation of KRIT1 and its correlated proteins, FoxO1, SOD2, and cyclin D1.	Reactive Oxygen Species	45-48	superoxide dismutase 2	Homo sapiens	118-122
26089937-6	2015	Moreover, compared with Cu/Zn-SOD, RT saponins (2 mg/kg/d dosage) significantly increased Mn-SOD activity after SAH.	Saponins	38-46	superoxide dismutase 2	Homo sapiens	90-96
25388628-4	2015	Long-term treatment of HUVECs with 3% w/v beta-d-glucan significantly increased the level of MnSOD by 200% +- 2% compared to control and by 50% +- 4% compared to untreated H2 O2 -stressed cells.	maltotriose	42-55	superoxide dismutase 2	Homo sapiens	93-98
25388628-7	2015	HUVECs overexpressing MnSOD demonstrated an increased activity of endothelial nitric oxide synthase (eNOS), reduced load of superoxide anion (O2 (-) ) and an increased survival under oxidative stress.	Superoxides	124-140	superoxide dismutase 2	Homo sapiens	22-27
25388628-7	2015	HUVECs overexpressing MnSOD demonstrated an increased activity of endothelial nitric oxide synthase (eNOS), reduced load of superoxide anion (O2 (-) ) and an increased survival under oxidative stress.	Superoxides	142-144	superoxide dismutase 2	Homo sapiens	22-27
25388628-11	2015	In conclusion, 3% w/v beta-d-glucan activates endothelial expression of MnSOD independent of histone acetylation level, thereby leading to adequate removal of O2 (-) , cell survival and angiogenic response to oxidative stress.	maltotriose	22-35	superoxide dismutase 2	Homo sapiens	72-77
25388628-11	2015	In conclusion, 3% w/v beta-d-glucan activates endothelial expression of MnSOD independent of histone acetylation level, thereby leading to adequate removal of O2 (-) , cell survival and angiogenic response to oxidative stress.	Superoxides	159-161	superoxide dismutase 2	Homo sapiens	72-77
25388628-12	2015	The identification of dietary beta-d-glucan as activator of MnSOD-related angiogenesis might lead to the development of nutritional approaches for the prevention of ischemic remodelling and heart failure.	maltotriose	30-43	superoxide dismutase 2	Homo sapiens	60-65
26596112-3	2015	In oral intake of hyperchlorination drinkable water products, the study revealed main genes having polymorphism associated with endocrine disorders: overweight and obesity--APOE, PPARG, HTR2A, characterizing antioxidant system state--SOD2 and detoxication--SULTA.	Water	46-51	superoxide dismutase 2	Homo sapiens	234-238
26596112-5	2015	Probability of increased serum serotonin and lower Cu/Zn in children with mutant homozygous genotype HTR2A and SOD2 is 1.2-1.3 times higher than in those with heterozygous and normal homozygous genotypes.	Serotonin	31-40	superoxide dismutase 2	Homo sapiens	111-115
25766656-3	2015	Although polyphenols can induce MnSOD expression, their mechanism of action remains unclear.	Polyphenols	9-20	superoxide dismutase 2	Homo sapiens	32-37
25766656-4	2015	We examined the effect of bavachalcone, a bioactive compound isolated from Psoralea corylifolia, on MnSOD protein expression and explored whether this effect is mediated through the AMP-activated protein kinase (AMPK) signaling pathway.	bavachalcone	26-38	superoxide dismutase 2	Homo sapiens	100-105
25766656-5	2015	Our data showed that bavachalcone enhanced the luciferase activity of the MnSOD promoter and increased MnSOD mRNA and protein expressions.	bavachalcone	21-33	superoxide dismutase 2	Homo sapiens	74-79
25766656-5	2015	Our data showed that bavachalcone enhanced the luciferase activity of the MnSOD promoter and increased MnSOD mRNA and protein expressions.	bavachalcone	21-33	superoxide dismutase 2	Homo sapiens	103-108
25766656-8	2015	mRNA interference by using short hairpin RNA (shRNA) of AMPK inhibited bavachalcone-induced MnSOD expression.	bavachalcone	71-83	superoxide dismutase 2	Homo sapiens	92-97
25766656-11	2015	These findings indicate that bavachalcone can protect the endothelial function by increasing AMPK activity and MnSOD expression and reducing mitochondrial oxidative stress.	bavachalcone	29-41	superoxide dismutase 2	Homo sapiens	111-116
25307178-12	2015	Further, MnSOD knockdown resulted in inhibited cell viability as well as increased mitochondrial ROS level and apoptosis upon radiation in PC3 and DU145 cells.	Reactive Oxygen Species	97-100	superoxide dismutase 2	Homo sapiens	9-14
25522270-6	2014	Moreover, the enzymatic activities of isocitrate dehydrogenase 2 (IDH2), glutathione peroxidase (GSH-Px) and manganese superoxide dismutase (SOD2) as well as deacetylation of SOD2 were increased by RSV pretreatment, suggesting RSV notably enhanced mtROS scavenging in t-BHP-induced endothelial cells.	Glutathione	97-100	superoxide dismutase 2	Homo sapiens	141-145
25522270-6	2014	Moreover, the enzymatic activities of isocitrate dehydrogenase 2 (IDH2), glutathione peroxidase (GSH-Px) and manganese superoxide dismutase (SOD2) as well as deacetylation of SOD2 were increased by RSV pretreatment, suggesting RSV notably enhanced mtROS scavenging in t-BHP-induced endothelial cells.	Resveratrol	198-201	superoxide dismutase 2	Homo sapiens	141-145
25522270-6	2014	Moreover, the enzymatic activities of isocitrate dehydrogenase 2 (IDH2), glutathione peroxidase (GSH-Px) and manganese superoxide dismutase (SOD2) as well as deacetylation of SOD2 were increased by RSV pretreatment, suggesting RSV notably enhanced mtROS scavenging in t-BHP-induced endothelial cells.	Resveratrol	198-201	superoxide dismutase 2	Homo sapiens	175-179
25522270-6	2014	Moreover, the enzymatic activities of isocitrate dehydrogenase 2 (IDH2), glutathione peroxidase (GSH-Px) and manganese superoxide dismutase (SOD2) as well as deacetylation of SOD2 were increased by RSV pretreatment, suggesting RSV notably enhanced mtROS scavenging in t-BHP-induced endothelial cells.	Resveratrol	227-230	superoxide dismutase 2	Homo sapiens	141-145
25522270-6	2014	Moreover, the enzymatic activities of isocitrate dehydrogenase 2 (IDH2), glutathione peroxidase (GSH-Px) and manganese superoxide dismutase (SOD2) as well as deacetylation of SOD2 were increased by RSV pretreatment, suggesting RSV notably enhanced mtROS scavenging in t-BHP-induced endothelial cells.	Resveratrol	227-230	superoxide dismutase 2	Homo sapiens	175-179
25522270-6	2014	Moreover, the enzymatic activities of isocitrate dehydrogenase 2 (IDH2), glutathione peroxidase (GSH-Px) and manganese superoxide dismutase (SOD2) as well as deacetylation of SOD2 were increased by RSV pretreatment, suggesting RSV notably enhanced mtROS scavenging in t-BHP-induced endothelial cells.	tert-Butylhydroperoxide	268-273	superoxide dismutase 2	Homo sapiens	141-145
25522270-6	2014	Moreover, the enzymatic activities of isocitrate dehydrogenase 2 (IDH2), glutathione peroxidase (GSH-Px) and manganese superoxide dismutase (SOD2) as well as deacetylation of SOD2 were increased by RSV pretreatment, suggesting RSV notably enhanced mtROS scavenging in t-BHP-induced endothelial cells.	tert-Butylhydroperoxide	268-273	superoxide dismutase 2	Homo sapiens	175-179
25224035-5	2014	Several studies display the biological significance of MnSOD level in proliferation as well as in invasive and angiogenic abilities of breast tumor cells by controlling superoxide anion radical (O2( -)) and hydrogen peroxide (H2O2).	Superoxides	169-193	superoxide dismutase 2	Homo sapiens	55-60
25450701-6	2014	Finally, we show that SRT3025 (Sirt1 activator) and Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP, a MnSOD mimetics) can markedly reduce mitochondrial oxidative stress and mtDNA damage.	manganese(III)-tetrakis(4-benzoic acid)porphyrin	52-96	superoxide dismutase 2	Homo sapiens	108-113
25224035-5	2014	Several studies display the biological significance of MnSOD level in proliferation as well as in invasive and angiogenic abilities of breast tumor cells by controlling superoxide anion radical (O2( -)) and hydrogen peroxide (H2O2).	Superoxides	195-197	superoxide dismutase 2	Homo sapiens	55-60
25224035-5	2014	Several studies display the biological significance of MnSOD level in proliferation as well as in invasive and angiogenic abilities of breast tumor cells by controlling superoxide anion radical (O2( -)) and hydrogen peroxide (H2O2).	Hydrogen Peroxide	207-224	superoxide dismutase 2	Homo sapiens	55-60
25224035-5	2014	Several studies display the biological significance of MnSOD level in proliferation as well as in invasive and angiogenic abilities of breast tumor cells by controlling superoxide anion radical (O2( -)) and hydrogen peroxide (H2O2).	Hydrogen Peroxide	226-230	superoxide dismutase 2	Homo sapiens	55-60
25211703-7	2014	The fold change in PGC-1alpha, SIRT1, and SOD2 gene expression following training was significantly (p &lt; 0.05) lower in the RSV group than placebo.	Resveratrol	127-130	superoxide dismutase 2	Homo sapiens	42-46
25372290-0	2014	Impact of the superoxide dismutase 2 Val16Ala polymorphism on the relationship between valproic acid exposure and elevation of gamma-glutamyltransferase in patients with epilepsy: a population pharmacokinetic-pharmacodynamic analysis.	Valproic Acid	87-100	superoxide dismutase 2	Homo sapiens	14-36
25448439-10	2014	Overexpression of catalase (CAT) or SOD2, eliminated Cr(VI)-induced malignant transformation.	chromium hexavalent ion	53-59	superoxide dismutase 2	Homo sapiens	36-40
25372290-7	2014	The predicted mean percentages of the subjects with gamma-GT elevation were about 2- to 3-fold, 3- to 4-fold and 4- to 8-fold greater in patients with the SOD2 Val/Val genotype but without any intellectual disability, those with the SOD2 Val/Ala or Ala/Ala genotype and intellectual disability and those with the SOD2 Val/Val genotype and intellectual disability, respectively, compared to those with the SOD2 Val/Ala or Ala/Ala genotype without intellectual disability.	Valine	160-163	superoxide dismutase 2	Homo sapiens	155-159
24754522-3	2014	Using primary cultured liver sinusoidal endothelial cells (LSECs), liver grafts from healthy and steatotic rats, and human liver samples, we aimed to characterize the effects of a new recombinant form of human manganese superoxide dismutase (rMnSOD) on hepatic CS+WR injury.	Cesium	261-263	superoxide dismutase 2	Homo sapiens	210-240
24953189-1	2014	Manganese superoxide dismutase (MnSOD), a critical anti-oxidant enzyme, detoxifies the mitochondrial-derived reactive oxygen species, superoxide, elicited through normal respiration or the inflammatory response.	Reactive Oxygen Species	109-132	superoxide dismutase 2	Homo sapiens	0-30
24953189-1	2014	Manganese superoxide dismutase (MnSOD), a critical anti-oxidant enzyme, detoxifies the mitochondrial-derived reactive oxygen species, superoxide, elicited through normal respiration or the inflammatory response.	Reactive Oxygen Species	109-132	superoxide dismutase 2	Homo sapiens	32-37
24953189-1	2014	Manganese superoxide dismutase (MnSOD), a critical anti-oxidant enzyme, detoxifies the mitochondrial-derived reactive oxygen species, superoxide, elicited through normal respiration or the inflammatory response.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
25220386-5	2014	Using the MnSOD as an oxidative stress marker, we showed here that ALA treatment of cultured cells induced ROS production, increasing with ALA concentration.	Aminolevulinic Acid	67-70	superoxide dismutase 2	Homo sapiens	10-15
25220386-5	2014	Using the MnSOD as an oxidative stress marker, we showed here that ALA treatment of cultured cells induced ROS production, increasing with ALA concentration.	ros	107-110	superoxide dismutase 2	Homo sapiens	10-15
25220386-5	2014	Using the MnSOD as an oxidative stress marker, we showed here that ALA treatment of cultured cells induced ROS production, increasing with ALA concentration.	Aminolevulinic Acid	139-142	superoxide dismutase 2	Homo sapiens	10-15
25398805-5	2014	RESULTS: After treatment with H2O2, DHT decreased tyrosine phosphorylation/transcriptional activity of STAT3 and promoter activity of MnSOD while E2 increased them.	Hydrogen Peroxide	30-34	superoxide dismutase 2	Homo sapiens	134-139
25330300-8	2014	The AA-PBMCs exposed to MTX showed decreasing SOD2 activity, but a concomitant up regulation of the SOD2 gene was observed.	Methotrexate	24-27	superoxide dismutase 2	Homo sapiens	100-104
25330300-11	2014	Caspase-8 and -3 levels were increased in cells exposed to MTX, but the modulation of these genes, as well as that of the Bax and Bcl-2 genes involved in the apoptosis pathway, presented a modulation that was dependent on the SOD2 genotype.	Methotrexate	59-62	superoxide dismutase 2	Homo sapiens	226-230
25330300-12	2014	MTX at a concentration of 10 microM also increased inflammatory cytokines (IL-1beta, IL-6, TNFalpha and Iggamma) and decreased the level of IL-10 anti-inflammatory cytokine, independent of SOD2 genetic background.	Methotrexate	0-3	superoxide dismutase 2	Homo sapiens	189-193
25330300-13	2014	The results suggest that potential pharmacogenetic effect on the cytotoxic response to MTX due differential redox status of cells carriers different SOD2 genotypes.	Methotrexate	87-90	superoxide dismutase 2	Homo sapiens	149-153
25398805-5	2014	RESULTS: After treatment with H2O2, DHT decreased tyrosine phosphorylation/transcriptional activity of STAT3 and promoter activity of MnSOD while E2 increased them.	Dihydrotestosterone	36-39	superoxide dismutase 2	Homo sapiens	134-139
25330300-0	2014	Methotrexate-related response on human peripheral blood mononuclear cells may be modulated by the Ala16Val-SOD2 gene polymorphism.	Methotrexate	0-12	superoxide dismutase 2	Homo sapiens	107-111
25330300-4	2014	Therefore, we analyzed here whether a genetic imbalance of the manganese-dependent superoxide dismutase (SOD2) gene could have some impact on the MTX cytotoxic response.	Methotrexate	146-149	superoxide dismutase 2	Homo sapiens	105-109
25330300-6	2014	AA-PBMCs that present higher SOD2 efficiencies were more resistance to high MTX doses (10 and 100 microM) than were the VV and AV genotypes.	Methotrexate	76-79	superoxide dismutase 2	Homo sapiens	29-33
25330300-8	2014	The AA-PBMCs exposed to MTX showed decreasing SOD2 activity, but a concomitant up regulation of the SOD2 gene was observed.	Methotrexate	24-27	superoxide dismutase 2	Homo sapiens	46-50
25136316-7	2014	In addition, curcumin with its versatile activities modulated the expression of many oxidative stress-regulating genes such as PDGF, VEGF, IGFBP-2, HO1, SOD2, and GPX1.	Curcumin	13-21	superoxide dismutase 2	Homo sapiens	153-157
25522535-6	2014	Treatment of HepG2 cells with flavone for 24 h reduced the accumulation of intracellular ROS, which correlated with upregulation of Gred, CuZnSOD and MnSOD mRNA levels.	flavone	30-37	superoxide dismutase 2	Homo sapiens	150-155
25522535-6	2014	Treatment of HepG2 cells with flavone for 24 h reduced the accumulation of intracellular ROS, which correlated with upregulation of Gred, CuZnSOD and MnSOD mRNA levels.	ros	89-92	superoxide dismutase 2	Homo sapiens	150-155
25109995-3	2014	Since superoxide formation, in particular in mitochondria, is often considered to be an initial step in the pathogenesis of these diseases, improper function of the MnSOD (mitochondrial superoxide dismutase; SOD2) may be critical for tissue homoeostasis.	Superoxides	6-16	superoxide dismutase 2	Homo sapiens	165-170
25109995-3	2014	Since superoxide formation, in particular in mitochondria, is often considered to be an initial step in the pathogenesis of these diseases, improper function of the MnSOD (mitochondrial superoxide dismutase; SOD2) may be critical for tissue homoeostasis.	Superoxides	6-16	superoxide dismutase 2	Homo sapiens	208-212
24865797-9	2014	Furthermore, the SOD2 T allele was significantly associated with increased activity of CK (females: p = 0.0144) and creatinine level (females: p = 0.0276; males: p = 0.0135) in athletes.	Creatinine	116-126	superoxide dismutase 2	Homo sapiens	17-21
25057809-5	2014	The expression of SOD1, SOD2, GSR, GPx1, GPX4, TXN, TXNRD1 and Nrf2 increased after the HSFA meal (p&lt;0.05).	hsfa	88-92	superoxide dismutase 2	Homo sapiens	24-28
24973648-8	2014	All of the above Sod2-dependent alterations are largely reversed by catalase coexpression, indicating that the redox control of MMP-1 is H2O2-dependent.	Hydrogen Peroxide	137-141	superoxide dismutase 2	Homo sapiens	17-21
24825124-3	2014	Unlike the other known SODs (MnSOD, FeSOD, and (CuZn)SOD), which utilize "typical" biological nitrogen and oxygen donors, NiSOD utilizes a rather unexpected ligand set.	Nitrogen	94-102	superoxide dismutase 2	Homo sapiens	29-34
24825124-3	2014	Unlike the other known SODs (MnSOD, FeSOD, and (CuZn)SOD), which utilize "typical" biological nitrogen and oxygen donors, NiSOD utilizes a rather unexpected ligand set.	Oxygen	107-113	superoxide dismutase 2	Homo sapiens	29-34
24825124-5	2014	These are unusual biological ligands, especially for an SOD: amine and amidate donors are underrepresented as biological ligands, whereas cysteinates are highly susceptible to oxidative damage.	Amines	61-66	superoxide dismutase 2	Homo sapiens	56-59
24825124-5	2014	These are unusual biological ligands, especially for an SOD: amine and amidate donors are underrepresented as biological ligands, whereas cysteinates are highly susceptible to oxidative damage.	Etomidate	71-78	superoxide dismutase 2	Homo sapiens	56-59
24825124-5	2014	These are unusual biological ligands, especially for an SOD: amine and amidate donors are underrepresented as biological ligands, whereas cysteinates are highly susceptible to oxidative damage.	cysteinates	138-149	superoxide dismutase 2	Homo sapiens	56-59
24700636-5	2014	Eckol recovered Mn SOD expression and activity that were decreased by H2O2.	Hydrogen Peroxide	70-74	superoxide dismutase 2	Homo sapiens	16-22
24486155-5	2014	The ROS genes gss, gstm2, gstt2 and sod2 were upregulated, and the presence of superoxide following 10 muM PX exposure was determined via dihydroethidium fluorescence studies further implicating PX-induced oxidative stress in HSG cells.	Reactive Oxygen Species	4-7	superoxide dismutase 2	Homo sapiens	36-40
24838005-8	2014	Superoxide dismutase (SOD) activities (Cu,Zn-SOD and Mn-SOD) and protein expression were adaptively increased after metal overloads (Cu,Zn-SOD: t1/2: 8-8.5h and Mn-SOD: t1/2: 8.5-8.0h).	Metals	116-121	superoxide dismutase 2	Homo sapiens	53-59
24838005-8	2014	Superoxide dismutase (SOD) activities (Cu,Zn-SOD and Mn-SOD) and protein expression were adaptively increased after metal overloads (Cu,Zn-SOD: t1/2: 8-8.5h and Mn-SOD: t1/2: 8.5-8.0h).	Metals	116-121	superoxide dismutase 2	Homo sapiens	161-167
24915901-0	2014	Structural, spectroscopic and functional investigation into Fe-substituted MnSOD from human pathogen Clostridium difficile.	Iron	60-62	superoxide dismutase 2	Homo sapiens	75-80
25158572-0	2014	Simvastatin inhibits the proliferation of A549 lung cancer cells through oxidative stress and up-regulation of SOD2.	Simvastatin	0-11	superoxide dismutase 2	Homo sapiens	111-115
25158572-5	2014	Treatment with 50 microM simvastatin for 48 h significantly increased reactive oxygen species (ROS) production and malondialdehyde (MDA), a lipid peroxidation production, and augmented the activity of total superoxide dismutase (SOD) and manganese SOD (SOD2).	Simvastatin	25-36	superoxide dismutase 2	Homo sapiens	229-232
25158572-5	2014	Treatment with 50 microM simvastatin for 48 h significantly increased reactive oxygen species (ROS) production and malondialdehyde (MDA), a lipid peroxidation production, and augmented the activity of total superoxide dismutase (SOD) and manganese SOD (SOD2).	Simvastatin	25-36	superoxide dismutase 2	Homo sapiens	248-251
25158572-5	2014	Treatment with 50 microM simvastatin for 48 h significantly increased reactive oxygen species (ROS) production and malondialdehyde (MDA), a lipid peroxidation production, and augmented the activity of total superoxide dismutase (SOD) and manganese SOD (SOD2).	Simvastatin	25-36	superoxide dismutase 2	Homo sapiens	253-257
25158572-6	2014	Moreover, western blotting analysis showed that simvastatin effectively up-regulated the SOD2 relative protein level.	Simvastatin	48-59	superoxide dismutase 2	Homo sapiens	89-93
25158572-7	2014	These findings suggested that simvastatin could inhibit the proliferation of A549 lung cells through oxidative stress and up-regulation of SOD2.	Simvastatin	30-41	superoxide dismutase 2	Homo sapiens	139-143
24939178-4	2014	Further study revealed that SOD2 acted as a negative regulator of beta-arrestin1 that is an important adaptor responsible for degradation of IGF-1R via the changes in ROS, as evidenced by observations that an antioxidant agent substantially attenuated beta-arrestin1 expression in vitro and in vivo.	Reactive Oxygen Species	167-170	superoxide dismutase 2	Homo sapiens	28-32
25073091-0	2014	Chikusetsu saponin V attenuates MPP+-induced neurotoxicity in SH-SY5Y cells via regulation of Sirt1/Mn-SOD and GRP78/caspase-12 pathways.	Saponins	11-18	superoxide dismutase 2	Homo sapiens	100-106
25073091-0	2014	Chikusetsu saponin V attenuates MPP+-induced neurotoxicity in SH-SY5Y cells via regulation of Sirt1/Mn-SOD and GRP78/caspase-12 pathways.	mangion-purified polysaccharide (Candida albicans)	32-36	superoxide dismutase 2	Homo sapiens	100-106
25073091-5	2014	We also found that levels of Sirt1 protein and Mn-SOD mRNA significantly decreased in MPP+-treated group but were restored with CsV treatment in a dose-dependent manner.	chikusetsusaponin V	128-131	superoxide dismutase 2	Homo sapiens	47-53
25073091-8	2014	Overall, these results suggest that Sirt1/Mn-SOD and GRP78/Caspase-12 pathways might be involved in the CsV-mediated neuroprotective effects.	chikusetsusaponin V	104-107	superoxide dismutase 2	Homo sapiens	42-48
24939178-0	2014	Regulation of SOD2 and beta-arrestin1 by interleukin-6 contributes to the increase of IGF-1R expression in docetaxel resistant prostate cancer cells.	Docetaxel	107-116	superoxide dismutase 2	Homo sapiens	14-18
24939178-2	2014	Proteomics-based analysis in this study revealed that SOD2, associated with downregulation of reactive oxygen species (ROS), was significantly up-regulated in docetaxel-resistant (PC3/Doc) cells if compared to sensitive cells, and the expression of redox-regulated genes such as IGF-1R, CXCR4, and BCL2 was increased as well.	Reactive Oxygen Species	94-117	superoxide dismutase 2	Homo sapiens	54-58
24939178-2	2014	Proteomics-based analysis in this study revealed that SOD2, associated with downregulation of reactive oxygen species (ROS), was significantly up-regulated in docetaxel-resistant (PC3/Doc) cells if compared to sensitive cells, and the expression of redox-regulated genes such as IGF-1R, CXCR4, and BCL2 was increased as well.	Reactive Oxygen Species	119-122	superoxide dismutase 2	Homo sapiens	54-58
24928367-10	2014	Moreover, maysin pretreatment (5-50 mug/ml) for 2h significantly and dose-dependently increased the mRNA levels of antioxidant enzymes (CAT, GPx-1, SOD-1, SOD-2 and HO-1) in H2O2 (200 muM)-insulted cells.	Deuterium	48-50	superoxide dismutase 2	Homo sapiens	155-160
24657218-8	2014	Our results show that patients treated with levosimendan had a significant reduction of glutathionylated proteins and an increase in the amount of the antioxidant enzyme MnSOD, underlining its antioxidant properties.	Simendan	44-56	superoxide dismutase 2	Homo sapiens	170-175
24939178-7	2014	Together, our data provide a novel explanation that high level of IL6 stimulated SOD2 expression that, at least partially, contributed to the low level of ROS that would likely result in a sustained increase in the expression of IGF-1R through abolishment of beta-arrestin1 in docetaxel resistant cells.	Reactive Oxygen Species	155-158	superoxide dismutase 2	Homo sapiens	81-85
24939178-2	2014	Proteomics-based analysis in this study revealed that SOD2, associated with downregulation of reactive oxygen species (ROS), was significantly up-regulated in docetaxel-resistant (PC3/Doc) cells if compared to sensitive cells, and the expression of redox-regulated genes such as IGF-1R, CXCR4, and BCL2 was increased as well.	Docetaxel	159-168	superoxide dismutase 2	Homo sapiens	54-58
24939178-7	2014	Together, our data provide a novel explanation that high level of IL6 stimulated SOD2 expression that, at least partially, contributed to the low level of ROS that would likely result in a sustained increase in the expression of IGF-1R through abolishment of beta-arrestin1 in docetaxel resistant cells.	Docetaxel	277-286	superoxide dismutase 2	Homo sapiens	81-85
24746671-4	2014	In the present study we demonstrate that acetaldehyde transiently impairs SOD2 activity in HepG2 cells, the decrease in the enzyme activity was associated to a reduction in the protein content, which was rapidly recovered, to basal values, by synthesis de novo in a mechanism mediated by NF-kappaB and PKC.	Acetaldehyde	41-53	superoxide dismutase 2	Homo sapiens	74-78
24483941-2	2014	MnSOD expression was analyzed immunohistochemically in 48 formalin-fixed and paraffin-embedded specimens from patients with UC who had undergone endoscopical biopsy.	Formaldehyde	58-66	superoxide dismutase 2	Homo sapiens	0-5
24497574-7	2014	An unbiased proteome screen of A2E-aged patient-specific iPS-derived RPE cell lines identified superoxide dismutase 2 (SOD2)-mediated antioxidative defense in the genetic allele"s susceptibility of AMD.	IPS	57-60	superoxide dismutase 2	Homo sapiens	95-117
24497574-7	2014	An unbiased proteome screen of A2E-aged patient-specific iPS-derived RPE cell lines identified superoxide dismutase 2 (SOD2)-mediated antioxidative defense in the genetic allele"s susceptibility of AMD.	IPS	57-60	superoxide dismutase 2	Homo sapiens	119-123
24716840-0	2014	MnSOD rs4880 and XPD rs13181 polymorphisms predict the survival of breast cancer patients treated with adjuvant tamoxifen.	Tamoxifen	112-121	superoxide dismutase 2	Homo sapiens	0-5
24716840-1	2014	UNLABELLED: The enzyme manganese superoxide dismutase (MnSOD) defends against oxidative stress caused by reactive oxygen species (ROS), whereas Xeroderma pigmentosum group D (XPD) protein is involved in DNA repair.	Reactive Oxygen Species	105-128	superoxide dismutase 2	Homo sapiens	23-53
24716840-1	2014	UNLABELLED: The enzyme manganese superoxide dismutase (MnSOD) defends against oxidative stress caused by reactive oxygen species (ROS), whereas Xeroderma pigmentosum group D (XPD) protein is involved in DNA repair.	Reactive Oxygen Species	105-128	superoxide dismutase 2	Homo sapiens	55-60
24716840-1	2014	UNLABELLED: The enzyme manganese superoxide dismutase (MnSOD) defends against oxidative stress caused by reactive oxygen species (ROS), whereas Xeroderma pigmentosum group D (XPD) protein is involved in DNA repair.	Reactive Oxygen Species	130-133	superoxide dismutase 2	Homo sapiens	23-53
24716840-1	2014	UNLABELLED: The enzyme manganese superoxide dismutase (MnSOD) defends against oxidative stress caused by reactive oxygen species (ROS), whereas Xeroderma pigmentosum group D (XPD) protein is involved in DNA repair.	Reactive Oxygen Species	130-133	superoxide dismutase 2	Homo sapiens	55-60
24716840-8	2014	CONCLUSION: This is the first study to show that the MnSOD rs4880 and XPD rs13181 polymorphisms may influence the outcome of breast cancer patients receiving adjuvant TAM monotherapy.	Tamoxifen	167-170	superoxide dismutase 2	Homo sapiens	53-58
23475579-5	2014	Overexpression of anti-oxidant enzymes superoxide dismutase 1 (SOD1), SOD2, and catalase, or pretreatment with the pharmacological inhibitor N-acetylcysteine (NAC) significantly attenuated both pso-mediated ROS generation and pso-mediated growth inhibition in CaP cells.	Acetylcysteine	141-157	superoxide dismutase 2	Homo sapiens	70-74
24483941-2	2014	MnSOD expression was analyzed immunohistochemically in 48 formalin-fixed and paraffin-embedded specimens from patients with UC who had undergone endoscopical biopsy.	Paraffin	77-85	superoxide dismutase 2	Homo sapiens	0-5
25071412-5	2014	Manganese Superoxide Dismutase (MnSOD) is a manganesedependant metallo-enzyme which plays a crucial role in protecting cells from anti-oxidative stress by eliminating reactive (superoxide) oxygen species.	Superoxides	177-187	superoxide dismutase 2	Homo sapiens	0-30
24486445-6	2014	The defence mechanism to counteract the excess of ROS production was by the upregulation of Ucp2, Ucp3 and MnSod gene expression.	Reactive Oxygen Species	50-53	superoxide dismutase 2	Homo sapiens	107-112
25071412-5	2014	Manganese Superoxide Dismutase (MnSOD) is a manganesedependant metallo-enzyme which plays a crucial role in protecting cells from anti-oxidative stress by eliminating reactive (superoxide) oxygen species.	Superoxides	177-187	superoxide dismutase 2	Homo sapiens	32-37
25071412-5	2014	Manganese Superoxide Dismutase (MnSOD) is a manganesedependant metallo-enzyme which plays a crucial role in protecting cells from anti-oxidative stress by eliminating reactive (superoxide) oxygen species.	Oxygen	189-195	superoxide dismutase 2	Homo sapiens	0-30
25071412-5	2014	Manganese Superoxide Dismutase (MnSOD) is a manganesedependant metallo-enzyme which plays a crucial role in protecting cells from anti-oxidative stress by eliminating reactive (superoxide) oxygen species.	Oxygen	189-195	superoxide dismutase 2	Homo sapiens	32-37
23964924-6	2014	Finally, we provide evidence to implicate peroxynitrite as the mechanism involved in the increased sensitivity to chemotherapy induced by MnSOD repression.	Peroxynitrous Acid	42-55	superoxide dismutase 2	Homo sapiens	138-143
24610415-5	2014	Patients with HCV and normal, healthy controls were investigated for a superoxide dismutase (SOD-2) polymorphism in the mitochondrial targeting sequence with Ala/Val (C-9T) substitution.	Alanine	158-161	superoxide dismutase 2	Homo sapiens	93-98
24610415-5	2014	Patients with HCV and normal, healthy controls were investigated for a superoxide dismutase (SOD-2) polymorphism in the mitochondrial targeting sequence with Ala/Val (C-9T) substitution.	Valine	162-165	superoxide dismutase 2	Homo sapiens	93-98
24610415-6	2014	Polymorphisms in antioxidant gene SOD-2 were carried out by PCR, restriction fragment length polymorphism assays and by polyacrylamide gel electrophoresis.	polyacrylamide	120-134	superoxide dismutase 2	Homo sapiens	34-39
24635018-3	2014	However, the importance of the reactive oxygen species (ROS)-scavenging ability of mitochondria through manganese superoxide dismutase (MnSOD) is not established.	Reactive Oxygen Species	31-54	superoxide dismutase 2	Homo sapiens	136-141
24635018-3	2014	However, the importance of the reactive oxygen species (ROS)-scavenging ability of mitochondria through manganese superoxide dismutase (MnSOD) is not established.	Reactive Oxygen Species	56-59	superoxide dismutase 2	Homo sapiens	136-141
24635018-5	2014	RESULTS AND INNOVATION: There is an inverse correlation between MnSOD expression and UV-induced activation of epidermal growth factor receptor (EGFR), as determined by phosphorylation at Tyr1068, both in vitro and in vivo, which correlates with increased ROS production (as measured by dihydroethidium fluorescence).	Reactive Oxygen Species	255-258	superoxide dismutase 2	Homo sapiens	64-69
24930516-9	2014	Treatment with rebamipide significantly decreased both the ROS concentration and the number of dying cells: this drug is prescribed clinically for gastric injury patients and has been reported to upregulate the expression of manganese superoxide dismutase.	rebamipide	15-25	superoxide dismutase 2	Homo sapiens	225-255
24858012-11	2014	Treatment with metformin resulted in an increase in p-p38 MAPK, catalase, MnSOD and Cu/Zn SOD protein expression.	Metformin	15-24	superoxide dismutase 2	Homo sapiens	74-79
24486139-4	2014	The expression of SOD-2, but not of SOD-1, markedly increased after PA exposure, which also elevated the number of cells generating ROS.	Palmitic Acid	68-70	superoxide dismutase 2	Homo sapiens	18-23
24819633-2	2014	Manganese superoxide dismutase (SOD2) catalyses the dismutation of superoxide, regulates the metabolism of reactive oxygen species in the mitochondria and is highly expressed in the kidney.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-36
24819633-2	2014	Manganese superoxide dismutase (SOD2) catalyses the dismutation of superoxide, regulates the metabolism of reactive oxygen species in the mitochondria and is highly expressed in the kidney.	Reactive Oxygen Species	107-130	superoxide dismutase 2	Homo sapiens	0-30
24819633-2	2014	Manganese superoxide dismutase (SOD2) catalyses the dismutation of superoxide, regulates the metabolism of reactive oxygen species in the mitochondria and is highly expressed in the kidney.	Reactive Oxygen Species	107-130	superoxide dismutase 2	Homo sapiens	32-36
24616096-4	2014	Susceptibility of T. cruzi Fe-SODA toward peroxynitrite was similar to that reported previously for Escherichia coli Mn- and Fe-SODs and mammalian Mn-SOD, whereas Fe-SODB was exceptionally resistant to oxidant-mediated inactivation.	fe-soda	27-34	superoxide dismutase 2	Homo sapiens	147-153
24635018-5	2014	RESULTS AND INNOVATION: There is an inverse correlation between MnSOD expression and UV-induced activation of epidermal growth factor receptor (EGFR), as determined by phosphorylation at Tyr1068, both in vitro and in vivo, which correlates with increased ROS production (as measured by dihydroethidium fluorescence).	dihydroethidium	286-301	superoxide dismutase 2	Homo sapiens	64-69
24635018-7	2014	Enhanced EGFR activation in MnSOD knockdown cells is abrogated by treatment with the SOD mimetic MnTnBuOE-2-PyP(5+).	-2-pyp	105-111	superoxide dismutase 2	Homo sapiens	28-33
24635018-7	2014	Enhanced EGFR activation in MnSOD knockdown cells is abrogated by treatment with the SOD mimetic MnTnBuOE-2-PyP(5+).	-2-pyp	105-111	superoxide dismutase 2	Homo sapiens	30-33
24635018-8	2014	CONCLUSIONS: Our data demonstrate that the ROS-scavenging ability of mitochondria, through the expression of MnSOD, is important for UV-induced inside-out signaling.	Reactive Oxygen Species	43-46	superoxide dismutase 2	Homo sapiens	109-114
24635018-10	2014	Inhibition of inside-out signaling by MnTnBuOE-2-PyP(5+) mimics the effect of endogenous MnSOD, suggesting that pharmacological intervention by SOD mimetics could play an important role in the prevention of aberrant cell signaling, which may contribute to carcinogenesis and may prove valuable for the treatment or prevention of cancer in the future.	-2-pyp	46-52	superoxide dismutase 2	Homo sapiens	89-94
24635018-10	2014	Inhibition of inside-out signaling by MnTnBuOE-2-PyP(5+) mimics the effect of endogenous MnSOD, suggesting that pharmacological intervention by SOD mimetics could play an important role in the prevention of aberrant cell signaling, which may contribute to carcinogenesis and may prove valuable for the treatment or prevention of cancer in the future.	-2-pyp	46-52	superoxide dismutase 2	Homo sapiens	91-94
24486139-4	2014	The expression of SOD-2, but not of SOD-1, markedly increased after PA exposure, which also elevated the number of cells generating ROS.	ros	132-135	superoxide dismutase 2	Homo sapiens	18-23
24585533-9	2014	By analyzing a dataset from the National Birth Defects Prevention Study (NBDPS), we identified seven genes (GSTA1, SOD2, MTRR, AHCYL2, GCLC, GSTM3, and RFC1) associated with the development of CTDs.	beta-cyclodextrin tetradecasulfate	193-197	superoxide dismutase 2	Homo sapiens	115-119
24573886-9	2014	In addition, genistein promoted a decrease of 5.5, 9.3, and 3.6 times of MnSOD, CuZnSOD, and TrxR mRNA expression, respectively, while the GPx expression was increased by 6.5 times.	Genistein	13-22	superoxide dismutase 2	Homo sapiens	73-78
24212762-2	2014	In this study, we aimed to examine to investigate possible associations between the manganese superoxide dismutase (MnSOD Ala-9Val) and glutathione peroxidase (GPx1 Pro198Leu) polymorphisms and psoriasis susceptibility and disease progression in a Turkish population.	ala-9val	122-130	superoxide dismutase 2	Homo sapiens	116-121
24212762-5	2014	Genotyping was performed to identify MnSOD Ala-9Val and GPx1 Pro198Leu polymorphisms by a method based on PCR amplification and detection of polymorphisms with hybridization probes labeled with fluorescent dyes.	ala-9val	43-51	superoxide dismutase 2	Homo sapiens	37-42
24212762-10	2014	This is the first report investigating the possible associations between the MnSOD Ala-9Val and GPx1 Pro198Leu polymorphisms and psoriasis susceptibility and disease progression in the Turkish population even if no significant difference was found between patient groups and control subjects.	ala-9val	83-91	superoxide dismutase 2	Homo sapiens	77-82
24530425-6	2014	Our results show that gestational exposure to CrVI resulted in (i) increased Cr concentration in the placenta, (ii) increased germ cell apoptosis by up-regulating p53/p27-Bax-caspase-3 proteins and by increasing p53-SOD-2 co-localization; (iii) accelerated germ cell cyst (GCC) breakdown; (iv) advanced primordial follicle assembly and primary follicle transition and (v) down regulation of p-AKT, p-ERK and XIAP.	Chromium	46-48	superoxide dismutase 2	Homo sapiens	216-221
23588476-0	2014	Cognitive function, plasma MnSOD activity, and MnSOD Ala-9Val polymorphism in patients with schizophrenia and normal controls.	ala-9val	53-61	superoxide dismutase 2	Homo sapiens	47-52
23588476-2	2014	The functional Ala-9Val polymorphism of the mitochondrial enzyme manganese superoxide dismutase (MnSOD), which detoxifies superoxide radicals to hydrogen peroxide, has been associated with schizophrenia.	ala-9val	15-23	superoxide dismutase 2	Homo sapiens	97-102
23588476-2	2014	The functional Ala-9Val polymorphism of the mitochondrial enzyme manganese superoxide dismutase (MnSOD), which detoxifies superoxide radicals to hydrogen peroxide, has been associated with schizophrenia.	Superoxides	75-85	superoxide dismutase 2	Homo sapiens	97-102
23588476-2	2014	The functional Ala-9Val polymorphism of the mitochondrial enzyme manganese superoxide dismutase (MnSOD), which detoxifies superoxide radicals to hydrogen peroxide, has been associated with schizophrenia.	Hydrogen Peroxide	145-162	superoxide dismutase 2	Homo sapiens	97-102
23588476-4	2014	We recruited 923 schizophrenic inpatients and 566 healthy controls and compared them on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), plasma MnSOD activity, and the MnSOD Ala-9Val polymorphism.	ala-9val	205-213	superoxide dismutase 2	Homo sapiens	199-204
23588476-6	2014	We showed that the MnSOD Ala-9Val polymorphism may not contribute directly to the susceptibility to schizophrenia.	ala-9val	25-33	superoxide dismutase 2	Homo sapiens	19-24
23588476-10	2014	We demonstrated an association between the MnSOD Ala-9Val variant and poor attention in schizophrenia.	Alanine	49-52	superoxide dismutase 2	Homo sapiens	43-48
23588476-10	2014	We demonstrated an association between the MnSOD Ala-9Val variant and poor attention in schizophrenia.	9val	53-57	superoxide dismutase 2	Homo sapiens	43-48
23588476-11	2014	The association between higher MnSOD activity and cognitive impairment in schizophrenia is dependent on the MnSOD Ala-9Val polymorphism.	ala-9val	114-122	superoxide dismutase 2	Homo sapiens	31-36
23588476-11	2014	The association between higher MnSOD activity and cognitive impairment in schizophrenia is dependent on the MnSOD Ala-9Val polymorphism.	ala-9val	114-122	superoxide dismutase 2	Homo sapiens	108-113
24736663-0	2014	The TrkAIII oncoprotein inhibits mitochondrial free radical ROS-induced death of SH-SY5Y neuroblastoma cells by augmenting SOD2 expression and activity at the mitochondria, within the context of a tumour stem cell-like phenotype.	Reactive Oxygen Species	60-63	superoxide dismutase 2	Homo sapiens	123-127
24736663-2	2014	In the present study, we report that constitutive TrkAIII expression in human SH-SY5Y NB cells inhibits Rotenone, Paraquat and LY83583-induced mitochondrial free radical reactive oxygen species (ROS)-mediated death by stimulating SOD2 expression, increasing mitochondrial SOD2 activity and attenuating mitochondrial free radical ROS production, in association with increased mitochondrial capacity to produce H2O2, within the context of a more tumour stem cell-like phenotype.	6-anilino-5,8-quinolinedione	127-134	superoxide dismutase 2	Homo sapiens	230-234
24736663-2	2014	In the present study, we report that constitutive TrkAIII expression in human SH-SY5Y NB cells inhibits Rotenone, Paraquat and LY83583-induced mitochondrial free radical reactive oxygen species (ROS)-mediated death by stimulating SOD2 expression, increasing mitochondrial SOD2 activity and attenuating mitochondrial free radical ROS production, in association with increased mitochondrial capacity to produce H2O2, within the context of a more tumour stem cell-like phenotype.	6-anilino-5,8-quinolinedione	127-134	superoxide dismutase 2	Homo sapiens	272-276
24736663-3	2014	This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Go6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death.	GW 441756	75-83	superoxide dismutase 2	Homo sapiens	162-166
24736663-3	2014	This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Go6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death.	GW 441756	75-83	superoxide dismutase 2	Homo sapiens	205-209
24736663-3	2014	This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Go6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death.	Rotenone	292-300	superoxide dismutase 2	Homo sapiens	162-166
24736663-3	2014	This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Go6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death.	Paraquat	302-310	superoxide dismutase 2	Homo sapiens	162-166
24736663-3	2014	This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Go6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death.	6-anilino-5,8-quinolinedione	315-322	superoxide dismutase 2	Homo sapiens	162-166
24736663-3	2014	This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Go6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death.	Reactive Oxygen Species	358-361	superoxide dismutase 2	Homo sapiens	162-166
24736663-3	2014	This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Go6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death.	Reactive Oxygen Species	377-380	superoxide dismutase 2	Homo sapiens	162-166
24722289-13	2014	Ruboxistaurin attenuated gut oxidative stress after I/R by suppressing the decreased expression of manganese superoxide dismutase (MnSOD), the exhaustion of the glutathione (GSH) system, and the overproduction of malondialdehyde (MDA).	ruboxistaurin	0-13	superoxide dismutase 2	Homo sapiens	99-129
24722289-13	2014	Ruboxistaurin attenuated gut oxidative stress after I/R by suppressing the decreased expression of manganese superoxide dismutase (MnSOD), the exhaustion of the glutathione (GSH) system, and the overproduction of malondialdehyde (MDA).	ruboxistaurin	0-13	superoxide dismutase 2	Homo sapiens	131-136
23581847-1	2014	SIGNIFICANCE: The mitochondrial antioxidant manganese superoxide dismutase (MnSOD) is encoded by genomic DNA and its dismutase function is fully activated in the mitochondria to detoxify free radical O2( -) generated by mitochondrial respiration.	Superoxides	200-202	superoxide dismutase 2	Homo sapiens	44-74
23581847-1	2014	SIGNIFICANCE: The mitochondrial antioxidant manganese superoxide dismutase (MnSOD) is encoded by genomic DNA and its dismutase function is fully activated in the mitochondria to detoxify free radical O2( -) generated by mitochondrial respiration.	Superoxides	200-202	superoxide dismutase 2	Homo sapiens	76-81
23581847-5	2014	These proteins modulate MnSOD superoxide scavenging activity via post-translational modifications in the mitochondria.	Superoxides	30-40	superoxide dismutase 2	Homo sapiens	24-29
23590434-7	2014	The periodic fluctuation in MnSOD activity during the cell cycle inversely correlates with cellular superoxide levels as well as glucose and oxygen consumption.	Superoxides	100-110	superoxide dismutase 2	Homo sapiens	28-33
23590434-7	2014	The periodic fluctuation in MnSOD activity during the cell cycle inversely correlates with cellular superoxide levels as well as glucose and oxygen consumption.	Glucose	129-136	superoxide dismutase 2	Homo sapiens	28-33
23590434-7	2014	The periodic fluctuation in MnSOD activity during the cell cycle inversely correlates with cellular superoxide levels as well as glucose and oxygen consumption.	Oxygen	141-147	superoxide dismutase 2	Homo sapiens	28-33
23590434-8	2014	Based on an inverse correlation between MnSOD activity and glucose consumption during the cell cycle, it is proposed that MnSOD is a central molecular player for the "Warburg effect."	Glucose	59-66	superoxide dismutase 2	Homo sapiens	40-45
23590434-8	2014	Based on an inverse correlation between MnSOD activity and glucose consumption during the cell cycle, it is proposed that MnSOD is a central molecular player for the "Warburg effect."	Glucose	59-66	superoxide dismutase 2	Homo sapiens	122-127
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Reactive Oxygen Species	9-12	superoxide dismutase 2	Homo sapiens	64-67
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Tyrosine	150-158	superoxide dismutase 2	Homo sapiens	64-67
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Reactive Oxygen Species	199-202	superoxide dismutase 2	Homo sapiens	64-67
24486397-4	2014	Aldosterone increased mineralocorticoid activity, NO and reactive oxygen species production, iNOS mRNA and protein expression, MnSOD and CuZnSOD activity.	Aldosterone	0-11	superoxide dismutase 2	Homo sapiens	127-132
24567128-1	2014	Superoxide dismutases (SOD) are able to remove the superoxide anion free radicals produced by environmental stress and thereby protect cells from being injured by reactive oxygen species.	Superoxides	51-67	superoxide dismutase 2	Homo sapiens	23-26
24567128-1	2014	Superoxide dismutases (SOD) are able to remove the superoxide anion free radicals produced by environmental stress and thereby protect cells from being injured by reactive oxygen species.	Reactive Oxygen Species	163-186	superoxide dismutase 2	Homo sapiens	23-26
24486397-5	2014	Eplerenone attenuated the effects of aldosterone on all but MnSOD and CuZnSOD variables.	Eplerenone	0-10	superoxide dismutase 2	Homo sapiens	60-65
24486397-5	2014	Eplerenone attenuated the effects of aldosterone on all but MnSOD and CuZnSOD variables.	Aldosterone	37-48	superoxide dismutase 2	Homo sapiens	60-65
24486397-6	2014	Eplerenone alone increased the production of NO, MnSOD and CuZnSOD activity, arginase I gene and protein expression, and mannose receptor gene and protein expression, but decreased mineralocorticoid activity only in "heart failure" macrophages.	Eplerenone	0-10	superoxide dismutase 2	Homo sapiens	49-54
24524627-13	2014	The multiplex mRNA expression study indicated that EADs-induced apoptosis was accompanied by upregulation of the expression of SOD1, SOD2, NF-kappaB, p53, p38 MAPK, and catalase, but downregulation of Akt1.	eads	51-55	superoxide dismutase 2	Homo sapiens	133-137
24291162-6	2014	On the other hand, exposure of NKE to different concentrations of CdCl2 (e.g. 0, 10, 20, 30 and 50muM) under the same conditions elevate stronger heat shock and SOD2 mediated protective responses.	Cadmium Chloride	66-71	superoxide dismutase 2	Homo sapiens	161-165
24586301-1	2014	BACKGROUND: The manganese superoxide dismutase (MnSOD) gene, which encodes a chief reactive oxygen species (ROS) scavenging enzyme, has been reported to be associated with the risk of developing sporadic Parkinson"s disease (PD) in some Asian races and the synapsin III (SYN3) gene with some neuropsychiatric diseases.	Reactive Oxygen Species	83-106	superoxide dismutase 2	Homo sapiens	16-46
24586301-1	2014	BACKGROUND: The manganese superoxide dismutase (MnSOD) gene, which encodes a chief reactive oxygen species (ROS) scavenging enzyme, has been reported to be associated with the risk of developing sporadic Parkinson"s disease (PD) in some Asian races and the synapsin III (SYN3) gene with some neuropsychiatric diseases.	Reactive Oxygen Species	83-106	superoxide dismutase 2	Homo sapiens	48-53
24586301-1	2014	BACKGROUND: The manganese superoxide dismutase (MnSOD) gene, which encodes a chief reactive oxygen species (ROS) scavenging enzyme, has been reported to be associated with the risk of developing sporadic Parkinson"s disease (PD) in some Asian races and the synapsin III (SYN3) gene with some neuropsychiatric diseases.	Reactive Oxygen Species	108-111	superoxide dismutase 2	Homo sapiens	16-46
24586301-1	2014	BACKGROUND: The manganese superoxide dismutase (MnSOD) gene, which encodes a chief reactive oxygen species (ROS) scavenging enzyme, has been reported to be associated with the risk of developing sporadic Parkinson"s disease (PD) in some Asian races and the synapsin III (SYN3) gene with some neuropsychiatric diseases.	Reactive Oxygen Species	108-111	superoxide dismutase 2	Homo sapiens	48-53
24375796-3	2014	We hypothesize that inducible heat shock protein 70 (iHSP70) targets SOD-2 to the mitochondria via a mechanism facilitated by ATP, and this process is impaired in persistent pulmonary hypertension of the newborn (PPHN).	Adenosine Triphosphate	126-129	superoxide dismutase 2	Homo sapiens	69-74
24375796-5	2014	Interruption of iHSP70-SOD-2 interaction with 2-phenylethylenesulfonamide-mu (PFT-mu, a specific inhibitor of substrate binding to iHSP70 COOH terminus) and siRNA-mediated knockdown of iHSP70 expression disrupted SOD-2 transport to mitochondria.	2-phenylethylenesulfonamide	46-73	superoxide dismutase 2	Homo sapiens	23-28
24375796-6	2014	Increasing intracellular ATP levels by stimulation of respiration with CaCl2 facilitated the mitochondrial import of SOD-2, increased SOD-2 activity, and decreased the mitochondrial superoxide (O2( -)) levels in PPHN pulmonary artery endothelial cells (PAEC) by promoting iHSP70-SOD-2 dissociation at the outer mitochondrial membrane.	Adenosine Triphosphate	25-28	superoxide dismutase 2	Homo sapiens	117-122
24375796-6	2014	Increasing intracellular ATP levels by stimulation of respiration with CaCl2 facilitated the mitochondrial import of SOD-2, increased SOD-2 activity, and decreased the mitochondrial superoxide (O2( -)) levels in PPHN pulmonary artery endothelial cells (PAEC) by promoting iHSP70-SOD-2 dissociation at the outer mitochondrial membrane.	Adenosine Triphosphate	25-28	superoxide dismutase 2	Homo sapiens	134-139
24375796-6	2014	Increasing intracellular ATP levels by stimulation of respiration with CaCl2 facilitated the mitochondrial import of SOD-2, increased SOD-2 activity, and decreased the mitochondrial superoxide (O2( -)) levels in PPHN pulmonary artery endothelial cells (PAEC) by promoting iHSP70-SOD-2 dissociation at the outer mitochondrial membrane.	Adenosine Triphosphate	25-28	superoxide dismutase 2	Homo sapiens	134-139
24375796-6	2014	Increasing intracellular ATP levels by stimulation of respiration with CaCl2 facilitated the mitochondrial import of SOD-2, increased SOD-2 activity, and decreased the mitochondrial superoxide (O2( -)) levels in PPHN pulmonary artery endothelial cells (PAEC) by promoting iHSP70-SOD-2 dissociation at the outer mitochondrial membrane.	Calcium Chloride	71-76	superoxide dismutase 2	Homo sapiens	117-122
24375796-6	2014	Increasing intracellular ATP levels by stimulation of respiration with CaCl2 facilitated the mitochondrial import of SOD-2, increased SOD-2 activity, and decreased the mitochondrial superoxide (O2( -)) levels in PPHN pulmonary artery endothelial cells (PAEC) by promoting iHSP70-SOD-2 dissociation at the outer mitochondrial membrane.	Calcium Chloride	71-76	superoxide dismutase 2	Homo sapiens	134-139
24375796-6	2014	Increasing intracellular ATP levels by stimulation of respiration with CaCl2 facilitated the mitochondrial import of SOD-2, increased SOD-2 activity, and decreased the mitochondrial superoxide (O2( -)) levels in PPHN pulmonary artery endothelial cells (PAEC) by promoting iHSP70-SOD-2 dissociation at the outer mitochondrial membrane.	Calcium Chloride	71-76	superoxide dismutase 2	Homo sapiens	134-139
24375796-7	2014	In contrast, oligomycin, an inhibitor of mitochondrial ATPase, decreased SOD-2 expression and activity and increased O2( -) levels in the mitochondria of control PAEC.	Oligomycins	13-23	superoxide dismutase 2	Homo sapiens	73-78
24375796-8	2014	The basal ATP levels and degree of iHSP70-SOD-2 dissociation were lower in PPHN PAEC and lead to increased SOD-2 degradation in cytosol.	Adenosine Triphosphate	10-13	superoxide dismutase 2	Homo sapiens	107-112
24151936-8	2014	Moreover, we indicate that the increase of ROS is, at least in part, due to impaired folding of the manganese superoxide dismutase (MnSOD), a key antioxidant enzyme.	Reactive Oxygen Species	43-46	superoxide dismutase 2	Homo sapiens	100-130
24001137-5	2014	An in vitro culture of human adipocytes with 1 muM potassium iodide (KI, dose similar to the human breast milk iodine concentration) produced a significant decrease in adiponectin, GSH-Px, SOD1, and SOD2 mRNA expression.	Potassium Iodide	51-67	superoxide dismutase 2	Homo sapiens	199-203
24151936-8	2014	Moreover, we indicate that the increase of ROS is, at least in part, due to impaired folding of the manganese superoxide dismutase (MnSOD), a key antioxidant enzyme.	Reactive Oxygen Species	43-46	superoxide dismutase 2	Homo sapiens	132-137
24465521-4	2014	The aim of this study is to determine whether the cytoprotection by estrogen involves regulation of manganese superoxide dismutase (MnSOD), a major mitochondrial ROS scavenging enzyme, via cardiac p38beta.	Reactive Oxygen Species	162-165	superoxide dismutase 2	Homo sapiens	100-130
24269899-10	2014	Further studies demonstrated a significant increase in posttranslational modifications of tyrosine and lysine residues in MnSOD protein and oxidation of Cys at the active site (Cys32 and Cys35) and the regulatory site (Cys62 and Cys69) of Trx1 in high-grade PCa compared to BN tissues.	Tyrosine	90-98	superoxide dismutase 2	Homo sapiens	122-127
24269899-10	2014	Further studies demonstrated a significant increase in posttranslational modifications of tyrosine and lysine residues in MnSOD protein and oxidation of Cys at the active site (Cys32 and Cys35) and the regulatory site (Cys62 and Cys69) of Trx1 in high-grade PCa compared to BN tissues.	Lysine	103-109	superoxide dismutase 2	Homo sapiens	122-127
24361291-0	2014	The stilbenes resveratrol, pterostilbene and piceid affect growth and stress resistance in mammalian cells via a mechanism requiring estrogen receptor beta and the induction of Mn-superoxide dismutase.	Stilbenes	4-13	superoxide dismutase 2	Homo sapiens	177-200
24361291-0	2014	The stilbenes resveratrol, pterostilbene and piceid affect growth and stress resistance in mammalian cells via a mechanism requiring estrogen receptor beta and the induction of Mn-superoxide dismutase.	Resveratrol	14-25	superoxide dismutase 2	Homo sapiens	177-200
24361291-0	2014	The stilbenes resveratrol, pterostilbene and piceid affect growth and stress resistance in mammalian cells via a mechanism requiring estrogen receptor beta and the induction of Mn-superoxide dismutase.	pterostilbene	27-40	superoxide dismutase 2	Homo sapiens	177-200
24361291-2	2014	Resveratrol, a phytoestrogen found in red wines and other foods, has been previously reported to increase MnSOD protein levels and activity both in vitro and in vivo.	Resveratrol	0-11	superoxide dismutase 2	Homo sapiens	106-111
24361291-9	2014	Using pharmacological and genetic approaches, it was found that the effects of pterostilbene and piceid required an induction of the mitochondrial enzyme MnSOD and intact mitochondrial respiration.	pterostilbene	79-92	superoxide dismutase 2	Homo sapiens	154-159
24361291-9	2014	Using pharmacological and genetic approaches, it was found that the effects of pterostilbene and piceid required an induction of the mitochondrial enzyme MnSOD and intact mitochondrial respiration.	polydatin	97-103	superoxide dismutase 2	Homo sapiens	154-159
24498107-3	2014	We examined the association of SOD2 genotype and breast cancer recurrence (BCR) among patients treated with cyclophosphamide-based chemotherapy (Cyclo).	Cyclophosphamide	108-124	superoxide dismutase 2	Homo sapiens	31-35
24498107-3	2014	We examined the association of SOD2 genotype and breast cancer recurrence (BCR) among patients treated with cyclophosphamide-based chemotherapy (Cyclo).	emodepside	145-150	superoxide dismutase 2	Homo sapiens	31-35
24465521-4	2014	The aim of this study is to determine whether the cytoprotection by estrogen involves regulation of manganese superoxide dismutase (MnSOD), a major mitochondrial ROS scavenging enzyme, via cardiac p38beta.	Reactive Oxygen Species	162-165	superoxide dismutase 2	Homo sapiens	132-137
24494199-5	2014	Here we show that this signaling complex can similarly be induced in a redox-engineered cell culture model that enables regulation of intracellular steady state H2O2 level by enforced expression of superoxide dismutase 2 (Sod2) and catalase.	Hydrogen Peroxide	161-165	superoxide dismutase 2	Homo sapiens	198-220
24494199-5	2014	Here we show that this signaling complex can similarly be induced in a redox-engineered cell culture model that enables regulation of intracellular steady state H2O2 level by enforced expression of superoxide dismutase 2 (Sod2) and catalase.	Hydrogen Peroxide	161-165	superoxide dismutase 2	Homo sapiens	222-226
24275138-8	2014	Downregulation of MnSOD and LDHA accompanied the toxicity induced by hypoxia and CoCl2 in 5mM glucose, and these changes were enhanced by oxamate or 2-deoxyglucose.	cobaltous chloride	81-86	superoxide dismutase 2	Homo sapiens	18-23
24275138-8	2014	Downregulation of MnSOD and LDHA accompanied the toxicity induced by hypoxia and CoCl2 in 5mM glucose, and these changes were enhanced by oxamate or 2-deoxyglucose.	Glucose	94-101	superoxide dismutase 2	Homo sapiens	18-23
24275138-8	2014	Downregulation of MnSOD and LDHA accompanied the toxicity induced by hypoxia and CoCl2 in 5mM glucose, and these changes were enhanced by oxamate or 2-deoxyglucose.	Oxamic Acid	138-145	superoxide dismutase 2	Homo sapiens	18-23
24275138-8	2014	Downregulation of MnSOD and LDHA accompanied the toxicity induced by hypoxia and CoCl2 in 5mM glucose, and these changes were enhanced by oxamate or 2-deoxyglucose.	Deoxyglucose	149-163	superoxide dismutase 2	Homo sapiens	18-23
24078003-7	2014	The MTT assay showed that proliferation of various cancer cell lines were inhibited by hMnSOD-R9 in a dose-dependent manner.	monooxyethylene trimethylolpropane tristearate	4-7	superoxide dismutase 2	Homo sapiens	87-93
24587799-9	2014	There was a significant difference in the MnSOD genotype distributions between the RCC patients and the controls in terms of Ala/Ala+Ala/Val and Val/Val genotypes (P = 0.039).	Alanine	125-128	superoxide dismutase 2	Homo sapiens	42-47
24587799-9	2014	There was a significant difference in the MnSOD genotype distributions between the RCC patients and the controls in terms of Ala/Ala+Ala/Val and Val/Val genotypes (P = 0.039).	Alanine	129-132	superoxide dismutase 2	Homo sapiens	42-47
24587799-9	2014	There was a significant difference in the MnSOD genotype distributions between the RCC patients and the controls in terms of Ala/Ala+Ala/Val and Val/Val genotypes (P = 0.039).	Alanine	129-132	superoxide dismutase 2	Homo sapiens	42-47
24587799-9	2014	There was a significant difference in the MnSOD genotype distributions between the RCC patients and the controls in terms of Ala/Ala+Ala/Val and Val/Val genotypes (P = 0.039).	Valine	137-140	superoxide dismutase 2	Homo sapiens	42-47
24587799-9	2014	There was a significant difference in the MnSOD genotype distributions between the RCC patients and the controls in terms of Ala/Ala+Ala/Val and Val/Val genotypes (P = 0.039).	Valine	145-148	superoxide dismutase 2	Homo sapiens	42-47
24587799-9	2014	There was a significant difference in the MnSOD genotype distributions between the RCC patients and the controls in terms of Ala/Ala+Ala/Val and Val/Val genotypes (P = 0.039).	Valine	145-148	superoxide dismutase 2	Homo sapiens	42-47
25400332-13	2014	Increased MnSOD activity indicates the mitochondrial source of ROS in patients with advanced heart failure.	ros	63-66	superoxide dismutase 2	Homo sapiens	10-15
24248464-0	2014	Importance of C/EBPbeta binding and histone acetylation status in the promoter regions for induction of IGFBP-1, PRL, and Mn-SOD by cAMP in human endometrial stromal cells.	Cyclic AMP	132-136	superoxide dismutase 2	Homo sapiens	122-128
24248464-4	2014	This study investigated the molecular and epigenetic mechanisms by which cAMP up-regulates the expression of IGF-binding protein-1 (IGFBP-1), prolactin (PRL), and manganese superoxide dismutase (Mn-SOD) in ESC.	Cyclic AMP	73-77	superoxide dismutase 2	Homo sapiens	163-193
24248464-4	2014	This study investigated the molecular and epigenetic mechanisms by which cAMP up-regulates the expression of IGF-binding protein-1 (IGFBP-1), prolactin (PRL), and manganese superoxide dismutase (Mn-SOD) in ESC.	Cyclic AMP	73-77	superoxide dismutase 2	Homo sapiens	195-201
24248464-11	2014	cAMP increased Mn-SOD mRNA levels and C/EBPbeta binding activities in the enhancer region.	Cyclic AMP	0-4	superoxide dismutase 2	Homo sapiens	15-21
24037914-2	2014	Glutathione peroxidase 1 (GPX1) and mitochondrial superoxide dismutase (MnSOD) are two key antioxidant enzymes in the defense system against reactive oxygen species.	Reactive Oxygen Species	141-164	superoxide dismutase 2	Homo sapiens	72-77
25462070-4	2014	The E2/ER-mediated SOD2 up-regulation results in minimized ROS generation, which highly favors healthy cardiovascular function.	ros	59-62	superoxide dismutase 2	Homo sapiens	19-23
23526725-5	2014	Five of these, resveratrol, coumestrol, kaempferol, genistein and daidzein, significantly increased MnSOD expression, slowed proliferative growth and enhanced stress resistance (hydrogen peroxide LD50) .	Resveratrol	15-26	superoxide dismutase 2	Homo sapiens	100-105
23526725-5	2014	Five of these, resveratrol, coumestrol, kaempferol, genistein and daidzein, significantly increased MnSOD expression, slowed proliferative growth and enhanced stress resistance (hydrogen peroxide LD50) .	Coumestrol	28-38	superoxide dismutase 2	Homo sapiens	100-105
23526725-5	2014	Five of these, resveratrol, coumestrol, kaempferol, genistein and daidzein, significantly increased MnSOD expression, slowed proliferative growth and enhanced stress resistance (hydrogen peroxide LD50) .	kaempferol	40-50	superoxide dismutase 2	Homo sapiens	100-105
23526725-5	2014	Five of these, resveratrol, coumestrol, kaempferol, genistein and daidzein, significantly increased MnSOD expression, slowed proliferative growth and enhanced stress resistance (hydrogen peroxide LD50) .	Genistein	52-61	superoxide dismutase 2	Homo sapiens	100-105
23526725-5	2014	Five of these, resveratrol, coumestrol, kaempferol, genistein and daidzein, significantly increased MnSOD expression, slowed proliferative growth and enhanced stress resistance (hydrogen peroxide LD50) .	daidzein	66-74	superoxide dismutase 2	Homo sapiens	100-105
23526725-6	2014	When siRNA was used to prevent the MnSOD induction by genistein, coumestrol or daidzein, none of these compounds exerted any effect on proliferative growth, and only the effect of coumestrol on stress resistance persisted.	Genistein	54-63	superoxide dismutase 2	Homo sapiens	35-40
23526725-6	2014	When siRNA was used to prevent the MnSOD induction by genistein, coumestrol or daidzein, none of these compounds exerted any effect on proliferative growth, and only the effect of coumestrol on stress resistance persisted.	Coumestrol	65-75	superoxide dismutase 2	Homo sapiens	35-40
23526725-6	2014	When siRNA was used to prevent the MnSOD induction by genistein, coumestrol or daidzein, none of these compounds exerted any effect on proliferative growth, and only the effect of coumestrol on stress resistance persisted.	daidzein	79-87	superoxide dismutase 2	Homo sapiens	35-40
23526725-7	2014	The estrogen antagonist ICI182780 prevented the increased MnSOD expression and also the changes in cell growth and stress resistance, indicating that these effects are mediated by estrogen receptors (ER).	Fulvestrant	24-33	superoxide dismutase 2	Homo sapiens	58-63
24732311-8	2014	The MnSOD expression was positively correlated with fasting plasma glucose and total cholesterol levels both at the transcript level (r = 0.4, P &lt;0.05 for both correlations) and at the protein level (r = 0.3 and r = 0.4, respectively, P &lt;0.05).	Glucose	67-74	superoxide dismutase 2	Homo sapiens	4-9
24732311-8	2014	The MnSOD expression was positively correlated with fasting plasma glucose and total cholesterol levels both at the transcript level (r = 0.4, P &lt;0.05 for both correlations) and at the protein level (r = 0.3 and r = 0.4, respectively, P &lt;0.05).	Cholesterol	85-96	superoxide dismutase 2	Homo sapiens	4-9
24225087-7	2013	Mice expressing HCV structural proteins on a background of reduced expression of superoxide dismutase 2 (SOD2; Sod2(+/-)) also had increased liver sensitivity to alcohol, with elevated ALT, steatosis, and lobular inflammation.	Alcohols	162-169	superoxide dismutase 2	Homo sapiens	105-109
23494737-7	2013	We have demonstrated that overexpression of SIRT3 under high glucose conditions reduces FOXO1 acetylation, suggesting that deacetylation of FOXO1 by SIRT3 elevates the expression of the FOXO1 target genes, catalase, and manganese superoxide dismutase (MnSOD) while decreasing senescence phenotypes.	Glucose	61-68	superoxide dismutase 2	Homo sapiens	220-250
23494737-7	2013	We have demonstrated that overexpression of SIRT3 under high glucose conditions reduces FOXO1 acetylation, suggesting that deacetylation of FOXO1 by SIRT3 elevates the expression of the FOXO1 target genes, catalase, and manganese superoxide dismutase (MnSOD) while decreasing senescence phenotypes.	Glucose	61-68	superoxide dismutase 2	Homo sapiens	252-257
24225087-7	2013	Mice expressing HCV structural proteins on a background of reduced expression of superoxide dismutase 2 (SOD2; Sod2(+/-)) also had increased liver sensitivity to alcohol, with elevated ALT, steatosis, and lobular inflammation.	Alcohols	162-169	superoxide dismutase 2	Homo sapiens	111-115
24225087-8	2013	Elevated ALT was associated with an alcohol-induced decrease in SOD2 and redistribution of FOXO3 to the cytosol.	Alcohols	36-43	superoxide dismutase 2	Homo sapiens	64-68
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Reactive Oxygen Species	207-210	superoxide dismutase 2	Homo sapiens	113-143
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Reactive Oxygen Species	207-210	superoxide dismutase 2	Homo sapiens	145-150
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Superoxides	123-133	superoxide dismutase 2	Homo sapiens	145-150
24055523-0	2013	Acid-degradable core-shell nanoparticles for reversed tamoxifen-resistance in breast cancer by silencing manganese superoxide dismutase (MnSOD).	Tamoxifen	54-63	superoxide dismutase 2	Homo sapiens	105-135
24055523-0	2013	Acid-degradable core-shell nanoparticles for reversed tamoxifen-resistance in breast cancer by silencing manganese superoxide dismutase (MnSOD).	Tamoxifen	54-63	superoxide dismutase 2	Homo sapiens	137-142
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Hydrogen Peroxide	247-264	superoxide dismutase 2	Homo sapiens	113-143
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Tamoxifen	32-41	superoxide dismutase 2	Homo sapiens	113-143
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Hydrogen Peroxide	247-264	superoxide dismutase 2	Homo sapiens	145-150
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Tamoxifen	32-41	superoxide dismutase 2	Homo sapiens	145-150
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Tamoxifen	43-46	superoxide dismutase 2	Homo sapiens	113-143
24090840-4	2013	At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.	Zinc Oxide	16-19	superoxide dismutase 2	Homo sapiens	90-94
24055523-9	2013	Sensitization of TAM-resistant MCF7-BK-TR breast cancer cells with (MnSOD siRNA/PAMAM)-PK NPs restored TAM-induced cellular apoptosis in vitro and significantly suppressed tumor growth in vivo, as confirmed by biochemical assays and histological observations.	Tamoxifen	17-20	superoxide dismutase 2	Homo sapiens	68-73
24090840-4	2013	At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.	Zinc Oxide	191-194	superoxide dismutase 2	Homo sapiens	90-94
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Tamoxifen	43-46	superoxide dismutase 2	Homo sapiens	145-150
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Tamoxifen	170-173	superoxide dismutase 2	Homo sapiens	113-143
24090840-4	2013	At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.	Reactive Oxygen Species	236-239	superoxide dismutase 2	Homo sapiens	90-94
24055523-9	2013	Sensitization of TAM-resistant MCF7-BK-TR breast cancer cells with (MnSOD siRNA/PAMAM)-PK NPs restored TAM-induced cellular apoptosis in vitro and significantly suppressed tumor growth in vivo, as confirmed by biochemical assays and histological observations.	Tamoxifen	103-106	superoxide dismutase 2	Homo sapiens	68-73
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Tamoxifen	170-173	superoxide dismutase 2	Homo sapiens	145-150
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Reactive Oxygen Species	182-205	superoxide dismutase 2	Homo sapiens	113-143
23566586-3	2013	Among the antioxidant enzymes, the manganese-dependent and mitochondria-specific isoform of SOD (MnSOD) represents the first line of defense against superoxide radicals attack.	Manganese	35-44	superoxide dismutase 2	Homo sapiens	59-95
24055523-3	2013	This study attempted to reverse tamoxifen (TAM)-resistance in breast cancer by silencing a mitochondrial enzyme, manganese superoxide dismutase (MnSOD), which dismutates TAM-induced reactive oxygen species (ROS) (i.e., superoxide) to less harmful hydrogen peroxide and hampers therapeutic effects.	Reactive Oxygen Species	182-205	superoxide dismutase 2	Homo sapiens	145-150
23770201-4	2013	Overexpression of Mn-superoxide dismutase or catalase or treatment with N-acetyl-l-cysteine suppressed 4-ClBQ-induced toxicity.	1-(4-chlorophenyl)-benzo-2,5-quinone	103-109	superoxide dismutase 2	Homo sapiens	18-41
23686423-6	2013	Interestingly, the validation at the protein level showed a strong expression of TXN, CXCL9, MT2A and SOD2 not only in macrophages of THRLBCL but also in the tumor cells of NLPHL and classical Hodgkin lymphoma (cHL).	thrlbcl	134-141	superoxide dismutase 2	Homo sapiens	102-106
24231355-3	2013	In primary human keratinocytes, we found that hypochlorite (HOCl) reversibly inhibited the expression of CCL2 and SOD2, two NF-kappaB-dependent genes.	Hypochlorous Acid	46-58	superoxide dismutase 2	Homo sapiens	114-118
24231355-3	2013	In primary human keratinocytes, we found that hypochlorite (HOCl) reversibly inhibited the expression of CCL2 and SOD2, two NF-kappaB-dependent genes.	Hypochlorous Acid	60-64	superoxide dismutase 2	Homo sapiens	114-118
24255720-2	2013	The level of reactive oxygen species is regulated by a number of enzymes and physiological antioxidants, including HO-1, Sod2, catalase and COX-2, etc.	Reactive Oxygen Species	13-36	superoxide dismutase 2	Homo sapiens	121-125
24255720-9	2013	CoPP induces HO-1 and other oxidative stress-responsive genes expression, such as catalase, cytochrome c, Sod2, and COX-2, and decreases mitochondria-derived reactive oxygen species production, which are mediated partially by FOXO1.	COPP protocol	0-4	superoxide dismutase 2	Homo sapiens	106-110
23991909-8	2013	We conclude that 1) the Ala allele is more frequent in athletes than in controls; and 2) the higher frequency of the Ala allele was noted in both endurance and power athletes compared with that in controls, suggesting that the positive association between the Ala allele and athletic performance may be related to ROS-related angiogenesis, mitochondrial biosynthesis, and muscle hypertrophy, and not to MnSOD aerobic properties.	Alanine	117-120	superoxide dismutase 2	Homo sapiens	403-408
23991909-8	2013	We conclude that 1) the Ala allele is more frequent in athletes than in controls; and 2) the higher frequency of the Ala allele was noted in both endurance and power athletes compared with that in controls, suggesting that the positive association between the Ala allele and athletic performance may be related to ROS-related angiogenesis, mitochondrial biosynthesis, and muscle hypertrophy, and not to MnSOD aerobic properties.	Alanine	117-120	superoxide dismutase 2	Homo sapiens	403-408
23991909-8	2013	We conclude that 1) the Ala allele is more frequent in athletes than in controls; and 2) the higher frequency of the Ala allele was noted in both endurance and power athletes compared with that in controls, suggesting that the positive association between the Ala allele and athletic performance may be related to ROS-related angiogenesis, mitochondrial biosynthesis, and muscle hypertrophy, and not to MnSOD aerobic properties.	ros	314-317	superoxide dismutase 2	Homo sapiens	403-408
23566586-3	2013	Among the antioxidant enzymes, the manganese-dependent and mitochondria-specific isoform of SOD (MnSOD) represents the first line of defense against superoxide radicals attack.	Manganese	35-44	superoxide dismutase 2	Homo sapiens	97-102
23566586-3	2013	Among the antioxidant enzymes, the manganese-dependent and mitochondria-specific isoform of SOD (MnSOD) represents the first line of defense against superoxide radicals attack.	Superoxides	149-159	superoxide dismutase 2	Homo sapiens	59-95
23566586-3	2013	Among the antioxidant enzymes, the manganese-dependent and mitochondria-specific isoform of SOD (MnSOD) represents the first line of defense against superoxide radicals attack.	Superoxides	149-159	superoxide dismutase 2	Homo sapiens	97-102
23952573-3	2013	The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against ROS within the mitochondria, which is considered the main ROS production locus in aerobes.	Reactive Oxygen Species	96-99	superoxide dismutase 2	Homo sapiens	4-34
23873331-6	2013	The relatively high correlation was found between IC50 values calculated for 3,3",4,4",5,5"-trans-hexahydroxystilbene and expression of MnSOD (r = 0.6562).	3,3",4,4",5,5"-trans-hexahydroxystilbene	77-117	superoxide dismutase 2	Homo sapiens	136-141
23994728-6	2013	Furthermore, both PG and LMNA-MSCs showed a decrease in manganese superoxide dismutase (MnSODM), an increase of mitochondrial MnSODM-dependent reactive oxygen species (ROS) and alterations in their migration capacity.	Reactive Oxygen Species	143-166	superoxide dismutase 2	Homo sapiens	126-132
23994728-7	2013	Finally, defects in chondrogenesis are partially reversed by periodic incubation with ROS-scavenger agent that mimics MnSODM effect.	Reactive Oxygen Species	86-89	superoxide dismutase 2	Homo sapiens	118-124
24093550-14	2013	ROS neutralizing enzymes SOD2 and CAT gene expression were downregulated.	Reactive Oxygen Species	0-3	superoxide dismutase 2	Homo sapiens	25-29
24144057-6	2013	Furthermore, there was a 20% reduction in SOD-specific activity in the glycine-treated group, which correlated with SOD2 expression.	Glycine	71-78	superoxide dismutase 2	Homo sapiens	42-45
24144057-6	2013	Furthermore, there was a 20% reduction in SOD-specific activity in the glycine-treated group, which correlated with SOD2 expression.	Glycine	71-78	superoxide dismutase 2	Homo sapiens	116-120
23917205-5	2013	Very interestingly, while acute treatment with L-NAME induced a transient increase in ROS formation, chronic NO deprivation by long term L-NAME exposure drastically reduced cellular ROS content giving rise to an antioxidant environment characterized by an increase in superoxide dismutase-2 (SOD-2) expression and activity, and by nuclear accumulation of the transcription factor NF-E2-related factor-2 (Nrf2).	NG-Nitroarginine Methyl Ester	137-143	superoxide dismutase 2	Homo sapiens	268-290
23917205-5	2013	Very interestingly, while acute treatment with L-NAME induced a transient increase in ROS formation, chronic NO deprivation by long term L-NAME exposure drastically reduced cellular ROS content giving rise to an antioxidant environment characterized by an increase in superoxide dismutase-2 (SOD-2) expression and activity, and by nuclear accumulation of the transcription factor NF-E2-related factor-2 (Nrf2).	NG-Nitroarginine Methyl Ester	137-143	superoxide dismutase 2	Homo sapiens	292-297
23685312-11	2013	Reactive oxygen species content was lower in FH+ myotubes when differentiated in high glucose/insulin (25mM/150pM), which could be due to higher oxidative stress defenses (SOD2 expression and uncoupled respiration).	Reactive Oxygen Species	0-23	superoxide dismutase 2	Homo sapiens	172-176
23952573-3	2013	The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against ROS within the mitochondria, which is considered the main ROS production locus in aerobes.	Reactive Oxygen Species	96-99	superoxide dismutase 2	Homo sapiens	36-41
23952573-3	2013	The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against ROS within the mitochondria, which is considered the main ROS production locus in aerobes.	Reactive Oxygen Species	154-157	superoxide dismutase 2	Homo sapiens	4-34
23952573-3	2013	The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against ROS within the mitochondria, which is considered the main ROS production locus in aerobes.	Reactive Oxygen Species	154-157	superoxide dismutase 2	Homo sapiens	36-41
23952573-4	2013	Structural and/or functional single nucleotide polymorphisms (SNP) within the MnSOD encoding gene may be relevant for ROS detoxification.	Reactive Oxygen Species	118-121	superoxide dismutase 2	Homo sapiens	78-83
23880762-3	2013	The antioxidant enzyme superoxide dismutase (SOD) catalyzes the dismutation of highly reactive O2 (-) into H2O2 and thus acts as an intracellular generator of H2O2.	Superoxides	95-101	superoxide dismutase 2	Homo sapiens	45-48
23463417-7	2013	In support of this finding, coadministration of bortezomib and 2-methoxyestradiol, a SOD inhibitor, rendered KMS20 cells sensitive to apoptosis.	Bortezomib	48-58	superoxide dismutase 2	Homo sapiens	85-88
23463417-7	2013	In support of this finding, coadministration of bortezomib and 2-methoxyestradiol, a SOD inhibitor, rendered KMS20 cells sensitive to apoptosis.	2-Methoxyestradiol	63-81	superoxide dismutase 2	Homo sapiens	85-88
24040102-8	2013	In p53-independent cell protective pathway, we found that FOXO1, FOXO3a, and FOXO4 were involved in SOD2"s upregulation by resveratrol.	Resveratrol	123-134	superoxide dismutase 2	Homo sapiens	100-104
24040102-9	2013	The knockdown of these three FOXOs by siRNAs completely abolished the SOD2 induction, ROS reduction, and anti-apoptotic function of resveratrol.	Resveratrol	132-143	superoxide dismutase 2	Homo sapiens	70-74
23123399-8	2013	Among them, manganese superoxide dismutase gene Ala-9Val polymorphisms show a relatively consistent association with TD susceptibility, although not all studies support this.	Alanine	48-51	superoxide dismutase 2	Homo sapiens	12-42
23123399-8	2013	Among them, manganese superoxide dismutase gene Ala-9Val polymorphisms show a relatively consistent association with TD susceptibility, although not all studies support this.	9val	52-56	superoxide dismutase 2	Homo sapiens	12-42
23880762-3	2013	The antioxidant enzyme superoxide dismutase (SOD) catalyzes the dismutation of highly reactive O2 (-) into H2O2 and thus acts as an intracellular generator of H2O2.	Hydrogen Peroxide	107-111	superoxide dismutase 2	Homo sapiens	45-48
23880762-3	2013	The antioxidant enzyme superoxide dismutase (SOD) catalyzes the dismutation of highly reactive O2 (-) into H2O2 and thus acts as an intracellular generator of H2O2.	Hydrogen Peroxide	159-163	superoxide dismutase 2	Homo sapiens	45-48
23880762-4	2013	As charged O2 (-) is unable to diffuse through intracellular membranes, cells express distinct SOD isoforms in the cytosol (Cu,Zn-SOD) and mitochondria (Mn-SOD), where they locally scavenge O2 (-) leading to production of H2O2.	Superoxides	190-192	superoxide dismutase 2	Homo sapiens	95-98
23880762-4	2013	As charged O2 (-) is unable to diffuse through intracellular membranes, cells express distinct SOD isoforms in the cytosol (Cu,Zn-SOD) and mitochondria (Mn-SOD), where they locally scavenge O2 (-) leading to production of H2O2.	Superoxides	190-192	superoxide dismutase 2	Homo sapiens	153-159
23880762-4	2013	As charged O2 (-) is unable to diffuse through intracellular membranes, cells express distinct SOD isoforms in the cytosol (Cu,Zn-SOD) and mitochondria (Mn-SOD), where they locally scavenge O2 (-) leading to production of H2O2.	Hydrogen Peroxide	222-226	superoxide dismutase 2	Homo sapiens	95-98
23880762-4	2013	As charged O2 (-) is unable to diffuse through intracellular membranes, cells express distinct SOD isoforms in the cytosol (Cu,Zn-SOD) and mitochondria (Mn-SOD), where they locally scavenge O2 (-) leading to production of H2O2.	Hydrogen Peroxide	222-226	superoxide dismutase 2	Homo sapiens	153-159
23880762-5	2013	A 2-fold organelle-specific overexpression of either SOD in Jurkat T cell lines increases intracellular production of H2O2 but does not alter the levels of intracellular H2O2 scavenging enzymes such as catalase, membrane-bound peroxiredoxin1 (Prx1), and cytosolic Prx2.	Hydrogen Peroxide	118-122	superoxide dismutase 2	Homo sapiens	53-56
23880762-6	2013	We report that overexpression of Mn-SOD enhances tyrosine phosphorylation of TCR-associated membrane proximal signal transduction molecules Lck, LAT, ZAP70, PLCgamma1, and SLP76 within 1 min of TCR cross-linking.	Tyrosine	49-57	superoxide dismutase 2	Homo sapiens	33-39
23602909-9	2013	In contrast, paraquat-induced oxidative stress and cell death were selectively reduced by MnSOD overexpression, but not by CuZnSOD or manganese-porphyrins.	Paraquat	13-21	superoxide dismutase 2	Homo sapiens	90-95
24007566-8	2013	The only pathways significant after multiple comparison corrections (FDR &lt;0.05) were the Nrf2-mediated reactive oxygen species (ROS) oxidative response (superoxide dismutase 2, catalase, peroxiredoxin 1, PIK3C3, DNAJC17, microsomal glutathione S-transferase 3) and superoxide radical degradation (SOD2, CAT).	Reactive Oxygen Species	106-129	superoxide dismutase 2	Homo sapiens	300-304
23727323-4	2013	Eukaryotic systems have evolved defenses against such damaging moieties, the chief member of which is superoxide dismutase (SOD2), an enzyme that efficiently converts superoxide to the less reactive hydrogen peroxide (H2O2), which can freely diffuse across the mitochondrial membrane.	Superoxides	102-112	superoxide dismutase 2	Homo sapiens	124-128
23727323-4	2013	Eukaryotic systems have evolved defenses against such damaging moieties, the chief member of which is superoxide dismutase (SOD2), an enzyme that efficiently converts superoxide to the less reactive hydrogen peroxide (H2O2), which can freely diffuse across the mitochondrial membrane.	Hydrogen Peroxide	199-216	superoxide dismutase 2	Homo sapiens	124-128
23727323-4	2013	Eukaryotic systems have evolved defenses against such damaging moieties, the chief member of which is superoxide dismutase (SOD2), an enzyme that efficiently converts superoxide to the less reactive hydrogen peroxide (H2O2), which can freely diffuse across the mitochondrial membrane.	Hydrogen Peroxide	218-222	superoxide dismutase 2	Homo sapiens	124-128
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Alanine	114-117	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Alanine	114-117	superoxide dismutase 2	Homo sapiens	161-165
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Alanine	118-121	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	126-129	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	126-129	superoxide dismutase 2	Homo sapiens	161-165
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Alanine	118-121	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	161-165
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	161-165
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Alanine	118-121	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Alanine	118-121	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	161-165
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Alanine	118-121	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	161-165
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	109-113
23967348-6	2013	Both the significant adjusted OR of 4.30 (95% CI, 1.23-15.03) and 4.53 (95% CI, 1.52-13.51) were observed in SOD2 Ala/Ala and Val/Ala compared to Val/Val and in SOD2 Ala/Ala compared to Val/Ala compared to Val/Val genetic analysis in the high chemical sensitivity case-control study.	Valine	146-149	superoxide dismutase 2	Homo sapiens	161-165
24023786-11	2013	Simvastatin significantly induced cellular reactive oxygen species levels along with expression of pro- and anti-oxidative genes such as Nox2, and MnSOD and catalase, respectively.	Simvastatin	0-11	superoxide dismutase 2	Homo sapiens	147-152
22820117-4	2013	The mitochondria-localized antioxidant enzyme manganese superoxide dismutase (MnSOD) is vital to survival in our oxygen-rich atmosphere because it scavenges mitochondrial ROS.	Oxygen	113-119	superoxide dismutase 2	Homo sapiens	46-76
23488678-7	2013	Real-time RT-PCR data suggested that melatonin treatment up-regulated the expression of CuZnSOD and MnSOD, while down-regulated the expression of Bax.	Melatonin	37-46	superoxide dismutase 2	Homo sapiens	100-105
23485335-5	2013	MnSOD was up-regulated by MG132 and celastrol, and GST-pi was up-regulated by MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	superoxide dismutase 2	Homo sapiens	0-5
23485335-5	2013	MnSOD was up-regulated by MG132 and celastrol, and GST-pi was up-regulated by MG132 and lactacystin.	celastrol	36-45	superoxide dismutase 2	Homo sapiens	0-5
23611775-2	2013	Down-regulation of the mitochondrial enzyme superoxide dismutase 2 (SOD2) contributes to the stabilization of HIF-1alpha under hypoxia due to the decreased dismutation of superoxide radical.	Superoxides	171-189	superoxide dismutase 2	Homo sapiens	44-66
23611775-2	2013	Down-regulation of the mitochondrial enzyme superoxide dismutase 2 (SOD2) contributes to the stabilization of HIF-1alpha under hypoxia due to the decreased dismutation of superoxide radical.	Superoxides	171-189	superoxide dismutase 2	Homo sapiens	68-72
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	superoxide dismutase 2	Homo sapiens	341-345
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	superoxide dismutase 2	Homo sapiens	341-345
23805295-8	2013	Anti-oxidant defense mechanisms of the lens epithelial cells were diminished as evidenced from loss of mitochondrial membrane integrity and lowered MnSOD after 72 h treatment with high glucose.	Glucose	185-192	superoxide dismutase 2	Homo sapiens	148-153
23801966-2	2013	ROS-control by FOXO is mediated by transcriptional activation of detoxifying enzymes such as Superoxide dismutase 2 (SOD2), Catalase or Sestrins or by the repression of mitochondrial respiratory chain proteins resulting in reduced mitochondrial activity.	Reactive Oxygen Species	0-3	superoxide dismutase 2	Homo sapiens	93-115
23801966-2	2013	ROS-control by FOXO is mediated by transcriptional activation of detoxifying enzymes such as Superoxide dismutase 2 (SOD2), Catalase or Sestrins or by the repression of mitochondrial respiratory chain proteins resulting in reduced mitochondrial activity.	Reactive Oxygen Species	0-3	superoxide dismutase 2	Homo sapiens	117-121
23243068-1	2013	Manganese superoxide dismutase (MnSOD), a major antioxidant enzyme within the mitochondria, is responsible for the detoxification of free radicals generated by cellular metabolism and environmental/therapeutic irradiation.	Free Radicals	133-146	superoxide dismutase 2	Homo sapiens	0-30
23243068-1	2013	Manganese superoxide dismutase (MnSOD), a major antioxidant enzyme within the mitochondria, is responsible for the detoxification of free radicals generated by cellular metabolism and environmental/therapeutic irradiation.	Free Radicals	133-146	superoxide dismutase 2	Homo sapiens	32-37
23717425-8	2013	On the other hand, pre-incubation of Caco-2/15 cells with 5-Aza-2"-deoxycytidine, a demethylating agent, or Trolox antioxidant normalized the activities of SOD2 and GPx, reduced lipid peroxidation and prevented inflammation.	Decitabine	58-80	superoxide dismutase 2	Homo sapiens	156-160
23717425-8	2013	On the other hand, pre-incubation of Caco-2/15 cells with 5-Aza-2"-deoxycytidine, a demethylating agent, or Trolox antioxidant normalized the activities of SOD2 and GPx, reduced lipid peroxidation and prevented inflammation.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	108-114	superoxide dismutase 2	Homo sapiens	156-160
23725507-3	2013	The patients with BD and MDD and the controls had a similar distribution of the genotypes and alleles in the Ala-9Val MnSOD gene polymorphism.	ala-9val	109-117	superoxide dismutase 2	Homo sapiens	118-123
22820117-4	2013	The mitochondria-localized antioxidant enzyme manganese superoxide dismutase (MnSOD) is vital to survival in our oxygen-rich atmosphere because it scavenges mitochondrial ROS.	Oxygen	113-119	superoxide dismutase 2	Homo sapiens	78-83
22820117-4	2013	The mitochondria-localized antioxidant enzyme manganese superoxide dismutase (MnSOD) is vital to survival in our oxygen-rich atmosphere because it scavenges mitochondrial ROS.	Reactive Oxygen Species	171-174	superoxide dismutase 2	Homo sapiens	46-76
22820117-4	2013	The mitochondria-localized antioxidant enzyme manganese superoxide dismutase (MnSOD) is vital to survival in our oxygen-rich atmosphere because it scavenges mitochondrial ROS.	Reactive Oxygen Species	171-174	superoxide dismutase 2	Homo sapiens	78-83
23613809-4	2013	Subsequent studies demonstrated that the electrotaxis of glioma cells were abolished by the superoxide inhibitor N-acetyl-l-cysteine (NAC) or overexpression of mitochondrial superoxide dismutase (MnSOD), but was not affected by inhibition of hydrogen peroxide through the overexpression of catalase.	Hydrogen Peroxide	242-259	superoxide dismutase 2	Homo sapiens	160-194
24024155-3	2013	Shifts in steady-state H2O2 concentrations (SS-[H2O2]) resulting from enforced expression of manganese superoxide dismutase (SOD2) drive IL-1alpha mRNA and protein expression.	Hydrogen Peroxide	23-27	superoxide dismutase 2	Homo sapiens	93-123
24024155-3	2013	Shifts in steady-state H2O2 concentrations (SS-[H2O2]) resulting from enforced expression of manganese superoxide dismutase (SOD2) drive IL-1alpha mRNA and protein expression.	Hydrogen Peroxide	23-27	superoxide dismutase 2	Homo sapiens	125-129
24024155-3	2013	Shifts in steady-state H2O2 concentrations (SS-[H2O2]) resulting from enforced expression of manganese superoxide dismutase (SOD2) drive IL-1alpha mRNA and protein expression.	Hydrogen Peroxide	48-52	superoxide dismutase 2	Homo sapiens	93-123
24024155-3	2013	Shifts in steady-state H2O2 concentrations (SS-[H2O2]) resulting from enforced expression of manganese superoxide dismutase (SOD2) drive IL-1alpha mRNA and protein expression.	Hydrogen Peroxide	48-52	superoxide dismutase 2	Homo sapiens	125-129
22572619-14	2013	Pterostilbene significantly increase MnSOD activity in MDA-MB-231 cells.	pterostilbene	0-13	superoxide dismutase 2	Homo sapiens	37-42
23274131-8	2013	The observed decrease of Bcl-2/Bax ratio and a parallel increase of caspase-3 activity confirmed the pro-apoptotic role exerted by diclofenac in melanoma cells; furthermore, the drug provoked an increase of the ROS levels, a decrease of mitochondrial superoxide dismutase (SOD2), the cytosolic translocation of both SOD2 and cytochrome c, and an increase of caspase-9 activity.	Diclofenac	131-141	superoxide dismutase 2	Homo sapiens	273-277
23274131-8	2013	The observed decrease of Bcl-2/Bax ratio and a parallel increase of caspase-3 activity confirmed the pro-apoptotic role exerted by diclofenac in melanoma cells; furthermore, the drug provoked an increase of the ROS levels, a decrease of mitochondrial superoxide dismutase (SOD2), the cytosolic translocation of both SOD2 and cytochrome c, and an increase of caspase-9 activity.	Diclofenac	131-141	superoxide dismutase 2	Homo sapiens	316-320
23274131-9	2013	Finally, the cytotoxic effect of diclofenac was amplified, in melanoma cells, by the silencing of SOD2.	Diclofenac	33-43	superoxide dismutase 2	Homo sapiens	98-102
23319113-4	2013	Our research also extended to the relationship between mtDNA copy number, ROS (reactive oxygen species) production and the MnSOD (manganese superoxide dismutase) expression level.	Reactive Oxygen Species	74-77	superoxide dismutase 2	Homo sapiens	123-128
23319113-4	2013	Our research also extended to the relationship between mtDNA copy number, ROS (reactive oxygen species) production and the MnSOD (manganese superoxide dismutase) expression level.	Reactive Oxygen Species	74-77	superoxide dismutase 2	Homo sapiens	130-160
23319113-4	2013	Our research also extended to the relationship between mtDNA copy number, ROS (reactive oxygen species) production and the MnSOD (manganese superoxide dismutase) expression level.	Reactive Oxygen Species	79-102	superoxide dismutase 2	Homo sapiens	123-128
23319113-4	2013	Our research also extended to the relationship between mtDNA copy number, ROS (reactive oxygen species) production and the MnSOD (manganese superoxide dismutase) expression level.	Reactive Oxygen Species	79-102	superoxide dismutase 2	Homo sapiens	130-160
32260906-5	2013	Superoxide dismutase 2 (SOD2) was apparently up-regulated on the ECAPed Ti surface, which could have contributed to the increase in SOD activity and the decrease in the reactive oxygen species (ROS) level.	Reactive Oxygen Species	169-192	superoxide dismutase 2	Homo sapiens	0-22
32260906-5	2013	Superoxide dismutase 2 (SOD2) was apparently up-regulated on the ECAPed Ti surface, which could have contributed to the increase in SOD activity and the decrease in the reactive oxygen species (ROS) level.	Reactive Oxygen Species	169-192	superoxide dismutase 2	Homo sapiens	24-28
32260906-5	2013	Superoxide dismutase 2 (SOD2) was apparently up-regulated on the ECAPed Ti surface, which could have contributed to the increase in SOD activity and the decrease in the reactive oxygen species (ROS) level.	Reactive Oxygen Species	169-192	superoxide dismutase 2	Homo sapiens	24-27
32260906-5	2013	Superoxide dismutase 2 (SOD2) was apparently up-regulated on the ECAPed Ti surface, which could have contributed to the increase in SOD activity and the decrease in the reactive oxygen species (ROS) level.	Reactive Oxygen Species	194-197	superoxide dismutase 2	Homo sapiens	0-22
32260906-5	2013	Superoxide dismutase 2 (SOD2) was apparently up-regulated on the ECAPed Ti surface, which could have contributed to the increase in SOD activity and the decrease in the reactive oxygen species (ROS) level.	Reactive Oxygen Species	194-197	superoxide dismutase 2	Homo sapiens	24-28
32260906-5	2013	Superoxide dismutase 2 (SOD2) was apparently up-regulated on the ECAPed Ti surface, which could have contributed to the increase in SOD activity and the decrease in the reactive oxygen species (ROS) level.	Reactive Oxygen Species	194-197	superoxide dismutase 2	Homo sapiens	24-27
23384600-8	2013	High glucose also enhanced podocyte expression of MnSOD and catalase.	Glucose	5-12	superoxide dismutase 2	Homo sapiens	50-55
22572619-16	2013	CONCLUSIONS: The natural dietary compound pterostilbene has an anti-proliferative effect and induces apoptosis in breast cancer cells in vitro via Bax activation and overexpression, resulting in increased MnSOD, Smac/DIABLO, and cytochrome C activity and cytosolic Ca(2+) overload.	pterostilbene	42-55	superoxide dismutase 2	Homo sapiens	205-210
23461587-2	2013	On the basis of electronic absorption, circular dichroism (CD), magnetic CD (MCD), and variable-temperature variable-field MCD data obtained for oxidized Mn(Fe)SOD, we propose that the active site of this species is virtually identical to that of wild-type manganese SOD (MnSOD), with both containing a metal ion that resides in a trigonal bipyramidal ligand environment.	Manganese	257-266	superoxide dismutase 2	Homo sapiens	160-163
23461587-7	2013	These computations properly reproduce the experimental trend and reveal that the drastically elevated E(m) of the metal substituted protein stems from a larger separation between the second-sphere Gln residue and the coordinated solvent in Mn(Fe)SOD relative to MnSOD, which causes a weakening of the corresponding H-bond interaction in the oxidized state and alleviates steric crowding in the reduced state.	Metals	114-119	superoxide dismutase 2	Homo sapiens	246-249
23461587-7	2013	These computations properly reproduce the experimental trend and reveal that the drastically elevated E(m) of the metal substituted protein stems from a larger separation between the second-sphere Gln residue and the coordinated solvent in Mn(Fe)SOD relative to MnSOD, which causes a weakening of the corresponding H-bond interaction in the oxidized state and alleviates steric crowding in the reduced state.	Metals	114-119	superoxide dismutase 2	Homo sapiens	262-267
23461587-7	2013	These computations properly reproduce the experimental trend and reveal that the drastically elevated E(m) of the metal substituted protein stems from a larger separation between the second-sphere Gln residue and the coordinated solvent in Mn(Fe)SOD relative to MnSOD, which causes a weakening of the corresponding H-bond interaction in the oxidized state and alleviates steric crowding in the reduced state.	Glutamine	197-200	superoxide dismutase 2	Homo sapiens	246-249
23461587-2	2013	On the basis of electronic absorption, circular dichroism (CD), magnetic CD (MCD), and variable-temperature variable-field MCD data obtained for oxidized Mn(Fe)SOD, we propose that the active site of this species is virtually identical to that of wild-type manganese SOD (MnSOD), with both containing a metal ion that resides in a trigonal bipyramidal ligand environment.	Metals	303-308	superoxide dismutase 2	Homo sapiens	160-163
23461587-4	2013	The major differences between the QM/MM optimized active sites of WT MnSOD and Mn(Fe)SOD are a smaller (His)N-Mn-N(His) equatorial angle and a longer (Gln146(69))NH   O(sol) H-bond distance in the metal-substituted protein.	Histidine	104-107	superoxide dismutase 2	Homo sapiens	69-74
23461587-4	2013	The major differences between the QM/MM optimized active sites of WT MnSOD and Mn(Fe)SOD are a smaller (His)N-Mn-N(His) equatorial angle and a longer (Gln146(69))NH   O(sol) H-bond distance in the metal-substituted protein.	Histidine	104-107	superoxide dismutase 2	Homo sapiens	71-74
23461587-4	2013	The major differences between the QM/MM optimized active sites of WT MnSOD and Mn(Fe)SOD are a smaller (His)N-Mn-N(His) equatorial angle and a longer (Gln146(69))NH   O(sol) H-bond distance in the metal-substituted protein.	Metals	197-202	superoxide dismutase 2	Homo sapiens	69-74
23461587-4	2013	The major differences between the QM/MM optimized active sites of WT MnSOD and Mn(Fe)SOD are a smaller (His)N-Mn-N(His) equatorial angle and a longer (Gln146(69))NH   O(sol) H-bond distance in the metal-substituted protein.	Metals	197-202	superoxide dismutase 2	Homo sapiens	71-74
23461587-6	2013	As Mn(Fe)SOD exhibits a reduction midpoint potential (E(m)) almost 700 mV higher than that of MnSOD, which has been shown to be sufficient for explaining the lack of SOD activity displayed by the metal-subtituted species (Vance, C. K.; Miller, A. F. Biochemistry 2001, 40, 13079-13087), E(m)"s were computed for our experimentally validated QM/MM optimized models of Mn(Fe)SOD and MnSOD.	Metals	196-201	superoxide dismutase 2	Homo sapiens	9-12
23461587-6	2013	As Mn(Fe)SOD exhibits a reduction midpoint potential (E(m)) almost 700 mV higher than that of MnSOD, which has been shown to be sufficient for explaining the lack of SOD activity displayed by the metal-subtituted species (Vance, C. K.; Miller, A. F. Biochemistry 2001, 40, 13079-13087), E(m)"s were computed for our experimentally validated QM/MM optimized models of Mn(Fe)SOD and MnSOD.	Metals	196-201	superoxide dismutase 2	Homo sapiens	94-99
23461587-6	2013	As Mn(Fe)SOD exhibits a reduction midpoint potential (E(m)) almost 700 mV higher than that of MnSOD, which has been shown to be sufficient for explaining the lack of SOD activity displayed by the metal-subtituted species (Vance, C. K.; Miller, A. F. Biochemistry 2001, 40, 13079-13087), E(m)"s were computed for our experimentally validated QM/MM optimized models of Mn(Fe)SOD and MnSOD.	Metals	196-201	superoxide dismutase 2	Homo sapiens	96-99
23461587-6	2013	As Mn(Fe)SOD exhibits a reduction midpoint potential (E(m)) almost 700 mV higher than that of MnSOD, which has been shown to be sufficient for explaining the lack of SOD activity displayed by the metal-subtituted species (Vance, C. K.; Miller, A. F. Biochemistry 2001, 40, 13079-13087), E(m)"s were computed for our experimentally validated QM/MM optimized models of Mn(Fe)SOD and MnSOD.	Metals	196-201	superoxide dismutase 2	Homo sapiens	96-99
23297859-1	2013	This study aimed to evaluate whether natural or synthetic steroid hormones could directly modulate the activity of the different superoxide dismutase (SOD) isoforms found in human blood fractions without changing enzyme expression.	Steroids	58-65	superoxide dismutase 2	Homo sapiens	151-154
23315858-1	2013	Manganese superoxide dismutase (MnSOD) is the most effective antioxidant enzyme in mitochondria and protects cells from reactive oxygen species-induced oxidative damage.	Reactive Oxygen Species	120-143	superoxide dismutase 2	Homo sapiens	0-30
23315858-1	2013	Manganese superoxide dismutase (MnSOD) is the most effective antioxidant enzyme in mitochondria and protects cells from reactive oxygen species-induced oxidative damage.	Reactive Oxygen Species	120-143	superoxide dismutase 2	Homo sapiens	32-37
23315858-4	2013	We observed an association between MnSOD Ala/Ala frequency and a higher PCa risk.	Alanine	41-44	superoxide dismutase 2	Homo sapiens	35-40
23315858-4	2013	We observed an association between MnSOD Ala/Ala frequency and a higher PCa risk.	Alanine	45-48	superoxide dismutase 2	Homo sapiens	35-40
23315858-6	2013	However, we determined that MnSOD Ala-9 Val genotype was not associated with the aggressiveness of the disease.	ala-9 val	34-43	superoxide dismutase 2	Homo sapiens	28-33
23315858-7	2013	The results of our study suggest that MnSOD Ala/Ala genotype may influence on early-onset of PCa patients, but no effect on subsequent development of the disease in Turkish men.	Alanine	44-47	superoxide dismutase 2	Homo sapiens	38-43
23315858-7	2013	The results of our study suggest that MnSOD Ala/Ala genotype may influence on early-onset of PCa patients, but no effect on subsequent development of the disease in Turkish men.	Alanine	48-51	superoxide dismutase 2	Homo sapiens	38-43
23313218-7	2013	This was coupled with concomitant increase in expression of antioxidant enzymes like Sod1, Sod2 and Pebp1 in cortex to neutralize the hypoxia-induced reactive oxygen species (ROS) generation.	Reactive Oxygen Species	150-173	superoxide dismutase 2	Homo sapiens	91-95
23271813-1	2013	Manganese superoxide dismutase (MnSOD) is an antioxidant enzyme responsible for the elimination of superoxide radical.	Superoxides	99-117	superoxide dismutase 2	Homo sapiens	0-30
23271813-1	2013	Manganese superoxide dismutase (MnSOD) is an antioxidant enzyme responsible for the elimination of superoxide radical.	Superoxides	99-117	superoxide dismutase 2	Homo sapiens	32-37
23456297-6	2013	RSV-induced SOD2 expression was observed in cancer cells, although the expression of SOD1, CAT and GPX1 was unaffected.	Resveratrol	0-3	superoxide dismutase 2	Homo sapiens	12-16
23313218-7	2013	This was coupled with concomitant increase in expression of antioxidant enzymes like Sod1, Sod2 and Pebp1 in cortex to neutralize the hypoxia-induced reactive oxygen species (ROS) generation.	Reactive Oxygen Species	175-178	superoxide dismutase 2	Homo sapiens	91-95
22607494-9	2013	Also, MDHAR and DHAR, via ascorbate regeneration, could constitute an essential antioxidant defense together with Mn-SOD, against NO and ONOO(-)  stress in plant mitochondria.	mdhar	6-11	superoxide dismutase 2	Homo sapiens	114-120
22057896-6	2013	Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet.	coenzyme Q10	14-17	superoxide dismutase 2	Homo sapiens	72-76
23412769-6	2013	Overexpression of Cu,Zn-superoxide dismutase (Cu,Zn-SOD) as well as Mn-SOD conferred significant protection against DATS-induced ROS production and apoptotic cell death in MDA-MB-231 and MCF-7 cells.	diallyl trisulfide	116-120	superoxide dismutase 2	Homo sapiens	68-74
23412769-6	2013	Overexpression of Cu,Zn-superoxide dismutase (Cu,Zn-SOD) as well as Mn-SOD conferred significant protection against DATS-induced ROS production and apoptotic cell death in MDA-MB-231 and MCF-7 cells.	Reactive Oxygen Species	129-132	superoxide dismutase 2	Homo sapiens	68-74
23412769-7	2013	Activation of Bak, but not Bax, resulting from DATS treatment was markedly suppressed by overexpression of Mn-SOD.	diallyl trisulfide	47-51	superoxide dismutase 2	Homo sapiens	107-113
23321237-8	2013	RESULTS: Pulp cells treated with long-term H(2)O(2) showed high reactive oxygen species formation, low cell viability, down-expression of antioxidant molecules (Cu/Zn and Mn superoxide dismutase), and odontogenic/osteogenic markers (eg, dentin sialophosphoprotein, dentin matrix protein-1, osteopontin, bone sialoprotein, Runx-2, and bone morphogenetic protein 2 and 7).	Hydrogen Peroxide	43-51	superoxide dismutase 2	Homo sapiens	171-194
23212700-6	2013	SOD2Val16Ala polymorphism was associated with dopamine plasma concentration and blood concentration ratio between reduced and oxidised form of glutathione, while GPX1Pro200Leu was related with concentration of reduced glutathione.	Dopamine	46-54	superoxide dismutase 2	Homo sapiens	0-4
23212700-6	2013	SOD2Val16Ala polymorphism was associated with dopamine plasma concentration and blood concentration ratio between reduced and oxidised form of glutathione, while GPX1Pro200Leu was related with concentration of reduced glutathione.	Glutathione	143-154	superoxide dismutase 2	Homo sapiens	0-4
23212700-6	2013	SOD2Val16Ala polymorphism was associated with dopamine plasma concentration and blood concentration ratio between reduced and oxidised form of glutathione, while GPX1Pro200Leu was related with concentration of reduced glutathione.	Glutathione	218-229	superoxide dismutase 2	Homo sapiens	0-4
23429290-3	2013	In the present study, we observed that upon detachment from matrix, human mammary epithelial cells strongly upregulate manganese superoxide dismutase (MnSOD, or SOD2), a principal mitochondrial antioxidant enzyme that detoxifies ROS through dismutation of superoxide.	Reactive Oxygen Species	229-232	superoxide dismutase 2	Homo sapiens	119-149
23429290-3	2013	In the present study, we observed that upon detachment from matrix, human mammary epithelial cells strongly upregulate manganese superoxide dismutase (MnSOD, or SOD2), a principal mitochondrial antioxidant enzyme that detoxifies ROS through dismutation of superoxide.	Reactive Oxygen Species	229-232	superoxide dismutase 2	Homo sapiens	151-156
23429290-3	2013	In the present study, we observed that upon detachment from matrix, human mammary epithelial cells strongly upregulate manganese superoxide dismutase (MnSOD, or SOD2), a principal mitochondrial antioxidant enzyme that detoxifies ROS through dismutation of superoxide.	Reactive Oxygen Species	229-232	superoxide dismutase 2	Homo sapiens	161-165
23429290-3	2013	In the present study, we observed that upon detachment from matrix, human mammary epithelial cells strongly upregulate manganese superoxide dismutase (MnSOD, or SOD2), a principal mitochondrial antioxidant enzyme that detoxifies ROS through dismutation of superoxide.	Superoxides	129-139	superoxide dismutase 2	Homo sapiens	151-156
23429290-5	2013	Detachment of mammary epithelial cells potently increases mitochondrial superoxide levels, which are further elevated by depletion of MnSOD in suspended cells.	Superoxides	72-82	superoxide dismutase 2	Homo sapiens	134-139
23429290-7	2013	These results suggest that detachment-induced MnSOD counters mitochondrial superoxide accumulation and confers anoikis resistance.	Superoxides	75-85	superoxide dismutase 2	Homo sapiens	46-51
22989570-0	2013	Recombinant human manganese superoxide dismutase reduces liver fibrosis and portal pressure in CCl4-cirrhotic rats.	Carbon Tetrachloride	95-99	superoxide dismutase 2	Homo sapiens	18-48
22607494-9	2013	Also, MDHAR and DHAR, via ascorbate regeneration, could constitute an essential antioxidant defense together with Mn-SOD, against NO and ONOO(-)  stress in plant mitochondria.	Ascorbic Acid	26-35	superoxide dismutase 2	Homo sapiens	114-120
22607494-9	2013	Also, MDHAR and DHAR, via ascorbate regeneration, could constitute an essential antioxidant defense together with Mn-SOD, against NO and ONOO(-)  stress in plant mitochondria.	onoo	137-141	superoxide dismutase 2	Homo sapiens	114-120
23111423-0	2013	The combination of mitochondrial low enzyme-activity aldehyde dehydrogenase 2 allele and superoxide dismutase 2 genotypes increases the risk of hypertension in relation to alcohol consumption.	Alcohols	172-179	superoxide dismutase 2	Homo sapiens	89-111
22983815-0	2013	Participation of 47C&gt;T SNP (Ala-9Val polymorphism) of the SOD2 gene in the intracellular environment of human peripheral blood mononuclear cells with and without lipopolysaccharides.	ala-9val	31-39	superoxide dismutase 2	Homo sapiens	61-65
23984360-5	2013	The associations between MnSOD Ala -9Val polymorphism and the risk of asbestosis and between iNOS genotypes and asbestosis were modified by CAT -262 C &gt; T polymorphism (P = 0.038; P = 0.031).	ala -9val	31-40	superoxide dismutase 2	Homo sapiens	25-30
22982047-1	2013	Manganese superoxide dismutase (MnSOD) is an integral mitochondrial protein known as a first-line antioxidant defense against superoxide radical anions produced as by-products of the electron transport chain.	Superoxides	10-20	superoxide dismutase 2	Homo sapiens	32-37
22982047-2	2013	Recent studies have shaped the idea that by regulating the mitochondrial redox status and H(2)O(2) outflow, MnSOD acts as a fundamental regulator of cellular proliferation, metabolism, and apoptosis, thereby assuming roles that extend far beyond its proposed antioxidant functions.	Hydrogen Peroxide	90-98	superoxide dismutase 2	Homo sapiens	108-113
22982047-5	2013	These facts led us to hypothesize that, like its Cu,ZnSOD counterpart, MnSOD may work as a peroxidase, utilizing H(2)O(2) to promote mitochondrial damage, a known cancer risk factor.	Hydrogen Peroxide	113-121	superoxide dismutase 2	Homo sapiens	71-76
23111423-1	2013	A cooperative role of mitochondrial aldehyde dehydrogenase 2 (ALDH2) and superoxide dismutase 2 (SOD2) to maintain the vascular function has recently been demonstrated in nitrate tolerance.	Nitrates	171-178	superoxide dismutase 2	Homo sapiens	73-95
23111423-1	2013	A cooperative role of mitochondrial aldehyde dehydrogenase 2 (ALDH2) and superoxide dismutase 2 (SOD2) to maintain the vascular function has recently been demonstrated in nitrate tolerance.	Nitrates	171-178	superoxide dismutase 2	Homo sapiens	97-101
23111423-2	2013	The present study examined whether the combination of low enzyme-activity variants of ALDH2 and SOD2 increases the risk of hypertension in relation to alcohol consumption.	Alcohols	151-158	superoxide dismutase 2	Homo sapiens	96-100
22517484-3	2012	In this study, the authors investigated the clinical significance of the single nucleotide polymorphisms (SNPs) of 2 ROS metabolic process-related genes: superoxide dismutase 2 (SOD2) and glutathione S-transferase pi (GSTP1).	Reactive Oxygen Species	117-120	superoxide dismutase 2	Homo sapiens	154-176
22267242-8	2012	Reactive oxygen species levels and expressions of AT(1)R, NAD(P)H oxidase subunits, SOD-1, and SOD-2 in SHR arteries were normalized by the chronic treatment with calcitriol.	Calcitriol	163-173	superoxide dismutase 2	Homo sapiens	95-100
23388485-4	2012	The aim of this study was to investigate the influence of MX therapy on enzymatic parameters of endogenous antioxidative status: manganese and copper/zinc superoxide dismutase (MnSOD, Cu/ZnSOD), catalase (CAT), glutathione peroxidase (GSH-Px) and lipid peroxidation marker--malondialdehyde (MDA) in blood serum and cerebrospinal fluid (CSF) in patients suffering from MS. After the MX therapy serum and the CSF MDA concentrations increased significantly.	Mitoxantrone	58-60	superoxide dismutase 2	Homo sapiens	177-182
23069381-7	2012	MnSODm also increased the production of ROS and the expression levels of cleaved caspase-9, caspase-3, poly (ADP-ribose) polymerase (PARP) and Bax in Raji cells.	Reactive Oxygen Species	40-43	superoxide dismutase 2	Homo sapiens	0-6
22517484-3	2012	In this study, the authors investigated the clinical significance of the single nucleotide polymorphisms (SNPs) of 2 ROS metabolic process-related genes: superoxide dismutase 2 (SOD2) and glutathione S-transferase pi (GSTP1).	Reactive Oxygen Species	117-120	superoxide dismutase 2	Homo sapiens	178-182
22621406-8	2012	We found that the expression of Mn-superoxide dismutase was significantly increased by 17-beta-estradiol and testosterone, myeloperoxidase expression was significantly elevated by cortisol and progesterone, and the expression of NADPH oxidase was significantly decreased by progesterone.	Estradiol	87-104	superoxide dismutase 2	Homo sapiens	32-55
22951908-3	2012	The most important reactive oxygen/nitrogen species (ROS/RNS) detoxification mechanisms include superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx).	reactive oxygen/nitrogen species	19-51	superoxide dismutase 2	Homo sapiens	118-121
22951908-3	2012	The most important reactive oxygen/nitrogen species (ROS/RNS) detoxification mechanisms include superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx).	ros	53-56	superoxide dismutase 2	Homo sapiens	118-121
22951908-3	2012	The most important reactive oxygen/nitrogen species (ROS/RNS) detoxification mechanisms include superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx).	Radon	57-60	superoxide dismutase 2	Homo sapiens	118-121
23000060-8	2012	These results provide evidence indicating that in addition to the enzymatic action of detoxifying superoxide, the antioxidant MnSOD may function as a signaling regulator in stress-induced adaptive protection through cell survival pathways.	Superoxides	98-108	superoxide dismutase 2	Homo sapiens	126-131
22621406-8	2012	We found that the expression of Mn-superoxide dismutase was significantly increased by 17-beta-estradiol and testosterone, myeloperoxidase expression was significantly elevated by cortisol and progesterone, and the expression of NADPH oxidase was significantly decreased by progesterone.	Testosterone	109-121	superoxide dismutase 2	Homo sapiens	32-55
22825700-6	2012	Statistically significant increased risks were also identified in women with the MnSOD genotypes containing the Ala allele who had a tobacco smoking history (OR, 1.17; 95% CI, 1.02-1.34), a higher body mass index (OR, 1.26; 95% CI, 1.02-1.56) or who used oral contraceptives (OR, 1.98; 95% CI, 1.34-2.93).	Alanine	112-115	superoxide dismutase 2	Homo sapiens	81-86
22884995-7	2012	In contrast, the cadmium-mediated increases in colony formation, cell invasion and migration were prevented by transfection with catalase, superoxide dismutase-1 (SOD1), or SOD2.	Cadmium	17-24	superoxide dismutase 2	Homo sapiens	173-177
22688013-2	2012	The superoxide dismutase manganese dependent (SOD2) catalyzes O(2)(-) in H(2)O(2) into mitochondria and is encoded by a single gene that presents a common polymorphism that results in the replacement of alanine (A) with a valine (V) in the 16 codon.	Superoxides	62-66	superoxide dismutase 2	Homo sapiens	46-50
22688013-2	2012	The superoxide dismutase manganese dependent (SOD2) catalyzes O(2)(-) in H(2)O(2) into mitochondria and is encoded by a single gene that presents a common polymorphism that results in the replacement of alanine (A) with a valine (V) in the 16 codon.	h(2)	73-77	superoxide dismutase 2	Homo sapiens	46-50
22688013-2	2012	The superoxide dismutase manganese dependent (SOD2) catalyzes O(2)(-) in H(2)O(2) into mitochondria and is encoded by a single gene that presents a common polymorphism that results in the replacement of alanine (A) with a valine (V) in the 16 codon.	Alanine	203-210	superoxide dismutase 2	Homo sapiens	46-50
22688013-2	2012	The superoxide dismutase manganese dependent (SOD2) catalyzes O(2)(-) in H(2)O(2) into mitochondria and is encoded by a single gene that presents a common polymorphism that results in the replacement of alanine (A) with a valine (V) in the 16 codon.	Valine	222-228	superoxide dismutase 2	Homo sapiens	46-50
23020916-3	2012	The aim of the present study was to determine whether pure methylchavicol applied on a human hepatoma cell line, HepG2, could promote oxidative stress and might alter the expression of procarcinogenic biomarkers such as the drug-metabolizing enzyme (CYP2E1), the inducible form of nitric oxide synthase (iNOS) and might induce the expression of Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and Mn-SOD that control the redox equilibrium of the cells.	estragole	59-73	superoxide dismutase 2	Homo sapiens	388-394
22836756-4	2012	We found that miR-21 inhibited the metabolism of superoxide to hydrogen peroxide, produced either by endogenous basal activities or exposure to ionizing radiation (IR), by directing attenuating SOD3 or by an indirect mechanism that limited TNFa production, thereby reducing SOD2 levels.	Superoxides	49-59	superoxide dismutase 2	Homo sapiens	274-278
22836756-4	2012	We found that miR-21 inhibited the metabolism of superoxide to hydrogen peroxide, produced either by endogenous basal activities or exposure to ionizing radiation (IR), by directing attenuating SOD3 or by an indirect mechanism that limited TNFa production, thereby reducing SOD2 levels.	Hydrogen Peroxide	63-80	superoxide dismutase 2	Homo sapiens	274-278
22704671-4	2012	Genotyping was performed to identify MnSOD Ala-9Val and GPx1 Pro198Leu polymorphisms by a method based on PCR amplification and detection of polymorphisms with hybridization probes labeled with fluorescent dyes.	ala-9val	43-51	superoxide dismutase 2	Homo sapiens	37-42
22704671-6	2012	RESULTS: The genotype distribution of the MnSOD Ala-9Val single nucleotide polymorphism was significantly different for the controls and the recurrent tonsillitis patients (P=0.009).	ala-9val	48-56	superoxide dismutase 2	Homo sapiens	42-47
22704671-9	2012	In addition, the frequency of tonsillitis was significantly higher in recurrent tonsillitis patients with the MnSOD Ala-9Val polymorphism than the patients with wild-type (P=0.008).	ala-9val	116-124	superoxide dismutase 2	Homo sapiens	110-115
22704671-11	2012	CONCLUSIONS: The MnSOD Ala-9Val polymorphism causes susceptibility to recurrent tonsillitis in Turkish children.	Alanine	23-26	superoxide dismutase 2	Homo sapiens	17-22
22704671-11	2012	CONCLUSIONS: The MnSOD Ala-9Val polymorphism causes susceptibility to recurrent tonsillitis in Turkish children.	9val	27-31	superoxide dismutase 2	Homo sapiens	17-22
22704671-12	2012	And we suggest that there may be a possible relation between local and recurrent infections or inflammation of the tonsillar tissue and the MnSOD Ala-9Val single nucleotide polymorphism in pediatric patients with RT.	ala-9val	146-154	superoxide dismutase 2	Homo sapiens	140-145
22656864-4	2012	Authentic MnSOD, but not MnSOD lacking MTS, protected against mitochondrial ROS, lipid peroxidation and apoptosis.	Reactive Oxygen Species	76-79	superoxide dismutase 2	Homo sapiens	10-15
22710948-2	2012	Immunofluorescence, immunoblotting             and immunogold labelling analyses of MCF7 cells exposed for up to 72 h to 2 nM             estradiol (E2) or to 2 microM 27OHC demonstrated similar responses in the expression             of MnSOD and ERbeta compared to the non-stimulated cells.	Estradiol	138-147	superoxide dismutase 2	Homo sapiens	238-243
22710948-2	2012	Immunofluorescence, immunoblotting             and immunogold labelling analyses of MCF7 cells exposed for up to 72 h to 2 nM             estradiol (E2) or to 2 microM 27OHC demonstrated similar responses in the expression             of MnSOD and ERbeta compared to the non-stimulated cells.	27-hydroxycholesterol	168-173	superoxide dismutase 2	Homo sapiens	238-243
22710435-2	2012	This study investigates the hypothesis that manganese superoxide dismutase (MnSOD) regulates cellular redox flux and glucose consumption during the cell cycle.	Glucose	117-124	superoxide dismutase 2	Homo sapiens	44-74
22710435-2	2012	This study investigates the hypothesis that manganese superoxide dismutase (MnSOD) regulates cellular redox flux and glucose consumption during the cell cycle.	Glucose	117-124	superoxide dismutase 2	Homo sapiens	76-81
22710435-3	2012	A direct correlation was observed between glucose consumption and percentage of S-phase cells in MnSOD wild-type fibroblasts, which was absent in MnSOD homozygous knockout fibroblasts.	Glucose	42-49	superoxide dismutase 2	Homo sapiens	97-102
22710435-4	2012	Results from electron paramagnetic resonance spectroscopy and flow cytometric assays showed a significant increase in cellular superoxide levels in S-phase cells, which was associated with an increase in glucose and oxygen consumption, and a decrease in MnSOD activity.	Superoxides	127-137	superoxide dismutase 2	Homo sapiens	254-259
22710435-5	2012	Mass spectrometry results showed a complex pattern of MnSOD-methylation at both lysine (68, 89, 122, and 202) and arginine (197 and 216) residues.	Lysine	80-86	superoxide dismutase 2	Homo sapiens	54-59
22710435-5	2012	Mass spectrometry results showed a complex pattern of MnSOD-methylation at both lysine (68, 89, 122, and 202) and arginine (197 and 216) residues.	Arginine	114-122	superoxide dismutase 2	Homo sapiens	54-59
22710435-7	2012	Computational-based simulations indicate that lysine and arginine methylation of MnSOD during quiescence would allow greater accessibility to the enzyme active site as well as increase the positive electrostatic potential around and within the active site.	Lysine	46-52	superoxide dismutase 2	Homo sapiens	81-86
22710435-7	2012	Computational-based simulations indicate that lysine and arginine methylation of MnSOD during quiescence would allow greater accessibility to the enzyme active site as well as increase the positive electrostatic potential around and within the active site.	Arginine	57-65	superoxide dismutase 2	Homo sapiens	81-86
22710435-8	2012	Methylation-dependent changes in the MnSOD conformation and subsequent changes in the electrostatic potential around the active site during quiescence versus proliferation could increase the accessibility of superoxide, a negatively charged substrate.	Superoxides	208-218	superoxide dismutase 2	Homo sapiens	37-42
21904836-3	2012	Genotyping of the MnSOD Ala-9Val and GPX1 Pro198Leu polymorphisms was carried out by PCR-RFLP.	ala-9val	24-32	superoxide dismutase 2	Homo sapiens	18-23
21904836-7	2012	Additionally, patients carrying both Ala/Ala of MnSOD and Leu/Leu of GPX1 had the highest risk of developing bladder cancer.	Alanine	37-40	superoxide dismutase 2	Homo sapiens	48-53
21904836-7	2012	Additionally, patients carrying both Ala/Ala of MnSOD and Leu/Leu of GPX1 had the highest risk of developing bladder cancer.	Alanine	41-44	superoxide dismutase 2	Homo sapiens	48-53
21904836-9	2012	In addition, the combination of the MnSOD Ala/Ala and GPX1 Leu/Leu genotypes may have a synergistic effect on disease risk.	Alanine	42-45	superoxide dismutase 2	Homo sapiens	36-41
21904836-9	2012	In addition, the combination of the MnSOD Ala/Ala and GPX1 Leu/Leu genotypes may have a synergistic effect on disease risk.	Alanine	46-49	superoxide dismutase 2	Homo sapiens	36-41
22907303-10	2012	With the pretreatment of NaHS, the up-regulations of XOD and p67(phox) levels and down-regulation of Mn-SOD level were inhibited.	sodium bisulfide	25-29	superoxide dismutase 2	Homo sapiens	101-107
22907303-11	2012	Compared with the young group, the old group showed lower SOD activity and higher H2O2 level, whereas NaHS pretreatment reversed the changes of SOD activity and H2O2 level.	sodium bisulfide	102-106	superoxide dismutase 2	Homo sapiens	144-147
22732184-3	2012	Manganese superoxide dismutase (MnSOD) is a primary mitochondrial ROS scavenging enzyme, and in 1983 Irwin Fridovich proposed an elegant chemical mechanism/model whereby acetylation directs MnSOD enzymatic activity.	Reactive Oxygen Species	66-69	superoxide dismutase 2	Homo sapiens	0-30
22732184-3	2012	Manganese superoxide dismutase (MnSOD) is a primary mitochondrial ROS scavenging enzyme, and in 1983 Irwin Fridovich proposed an elegant chemical mechanism/model whereby acetylation directs MnSOD enzymatic activity.	Reactive Oxygen Species	66-69	superoxide dismutase 2	Homo sapiens	32-37
22732184-3	2012	Manganese superoxide dismutase (MnSOD) is a primary mitochondrial ROS scavenging enzyme, and in 1983 Irwin Fridovich proposed an elegant chemical mechanism/model whereby acetylation directs MnSOD enzymatic activity.	Reactive Oxygen Species	66-69	superoxide dismutase 2	Homo sapiens	190-195
22732184-6	2012	In this regard, we and others have shown that MnSOD is regulated, at least in part, by the deacetylation of specific conserved lysines in a reaction catalyzed by the mitochondrial sirtuin, Sirt3.	Lysine	127-134	superoxide dismutase 2	Homo sapiens	46-51
22732184-7	2012	We speculate that the regulation of MnSOD activity by lysine acetylation via an electrostatic repulsion mechanism is a conserved and critical aspect of MnSOD regulation necessary to maintain mitochondrial homeostasis.	Lysine	54-60	superoxide dismutase 2	Homo sapiens	36-41
22732184-7	2012	We speculate that the regulation of MnSOD activity by lysine acetylation via an electrostatic repulsion mechanism is a conserved and critical aspect of MnSOD regulation necessary to maintain mitochondrial homeostasis.	Lysine	54-60	superoxide dismutase 2	Homo sapiens	152-157
22656864-5	2012	In addition, the levels of mitochondrial ROS were consistently found to always correlate with the levels of authentic MnSOD in mitochondria.	Reactive Oxygen Species	41-44	superoxide dismutase 2	Homo sapiens	118-123
22684917-9	2012	Moreover, superoxide             dismutase (SOD2) or thioredoxin (TXN) siRNAs attenuated HPF cell death by ATO,             which was not correlated with ROS and GSH level changes.	Arsenic Trioxide	107-110	superoxide dismutase 2	Homo sapiens	44-48
22316666-5	2012	RESULTS: MnSOD expression in Het-1A cells was decreased after bile salt exposure.	Bile Acids and Salts	62-71	superoxide dismutase 2	Homo sapiens	9-14
22316666-6	2012	The cells that received MnTBAP or curcumin oil pretreatment showed increased MnSOD expression compared with control untreated cells.	curcumin oil	34-46	superoxide dismutase 2	Homo sapiens	77-82
22316666-7	2012	The Bar-T cells showed an increase in MnSOD expression after treatment with bile salts.	Bile Acids and Salts	76-86	superoxide dismutase 2	Homo sapiens	38-43
22316666-9	2012	The MnSOD activity was significantly different between the untreated cell lines (P = 0.01) and after treatment with bile salt (P = 0.03).	Bile Acids and Salts	116-125	superoxide dismutase 2	Homo sapiens	4-9
22316666-11	2012	CONCLUSIONS: We demonstrated preservation of MnSOD expression in Het-1A cells that were pretreated with antioxidants including MnTBAP, curcumin oil, and certain berry extracts.	curcumin oil	135-147	superoxide dismutase 2	Homo sapiens	45-50
22580338-4	2012	Upon knockdown of SOD2 by RNA interference, UM1 cells displayed significantly reduced migration and invasion abilities; reduced activities of SOD2; lower intracellular H(2)O(2); decreased protein levels of Snail, MMP1, and pERK1/2; and increased protein levels of E-cadherin.	Water	168-173	superoxide dismutase 2	Homo sapiens	18-22
22580338-7	2012	Thus, we conclude that the SOD2-dependent production of H(2)O(2) contributes to both the migration and the invasion of TSCC via the Snail signaling pathway, through increased Snail, MMP1, and pERK1/2 protein levels and the repression of the E-cadherin protein.	Hydrogen Peroxide	56-64	superoxide dismutase 2	Homo sapiens	27-31
22432908-1	2012	OBJECTIVE: To check whether individual or combined mutated genotypes for Ala-9Val (Mn-SOD) and Arg213Gly (EC-SOD) are associated with preeclampsia; to check the influence of the mutated genotypes on the degree of severity and perinatal outcome of preeclampsia.	Alanine	73-76	superoxide dismutase 2	Homo sapiens	83-89
22432908-1	2012	OBJECTIVE: To check whether individual or combined mutated genotypes for Ala-9Val (Mn-SOD) and Arg213Gly (EC-SOD) are associated with preeclampsia; to check the influence of the mutated genotypes on the degree of severity and perinatal outcome of preeclampsia.	9val	77-81	superoxide dismutase 2	Homo sapiens	83-89
22193621-2	2012	Manganese superoxide dismutase (MnSOD) is a scavenger of reactive oxygen species, and 8-oxoguanine DNA glycosylase (OGG1) is the major glycosylase that repairs DNA lesions.	Reactive Oxygen Species	57-80	superoxide dismutase 2	Homo sapiens	0-30
22218650-4	2012	Superoxide dismutase 2 (SOD2), at candidate modifier locus 6q25.3, detoxifies superoxide radicals protecting against oxidative stress and damage.	Superoxides	78-97	superoxide dismutase 2	Homo sapiens	0-22
22218650-4	2012	Superoxide dismutase 2 (SOD2), at candidate modifier locus 6q25.3, detoxifies superoxide radicals protecting against oxidative stress and damage.	Superoxides	78-97	superoxide dismutase 2	Homo sapiens	24-28
22469513-5	2012	Ectopic expression of mitochondrial superoxide scavenging enzyme (MnSOD) or treatment with MnSOD mimetic (MnTBAP) inhibited DOX-induced superoxide generation and apoptosis.	Superoxides	36-46	superoxide dismutase 2	Homo sapiens	66-71
22469513-5	2012	Ectopic expression of mitochondrial superoxide scavenging enzyme (MnSOD) or treatment with MnSOD mimetic (MnTBAP) inhibited DOX-induced superoxide generation and apoptosis.	Doxorubicin	124-127	superoxide dismutase 2	Homo sapiens	66-71
22469513-5	2012	Ectopic expression of mitochondrial superoxide scavenging enzyme (MnSOD) or treatment with MnSOD mimetic (MnTBAP) inhibited DOX-induced superoxide generation and apoptosis.	Doxorubicin	124-127	superoxide dismutase 2	Homo sapiens	91-96
22469513-5	2012	Ectopic expression of mitochondrial superoxide scavenging enzyme (MnSOD) or treatment with MnSOD mimetic (MnTBAP) inhibited DOX-induced superoxide generation and apoptosis.	Superoxides	136-146	superoxide dismutase 2	Homo sapiens	66-71
22469513-5	2012	Ectopic expression of mitochondrial superoxide scavenging enzyme (MnSOD) or treatment with MnSOD mimetic (MnTBAP) inhibited DOX-induced superoxide generation and apoptosis.	Superoxides	136-146	superoxide dismutase 2	Homo sapiens	91-96
22471522-6	2012	In myeloma cells, upon combination with hydrogen peroxide treatment, relative to TNF (tumour necrosis factor)-alpha, IL-6 induced an early perturbation in reduced glutathione level and increased NF-kappaB-dependent MnSOD (manganese superoxide dismutase) expression.	Hydrogen Peroxide	40-57	superoxide dismutase 2	Homo sapiens	215-220
22471522-6	2012	In myeloma cells, upon combination with hydrogen peroxide treatment, relative to TNF (tumour necrosis factor)-alpha, IL-6 induced an early perturbation in reduced glutathione level and increased NF-kappaB-dependent MnSOD (manganese superoxide dismutase) expression.	Hydrogen Peroxide	40-57	superoxide dismutase 2	Homo sapiens	222-252
22471522-9	2012	The present study provides evidence that increases in MnSOD expression mediate IL-6-induced resistance to Dex and radiation in myeloma cells.	Dexamethasone	106-109	superoxide dismutase 2	Homo sapiens	54-59
22193621-2	2012	Manganese superoxide dismutase (MnSOD) is a scavenger of reactive oxygen species, and 8-oxoguanine DNA glycosylase (OGG1) is the major glycosylase that repairs DNA lesions.	Reactive Oxygen Species	57-80	superoxide dismutase 2	Homo sapiens	32-37
22193621-3	2012	Interestingly, whether there is an elevated risk of hypertension with arsenic or lead exposure in individuals with genetic variations in MnSOD or OGG1 has not yet been investigated.	Arsenic	70-77	superoxide dismutase 2	Homo sapiens	137-142
22193621-9	2012	Individuals with high urinary arsenic levels and the MnSOD Val-Ala/Ala-Ala genotypes had a greater risk of hypertension than those with low urinary arsenic levels and the MnSOD Val-Val genotype (odds ratio [OR] = 4.2, 95% confidence interval [CI] = 1.7-10.3).	H-VAL-ALA-OH	59-66	superoxide dismutase 2	Homo sapiens	53-58
22193621-9	2012	Individuals with high urinary arsenic levels and the MnSOD Val-Ala/Ala-Ala genotypes had a greater risk of hypertension than those with low urinary arsenic levels and the MnSOD Val-Val genotype (odds ratio [OR] = 4.2, 95% confidence interval [CI] = 1.7-10.3).	alanylalanine	67-74	superoxide dismutase 2	Homo sapiens	53-58
22193621-9	2012	Individuals with high urinary arsenic levels and the MnSOD Val-Ala/Ala-Ala genotypes had a greater risk of hypertension than those with low urinary arsenic levels and the MnSOD Val-Val genotype (odds ratio [OR] = 4.2, 95% confidence interval [CI] = 1.7-10.3).	valylvaline	177-184	superoxide dismutase 2	Homo sapiens	171-176
22193621-11	2012	Thus, both MnSOD and OGG1 genotypes may be prone to an increased risk of hypertension associated with arsenic exposure.	Arsenic	102-109	superoxide dismutase 2	Homo sapiens	11-16
22139133-7	2012	FOXO3a has been previously implicated in the detoxification of reactive oxygen species (ROS) through induction of manganese-containing superoxide dismutase (SOD2).	Reactive Oxygen Species	63-86	superoxide dismutase 2	Homo sapiens	157-161
22139133-7	2012	FOXO3a has been previously implicated in the detoxification of reactive oxygen species (ROS) through induction of manganese-containing superoxide dismutase (SOD2).	Reactive Oxygen Species	88-91	superoxide dismutase 2	Homo sapiens	157-161
22139133-8	2012	We observed that reduction in ROS levels following FOXO3a activation was independent of SOD2, but required c-Myc inhibition.	Reactive Oxygen Species	30-33	superoxide dismutase 2	Homo sapiens	88-92
22807932-4	2012	MnSOD enzyme activity was determined using an indirect competitive inhibition assay and MnSOD gene polymorphism using poly merase chain reaction and agarose gel electrophoresis.	Sepharose	149-156	superoxide dismutase 2	Homo sapiens	0-5
22561706-5	2012	The major antioxidant enzyme that scavenges superoxide anion radical in mitochondria is manganese superoxide dismutase (MnSOD).	Superoxides	44-68	superoxide dismutase 2	Homo sapiens	88-118
22561706-5	2012	The major antioxidant enzyme that scavenges superoxide anion radical in mitochondria is manganese superoxide dismutase (MnSOD).	Superoxides	44-68	superoxide dismutase 2	Homo sapiens	120-125
22807932-11	2012	MnSOD gene polymorphism Ala/Val may be a risk factor associated with more advanced breast cancer stage, and reduction of MnSOD activity may be a mechanism of the progression of benign to malignant tumors.	Alanine	24-27	superoxide dismutase 2	Homo sapiens	0-5
22807932-11	2012	MnSOD gene polymorphism Ala/Val may be a risk factor associated with more advanced breast cancer stage, and reduction of MnSOD activity may be a mechanism of the progression of benign to malignant tumors.	Valine	28-31	superoxide dismutase 2	Homo sapiens	0-5
22699057-3	2012	Genotyping of the SNP Ala-9Val of MnSOD gene was performed by PCR and direct sequencing of the PCR products.	Alanine	22-25	superoxide dismutase 2	Homo sapiens	34-39
22547077-9	2012	One protein identified to be upregulated in the resistant cells was manganese superoxide dismutase (SOD2), a mitochondrial protein that converts superoxide radicals to hydrogen peroxides.	Superoxides	78-88	superoxide dismutase 2	Homo sapiens	100-104
22547077-9	2012	One protein identified to be upregulated in the resistant cells was manganese superoxide dismutase (SOD2), a mitochondrial protein that converts superoxide radicals to hydrogen peroxides.	Hydrogen Peroxide	168-186	superoxide dismutase 2	Homo sapiens	100-104
22547077-10	2012	Silencing of SOD2 resensitized the resistant cells to 2-ME, and overexpression of SOD2 led the parental cells to 2-ME resistance.	2-Methoxyestradiol	54-58	superoxide dismutase 2	Homo sapiens	13-17
22547077-10	2012	Silencing of SOD2 resensitized the resistant cells to 2-ME, and overexpression of SOD2 led the parental cells to 2-ME resistance.	2-Methoxyestradiol	113-117	superoxide dismutase 2	Homo sapiens	82-86
22547077-12	2012	Our results suggest that upregulation of SOD2 expression is an important mechanism by which pancreatic cancer cells acquire resistance to ROS-inducing, anticancer drugs, and potentially also to IR.	Reactive Oxygen Species	138-141	superoxide dismutase 2	Homo sapiens	41-45
22699057-9	2012	CONCLUSION: MnSOD Ala-9Val polymorphism can be region- and race-related, and it is not correlated to the genetic susceptibility of NPC in Cantonese.	ala-9val	18-26	superoxide dismutase 2	Homo sapiens	12-17
22367629-12	2012	The increase in SOD2 was dependent on PrP expression and suggests increased scavenging of reactive oxygen species as mechanism of action.	Reactive Oxygen Species	90-113	superoxide dismutase 2	Homo sapiens	16-20
22261313-8	2012	Treatment with nuclear factor kappaB inhibitor, PDTC, or JNK inhibitor, SP600125, attenuated BDNF-augmented MnSOD protein expression.	pyrazolanthrone	72-80	superoxide dismutase 2	Homo sapiens	108-113
22429591-3	2012	Analysis of the kinetics of T cell receptor (TCR)-triggered ROS production revealed a temporal association between higher MnSOD abundance/activity and a shut-down phase of oxidative signal generation.	Reactive Oxygen Species	60-63	superoxide dismutase 2	Homo sapiens	122-127
22429591-4	2012	Transient or inducible MnSOD overexpression abrogated T cell activation-triggered mitochondrial ROS production as well as NF-kappaB- and AP-1-mediated transcription.	Reactive Oxygen Species	96-99	superoxide dismutase 2	Homo sapiens	23-28
22429591-7	2012	Thus, MnSOD-mediated negative feedback regulation of activation-induced mitochondrial ROS generation exemplifies a process of retrograde mitochondria-to-nucleus communication.	Reactive Oxygen Species	86-89	superoxide dismutase 2	Homo sapiens	6-11
22503984-0	2012	Hydrogen sulfide decreases the levels of ROS by inhibiting mitochondrial complex IV and increasing SOD activities in cardiomyocytes under ischemia/reperfusion.	Hydrogen Sulfide	0-16	superoxide dismutase 2	Homo sapiens	99-102
22503984-0	2012	Hydrogen sulfide decreases the levels of ROS by inhibiting mitochondrial complex IV and increasing SOD activities in cardiomyocytes under ischemia/reperfusion.	Reactive Oxygen Species	41-44	superoxide dismutase 2	Homo sapiens	99-102
22503984-5	2012	We found that H(2)S inhibited mitochondrial complex IV activity and increased the activities of superoxide dismutases (SODs), including Mn-SOD and CuZn-SOD.	Hydrogen Sulfide	14-19	superoxide dismutase 2	Homo sapiens	136-142
22406317-4	2012	Subsequent studies demonstrate that the electrotaxis of HT-1080 fibrosarcoma cells is abolished by NADPH oxidase inhibitor and overexpression of manganese superoxide dismutase (MnSOD), an enzyme that hydrolyzes superoxide.	Superoxides	155-165	superoxide dismutase 2	Homo sapiens	177-182
22247543-2	2012	As a cofactor for manganese superoxide dismutase or through formation of non-proteinaceous manganese antioxidants, this metal can combat oxidative damage without deleterious side effects of Fenton chemistry.	Metals	120-125	superoxide dismutase 2	Homo sapiens	18-48
22247543-4	2012	Cellular pools of iron can outcompete manganese for binding to manganese superoxide dismutase, and through Fenton chemistry, iron may counteract the benefits of non-proteinaceous manganese antioxidants.	Iron	18-22	superoxide dismutase 2	Homo sapiens	63-93
22247543-4	2012	Cellular pools of iron can outcompete manganese for binding to manganese superoxide dismutase, and through Fenton chemistry, iron may counteract the benefits of non-proteinaceous manganese antioxidants.	Manganese	38-47	superoxide dismutase 2	Homo sapiens	63-93
23552603-5	2012	We demonstrate that COX-2 inhibition, via its chemical inhibitors (NS-398 or celecoxib), reduced v-FLIP/K13-mediated NF-kappaB induction, and extracellular matrix (ECM) interaction-mediated signaling, mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) levels, and subsequently downregulated detachment-induced apoptosis (anoikis) resistance.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	67-73	superoxide dismutase 2	Homo sapiens	234-264
23552603-5	2012	We demonstrate that COX-2 inhibition, via its chemical inhibitors (NS-398 or celecoxib), reduced v-FLIP/K13-mediated NF-kappaB induction, and extracellular matrix (ECM) interaction-mediated signaling, mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) levels, and subsequently downregulated detachment-induced apoptosis (anoikis) resistance.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	67-73	superoxide dismutase 2	Homo sapiens	266-271
23552603-5	2012	We demonstrate that COX-2 inhibition, via its chemical inhibitors (NS-398 or celecoxib), reduced v-FLIP/K13-mediated NF-kappaB induction, and extracellular matrix (ECM) interaction-mediated signaling, mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) levels, and subsequently downregulated detachment-induced apoptosis (anoikis) resistance.	Celecoxib	77-86	superoxide dismutase 2	Homo sapiens	234-264
22237152-12	2012	CONCLUSION: Elevated serum uric acid is not associated with endothelial dysfunction among healthy adults, but is inversely related to EID and EC MnSOD, and positively related to systemic inflammation.	Uric Acid	27-36	superoxide dismutase 2	Homo sapiens	145-150
23552603-5	2012	We demonstrate that COX-2 inhibition, via its chemical inhibitors (NS-398 or celecoxib), reduced v-FLIP/K13-mediated NF-kappaB induction, and extracellular matrix (ECM) interaction-mediated signaling, mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) levels, and subsequently downregulated detachment-induced apoptosis (anoikis) resistance.	Celecoxib	77-86	superoxide dismutase 2	Homo sapiens	266-271
22187010-4	2012	Bafilomycin A1, an inhibitor of ER function, effectively blocked poly(I:C)-induced activation of caspase-8, -9, and -3, MnSOD and glutathione peroxidase 1 and reduced poly(I:C)-induced SK-N-AS apoptosis.	bafilomycin	0-11	superoxide dismutase 2	Homo sapiens	120-125
22187010-4	2012	Bafilomycin A1, an inhibitor of ER function, effectively blocked poly(I:C)-induced activation of caspase-8, -9, and -3, MnSOD and glutathione peroxidase 1 and reduced poly(I:C)-induced SK-N-AS apoptosis.	Poly I-C	65-74	superoxide dismutase 2	Homo sapiens	120-125
22187010-4	2012	Bafilomycin A1, an inhibitor of ER function, effectively blocked poly(I:C)-induced activation of caspase-8, -9, and -3, MnSOD and glutathione peroxidase 1 and reduced poly(I:C)-induced SK-N-AS apoptosis.	Poly I-C	65-73	superoxide dismutase 2	Homo sapiens	120-125
22246134-12	2012	Antioxidant enzymes, including GPx-1, PRX-1 and SOD-2, had an increased expression at 1% ethanol.	Ethanol	89-96	superoxide dismutase 2	Homo sapiens	48-53
22167619-0	2012	Polymorphic variations in manganese superoxide dismutase (MnSOD), glutathione peroxidase-1 (GPX1), and catalase (CAT) contribute to elevated plasma triglyceride levels in Chinese patients with type 2 diabetes or diabetic cardiovascular disease.	Triglycerides	148-160	superoxide dismutase 2	Homo sapiens	26-56
22167619-0	2012	Polymorphic variations in manganese superoxide dismutase (MnSOD), glutathione peroxidase-1 (GPX1), and catalase (CAT) contribute to elevated plasma triglyceride levels in Chinese patients with type 2 diabetes or diabetic cardiovascular disease.	Triglycerides	148-160	superoxide dismutase 2	Homo sapiens	58-63
21804600-3	2012	Human MnSOD has two poly(A) sites resulting in two transcripts: 1.5 and 4.2 kb.	Poly A	20-27	superoxide dismutase 2	Homo sapiens	6-11
22266922-9	2012	Furthermore, superoxide             dismutase (SOD) 2, catalase (CTX) and GSH peroxidase (GPX) siRNAs enhanced HPF             cell death by MG132, which was not correlated with ROS and GSH level changes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	superoxide dismutase 2	Homo sapiens	13-53
22386763-0	2012	Influence of Val16Ala SOD2 polymorphism on the in-vitro effect of clomiphene citrate in oxidative metabolism.	Clomiphene	66-84	superoxide dismutase 2	Homo sapiens	22-26
22386763-8	2012	The results suggest that clomiphene citrate exhibits antioxidant activity similar to that observed with other selective oestrogen receptor modulators, and the intensity of the effect appears to be SOD2 polymorphism dependent.	Clomiphene	25-43	superoxide dismutase 2	Homo sapiens	197-201
22386763-12	2012	Significant differences of the clomiphene citrate antioxidant effect on PBMC with different Val16Ala SOD genotypes were observed in this study.	Clomiphene	31-49	superoxide dismutase 2	Homo sapiens	101-104
22386763-13	2012	Based on these results, we could speculate that alterations in SOD2 activity caused by the Val16Ala polymorphism can result in differential responses to drugs such as clomiphene citrate.	Clomiphene	167-185	superoxide dismutase 2	Homo sapiens	63-67
21827635-7	2012	Analysis of exercise and/or ROS-sensitive genes demonstrated that exercise-induced mRNA expression is ROS dependent of MnSOD, but not PGC-1alpha, interleukin-6, monocyte chemotactic protein-1, or heat-shock protein 70.	Reactive Oxygen Species	28-31	superoxide dismutase 2	Homo sapiens	119-124
21827635-7	2012	Analysis of exercise and/or ROS-sensitive genes demonstrated that exercise-induced mRNA expression is ROS dependent of MnSOD, but not PGC-1alpha, interleukin-6, monocyte chemotactic protein-1, or heat-shock protein 70.	Reactive Oxygen Species	102-105	superoxide dismutase 2	Homo sapiens	119-124
22108091-4	2012	Telomerase overexpression also considerably diminished TNF-alpha-induced transcription of SOD2 Superoxide Dismutase 2 gene by reducing ROS contribution to SOD2 gene induction, both in normal fibroblasts and in cancer cells.	Reactive Oxygen Species	135-138	superoxide dismutase 2	Homo sapiens	90-94
22130631-1	2012	BACKGROUND: Mitochondrial manganese superoxide dismutase (MnSOD) converts superoxide anion into H(2)O(2), which is neutralized sequentially by either catalase (CAT) or glutathione peroxidase 1 (Gpx 1) into water or converted into highly reactive hypochlorous acid by myeloperoxidase (MPO).	Superoxides	74-90	superoxide dismutase 2	Homo sapiens	26-56
22130631-1	2012	BACKGROUND: Mitochondrial manganese superoxide dismutase (MnSOD) converts superoxide anion into H(2)O(2), which is neutralized sequentially by either catalase (CAT) or glutathione peroxidase 1 (Gpx 1) into water or converted into highly reactive hypochlorous acid by myeloperoxidase (MPO).	Superoxides	74-90	superoxide dismutase 2	Homo sapiens	58-63
22130631-1	2012	BACKGROUND: Mitochondrial manganese superoxide dismutase (MnSOD) converts superoxide anion into H(2)O(2), which is neutralized sequentially by either catalase (CAT) or glutathione peroxidase 1 (Gpx 1) into water or converted into highly reactive hypochlorous acid by myeloperoxidase (MPO).	h(2)	96-100	superoxide dismutase 2	Homo sapiens	26-56
22130631-1	2012	BACKGROUND: Mitochondrial manganese superoxide dismutase (MnSOD) converts superoxide anion into H(2)O(2), which is neutralized sequentially by either catalase (CAT) or glutathione peroxidase 1 (Gpx 1) into water or converted into highly reactive hypochlorous acid by myeloperoxidase (MPO).	h(2)	96-100	superoxide dismutase 2	Homo sapiens	58-63
22130631-1	2012	BACKGROUND: Mitochondrial manganese superoxide dismutase (MnSOD) converts superoxide anion into H(2)O(2), which is neutralized sequentially by either catalase (CAT) or glutathione peroxidase 1 (Gpx 1) into water or converted into highly reactive hypochlorous acid by myeloperoxidase (MPO).	Water	206-211	superoxide dismutase 2	Homo sapiens	26-56
22130631-1	2012	BACKGROUND: Mitochondrial manganese superoxide dismutase (MnSOD) converts superoxide anion into H(2)O(2), which is neutralized sequentially by either catalase (CAT) or glutathione peroxidase 1 (Gpx 1) into water or converted into highly reactive hypochlorous acid by myeloperoxidase (MPO).	Water	206-211	superoxide dismutase 2	Homo sapiens	58-63
22130631-1	2012	BACKGROUND: Mitochondrial manganese superoxide dismutase (MnSOD) converts superoxide anion into H(2)O(2), which is neutralized sequentially by either catalase (CAT) or glutathione peroxidase 1 (Gpx 1) into water or converted into highly reactive hypochlorous acid by myeloperoxidase (MPO).	Hypochlorous Acid	246-263	superoxide dismutase 2	Homo sapiens	26-56
22130631-1	2012	BACKGROUND: Mitochondrial manganese superoxide dismutase (MnSOD) converts superoxide anion into H(2)O(2), which is neutralized sequentially by either catalase (CAT) or glutathione peroxidase 1 (Gpx 1) into water or converted into highly reactive hypochlorous acid by myeloperoxidase (MPO).	Hypochlorous Acid	246-263	superoxide dismutase 2	Homo sapiens	58-63
22108091-4	2012	Telomerase overexpression also considerably diminished TNF-alpha-induced transcription of SOD2 Superoxide Dismutase 2 gene by reducing ROS contribution to SOD2 gene induction, both in normal fibroblasts and in cancer cells.	Reactive Oxygen Species	135-138	superoxide dismutase 2	Homo sapiens	155-159
22119635-0	2012	Superoxide dismutase 2 Val16Ala polymorphism is a risk factor for the valproic acid-related elevation of serum aminotransferases.	Valproic Acid	70-83	superoxide dismutase 2	Homo sapiens	0-22
22119635-1	2012	The association between the superoxide dismutase 2 (SOD2) Val16Ala polymorphism and the serum aminotransferase levels was retrospectively investigated in 207 valproic acid-treated patients with epilepsy.	Valproic Acid	158-171	superoxide dismutase 2	Homo sapiens	28-50
22119635-4	2012	The SOD2 Val/Val genotype may therefore contribute to a valproic acid-induced elevation in the serum aminotransferase levels.	Valproic Acid	56-69	superoxide dismutase 2	Homo sapiens	4-8
23109835-4	2012	Here, we discuss how Damaged DNA binding Protein-2 (DDB2), a nucleotide excision repair protein, plays an important role in ROS regulation by epigenetically repressing the antioxidant genes MnSOD and Catalase.	Reactive Oxygen Species	124-127	superoxide dismutase 2	Homo sapiens	190-195
22206979-7	2012	Moreover, linear regression analysis showed that individuals carrying the PON1 Arg192Glu (rs662) or SOD2 Val16Ala (rs4880) variants have significantly higher levels of sperm DNA fragmentation and 8-OHdG.	8-ohdg	196-202	superoxide dismutase 2	Homo sapiens	100-104
21384152-0	2012	MnSOD activity regulates hydroxytyrosol-induced extension of chronological lifespan.	3,4-dihydroxyphenylethanol	25-39	superoxide dismutase 2	Homo sapiens	0-5
21384152-9	2012	Results from spectroscopy assays indicate that HT in the presence of peroxidases can undergo catechol-semiquinone-quinone redox cycling generating superoxide, which in a cellular context can activate the antioxidant system, e.g., MnSOD expression.	catechol-semiquinone	93-113	superoxide dismutase 2	Homo sapiens	230-235
21384152-9	2012	Results from spectroscopy assays indicate that HT in the presence of peroxidases can undergo catechol-semiquinone-quinone redox cycling generating superoxide, which in a cellular context can activate the antioxidant system, e.g., MnSOD expression.	quinone	106-113	superoxide dismutase 2	Homo sapiens	230-235
21384152-9	2012	Results from spectroscopy assays indicate that HT in the presence of peroxidases can undergo catechol-semiquinone-quinone redox cycling generating superoxide, which in a cellular context can activate the antioxidant system, e.g., MnSOD expression.	Superoxides	147-157	superoxide dismutase 2	Homo sapiens	230-235
22938422-8	2012	A similar tendency was noted for TBRS.We suggested that elevated total SOD might reflect a response to oxidative stress, and then may predict a state of excess reactive oxygen species in the carcinogenesis process.	tbrs	33-37	superoxide dismutase 2	Homo sapiens	71-74
22938422-8	2012	A similar tendency was noted for TBRS.We suggested that elevated total SOD might reflect a response to oxidative stress, and then may predict a state of excess reactive oxygen species in the carcinogenesis process.	Reactive Oxygen Species	160-183	superoxide dismutase 2	Homo sapiens	71-74
22078782-11	2012	Moreover, DHT enhanced FOXO1 expression in parallel with increased SOD2 protein but not with SOD1.	Dihydrotestosterone	10-13	superoxide dismutase 2	Homo sapiens	67-71
21559822-6	2012	The GW583340-resistant IBC cells displayed increased SOD1, SOD2, and glutathione expression, which correlated with decreased sensitivity to the apoptotic-inducing effects of GW583340, H(2)O(2), and paraquat.	GW 583340	4-12	superoxide dismutase 2	Homo sapiens	59-63
22330623-5	2012	RESULTS: The highest triglyceride level was observed in patients with MnSOD Val/Val genotype.	Triglycerides	21-33	superoxide dismutase 2	Homo sapiens	70-75
22139847-2	2012	The presence of p38alpha increases basal and H(2)O(2)-induced expression of the antioxidant enzymes: superoxide-dismutase 1 (SOD-1), SOD-2, and catalase through different mechanisms, which protects from reactive oxygen species (ROS) accumulation and prevents cell death.	Hydrogen Peroxide	45-53	superoxide dismutase 2	Homo sapiens	133-138
21351093-11	2012	Patients carrying the high activity Ala/Ala genotype in SOD2 (rs4880) had significantly poorer PFS than Val allele carriers in the group treated by cyclophosphamide but not hormonal regimens (p = 0.004).	Alanine	36-39	superoxide dismutase 2	Homo sapiens	56-60
21351093-11	2012	Patients carrying the high activity Ala/Ala genotype in SOD2 (rs4880) had significantly poorer PFS than Val allele carriers in the group treated by cyclophosphamide but not hormonal regimens (p = 0.004).	Alanine	40-43	superoxide dismutase 2	Homo sapiens	56-60
21351093-11	2012	Patients carrying the high activity Ala/Ala genotype in SOD2 (rs4880) had significantly poorer PFS than Val allele carriers in the group treated by cyclophosphamide but not hormonal regimens (p = 0.004).	Valine	104-107	superoxide dismutase 2	Homo sapiens	56-60
21351093-11	2012	Patients carrying the high activity Ala/Ala genotype in SOD2 (rs4880) had significantly poorer PFS than Val allele carriers in the group treated by cyclophosphamide but not hormonal regimens (p = 0.004).	Cyclophosphamide	148-164	superoxide dismutase 2	Homo sapiens	56-60
23080136-4	2012	Loss of HIF-2 activity leads to decreased transcription of the Sod2 gene, encoding manganese superoxide dismutase, which converts superoxide to hydrogen peroxide.	Superoxides	93-103	superoxide dismutase 2	Homo sapiens	63-67
23080136-4	2012	Loss of HIF-2 activity leads to decreased transcription of the Sod2 gene, encoding manganese superoxide dismutase, which converts superoxide to hydrogen peroxide.	Hydrogen Peroxide	144-161	superoxide dismutase 2	Homo sapiens	63-67
22994704-3	2012	We previously determined that changes in MnSOD expression had bidirectional effects on adriamycin (ADR) when combined with nitric oxide (NO).	Doxorubicin	87-97	superoxide dismutase 2	Homo sapiens	41-46
21553226-8	2012	Ala/Ala genotype of MnSOD polymorphism may have an effect on adverse features of PCa such as high stage disease.	Alanine	0-3	superoxide dismutase 2	Homo sapiens	20-25
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	99-115	superoxide dismutase 2	Homo sapiens	28-32
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	117-120	superoxide dismutase 2	Homo sapiens	28-32
21741706-5	2012	SOD2 rs4880 V16A polymorphism was associated with significantly less CPA-related overall toxicity and significantly lower relapse rates by Kaplan-Meier analysis although the SOD2 finding regarding relapse was not significant when evaluated by the cumulative incidence function.	Cyclophosphamide	69-72	superoxide dismutase 2	Homo sapiens	0-4
22057568-6	2012	Superoxide dismutase (MnSOD, SOD2) from the mitochondrial matrix as well as superoxide dismutase (Cu/ZnSOD, SOD1) present in small amounts in the mitochondrial intramembrane space, convert superoxide anion to hydrogen peroxide, which can be then converted by catalase to harmless H(2)O.	Superoxides	189-205	superoxide dismutase 2	Homo sapiens	22-27
22057568-6	2012	Superoxide dismutase (MnSOD, SOD2) from the mitochondrial matrix as well as superoxide dismutase (Cu/ZnSOD, SOD1) present in small amounts in the mitochondrial intramembrane space, convert superoxide anion to hydrogen peroxide, which can be then converted by catalase to harmless H(2)O.	Superoxides	189-205	superoxide dismutase 2	Homo sapiens	29-33
22057568-6	2012	Superoxide dismutase (MnSOD, SOD2) from the mitochondrial matrix as well as superoxide dismutase (Cu/ZnSOD, SOD1) present in small amounts in the mitochondrial intramembrane space, convert superoxide anion to hydrogen peroxide, which can be then converted by catalase to harmless H(2)O.	Hydrogen Peroxide	209-226	superoxide dismutase 2	Homo sapiens	22-27
22302046-5	2012	The levels of gammaH2AX significantly decreased in HeLa S3/SOD2 and T-REx HeLa/SOD2 cells compared with those in the control cells.	gammah2ax	14-23	superoxide dismutase 2	Homo sapiens	59-63
22302046-5	2012	The levels of gammaH2AX significantly decreased in HeLa S3/SOD2 and T-REx HeLa/SOD2 cells compared with those in the control cells.	gammah2ax	14-23	superoxide dismutase 2	Homo sapiens	79-83
22302046-6	2012	MitoSox(TM) Red assays showed that both lines of SOD2-expressing cells showed suppression of the superoxide generation in mitochondria.	Superoxides	97-107	superoxide dismutase 2	Homo sapiens	49-53
22302046-7	2012	Furthermore, flow cytometry with a fluorescent probe (2",7"-dichlorofluorescein) revealed that the cellular levels of ROS increased in HeLa S3 cells during post-irradiation incubation, but the increase was markedly attenuated in HeLa S3/SOD2 cells.	2',7'-dichlorofluorescein	54-79	superoxide dismutase 2	Homo sapiens	237-241
22302046-7	2012	Furthermore, flow cytometry with a fluorescent probe (2",7"-dichlorofluorescein) revealed that the cellular levels of ROS increased in HeLa S3 cells during post-irradiation incubation, but the increase was markedly attenuated in HeLa S3/SOD2 cells.	Reactive Oxygen Species	118-121	superoxide dismutase 2	Homo sapiens	237-241
22302046-10	2012	These results indicate that SOD2 protects HeLa cells against cellular effects of gamma-rays through suppressing oxidative stress in irradiated cells caused by ROS generated in the mitochondria and through regulating the expression of genes which play a critical role in protection against ionizing radiation.	Reactive Oxygen Species	159-162	superoxide dismutase 2	Homo sapiens	28-32
21553226-0	2012	Increased risk of advanced prostate cancer associated with MnSOD Ala-9-Val gene polymorphism.	ala-9-val	65-74	superoxide dismutase 2	Homo sapiens	59-64
21553226-2	2012	MnSOD Ala-9-Val gene polymorphism was carried out in 134 (mean age 64.1+-7.48) PCa patients and 159 (mean age 62.5+-7.53) healthy controls with serum prostate specific antigen (PSA) levels (&lt;4 ng/ml) and normal digital rectal examination (DRE) findings in this prospectively designed study.	ala-9-val	6-15	superoxide dismutase 2	Homo sapiens	0-5
21553226-8	2012	Ala/Ala genotype of MnSOD polymorphism may have an effect on adverse features of PCa such as high stage disease.	Alanine	4-7	superoxide dismutase 2	Homo sapiens	20-25
22973466-5	2012	Among genes required for the control of oxidative stress, only the expression patterns of sod-2 and sod-3 genes encoding Mn-SODs in animals exposed to small sizes TiO2-NPs were significantly different from those in animals exposed to large sizes of TiO2-NPs.	titanium dioxide	163-167	superoxide dismutase 2	Homo sapiens	90-95
20674094-7	2012	Al-treated flies accumulated large amount of iron and reactive oxygen species (ROS), and exhibited elevated SOD2 activity.	Aluminum	0-2	superoxide dismutase 2	Homo sapiens	108-112
22172488-5	2012	Treatment with Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl), a SOD mimetic, not only lowered cellular superoxide levels but also concomitantly attenuated AR transcriptional activity and AR target gene expression in a dose- and time-dependent manner, in the presence and absence of dihydrotestosterone, the major endogenous AR agonist.	tempol	15-21	superoxide dismutase 2	Homo sapiens	74-77
22172488-5	2012	Treatment with Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl), a SOD mimetic, not only lowered cellular superoxide levels but also concomitantly attenuated AR transcriptional activity and AR target gene expression in a dose- and time-dependent manner, in the presence and absence of dihydrotestosterone, the major endogenous AR agonist.	tempol	23-69	superoxide dismutase 2	Homo sapiens	74-77
22172488-5	2012	Treatment with Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl), a SOD mimetic, not only lowered cellular superoxide levels but also concomitantly attenuated AR transcriptional activity and AR target gene expression in a dose- and time-dependent manner, in the presence and absence of dihydrotestosterone, the major endogenous AR agonist.	Superoxides	113-123	superoxide dismutase 2	Homo sapiens	74-77
22172488-5	2012	Treatment with Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl), a SOD mimetic, not only lowered cellular superoxide levels but also concomitantly attenuated AR transcriptional activity and AR target gene expression in a dose- and time-dependent manner, in the presence and absence of dihydrotestosterone, the major endogenous AR agonist.	Dihydrotestosterone	292-311	superoxide dismutase 2	Homo sapiens	74-77
23056314-7	2012	VASH1 increased the expression of (superoxide dismutase 2) SOD2, an enzyme known to quench reactive oxygen species (ROS).	Reactive Oxygen Species	91-114	superoxide dismutase 2	Homo sapiens	59-63
23056314-7	2012	VASH1 increased the expression of (superoxide dismutase 2) SOD2, an enzyme known to quench reactive oxygen species (ROS).	Reactive Oxygen Species	116-119	superoxide dismutase 2	Homo sapiens	59-63
22973466-5	2012	Among genes required for the control of oxidative stress, only the expression patterns of sod-2 and sod-3 genes encoding Mn-SODs in animals exposed to small sizes TiO2-NPs were significantly different from those in animals exposed to large sizes of TiO2-NPs.	titanium dioxide	249-253	superoxide dismutase 2	Homo sapiens	90-95
22973466-6	2012	sod-2 and sod-3 gene expressions were closely correlated with lethality, growth, reproduction, locomotion behavior, intestinal autofluorescence, and ROS production in TiO2-NPs-exposed animals.	Reactive Oxygen Species	149-152	superoxide dismutase 2	Homo sapiens	0-5
22973466-6	2012	sod-2 and sod-3 gene expressions were closely correlated with lethality, growth, reproduction, locomotion behavior, intestinal autofluorescence, and ROS production in TiO2-NPs-exposed animals.	titanium dioxide	167-171	superoxide dismutase 2	Homo sapiens	0-5
22859959-12	2012	In addition, we present evidence for increased LDHA and SOD2 expression in SDHB-PHEOs/PGLs, proteins that have been proposed as promising therapeutic targets in other cancers.	pheos	80-85	superoxide dismutase 2	Homo sapiens	56-60
22077216-1	2011	Human MnSOD is significantly more product-inhibited than bacterial MnSODs at high concentrations of superoxide (O(2)(-)).	Superoxides	100-110	superoxide dismutase 2	Homo sapiens	6-11
22077216-1	2011	Human MnSOD is significantly more product-inhibited than bacterial MnSODs at high concentrations of superoxide (O(2)(-)).	Superoxides	112-116	superoxide dismutase 2	Homo sapiens	6-11
22077216-10	2011	Our studies on yeast MnSODs indicate the unique nature of human MnSOD in that it predominantly undergoes the inhibited pathway at high [O(2)(-)].	Superoxides	136-140	superoxide dismutase 2	Homo sapiens	21-26
21960467-1	2011	We used two theoretical methods to estimate reduction potentials and acidity constants in Mn superoxide dismutase (MnSOD), namely combined quantum mechanical and molecular mechanics (QM/MM) thermodynamic cycle perturbation (QTCP) and the QM/MM-PBSA approach.	qtcp	224-228	superoxide dismutase 2	Homo sapiens	115-120
21960467-1	2011	We used two theoretical methods to estimate reduction potentials and acidity constants in Mn superoxide dismutase (MnSOD), namely combined quantum mechanical and molecular mechanics (QM/MM) thermodynamic cycle perturbation (QTCP) and the QM/MM-PBSA approach.	poly(tetramethylene succinate-co-tetramethylene adipate)	244-248	superoxide dismutase 2	Homo sapiens	90-113
21960467-1	2011	We used two theoretical methods to estimate reduction potentials and acidity constants in Mn superoxide dismutase (MnSOD), namely combined quantum mechanical and molecular mechanics (QM/MM) thermodynamic cycle perturbation (QTCP) and the QM/MM-PBSA approach.	poly(tetramethylene succinate-co-tetramethylene adipate)	244-248	superoxide dismutase 2	Homo sapiens	115-120
21960467-3	2011	We show that using the QTCP method, we can obtain accurate and precise estimates of the proton-coupled reduction potential for MnSOD, 0.30+-0.01 V, which compares favourably with experimental estimates of 0.26-0.40 V. However, the calculated potentials depend strongly on the DFT functional used: The B3LYP functional gives 0.6 V more positive potentials than the PBE functional.	qtcp	23-27	superoxide dismutase 2	Homo sapiens	127-132
21956414-6	2011	SDHx mutation analysis occurred in those without PTEN mutations/variations and elevated manganese superoxide dismutase (MnSOD) levels.	sdhx	0-4	superoxide dismutase 2	Homo sapiens	88-118
21671088-0	2011	Manganese regulates manganese-containing superoxide dismutase (MnSOD) expression in the primary broiler myocardial cells.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	20-61
21671088-0	2011	Manganese regulates manganese-containing superoxide dismutase (MnSOD) expression in the primary broiler myocardial cells.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	63-68
21671088-1	2011	Previous studies showed that dietary manganese can increase the MnSOD mRNA expression in a dose-dependent manner in the heart of broilers.	Manganese	37-46	superoxide dismutase 2	Homo sapiens	64-69
21671088-2	2011	In order to explore the specific mechanism of the MnSOD expression induced by manganese, a model of MnSOD expression was developed with primary cultured broiler myocardial cells.	Manganese	78-87	superoxide dismutase 2	Homo sapiens	50-55
21671088-6	2011	The results showed that MnSOD mRNA, MnSOD protein, and MnSOD activity were induced by manganese in dose- and time-dependent manner.	Manganese	86-95	superoxide dismutase 2	Homo sapiens	24-29
21671088-6	2011	The results showed that MnSOD mRNA, MnSOD protein, and MnSOD activity were induced by manganese in dose- and time-dependent manner.	Manganese	86-95	superoxide dismutase 2	Homo sapiens	36-41
21671088-6	2011	The results showed that MnSOD mRNA, MnSOD protein, and MnSOD activity were induced by manganese in dose- and time-dependent manner.	Manganese	86-95	superoxide dismutase 2	Homo sapiens	36-41
21671088-7	2011	Manganese regulates MnSOD expression not only at transcriptional level but also at translational and/or posttranslational levels.	Manganese	0-9	superoxide dismutase 2	Homo sapiens	20-25
21833471-7	2011	It was found that the cell line, called Tumor2 with down-regulation of basal ROS and manganese superoxide dismutase (MnSOD) expression as a constitutive pattern of this cell line, presented alterations in genes that confer metastatic potential in comparison to the Alpha5 cell line, showing overexpression of basal MnSOD and high levels of ROS.	Reactive Oxygen Species	340-343	superoxide dismutase 2	Homo sapiens	117-122
21833471-8	2011	Interesting, it was to found that CD44, considered a metastatic suppressor gene, was influenced by ROS, measured by hydrogen peroxide treatments, as seen by decreased CD44 protein expression in the Alpha5 cell line in a compensatory response to increased MnSOD protein expression.	Reactive Oxygen Species	99-102	superoxide dismutase 2	Homo sapiens	255-260
21833471-8	2011	Interesting, it was to found that CD44, considered a metastatic suppressor gene, was influenced by ROS, measured by hydrogen peroxide treatments, as seen by decreased CD44 protein expression in the Alpha5 cell line in a compensatory response to increased MnSOD protein expression.	Hydrogen Peroxide	116-133	superoxide dismutase 2	Homo sapiens	255-260
21956414-6	2011	SDHx mutation analysis occurred in those without PTEN mutations/variations and elevated manganese superoxide dismutase (MnSOD) levels.	sdhx	0-4	superoxide dismutase 2	Homo sapiens	120-125
20638682-0	2011	The resistance of esophageal adenocarcinoma to bile salt insult is associated with manganese superoxide dismutase expression.	Bile Acids and Salts	47-56	superoxide dismutase 2	Homo sapiens	83-113
20638682-12	2011	Exposure of ESC cells to bile salt increased MnSOD expression.	Bile Acids and Salts	25-34	superoxide dismutase 2	Homo sapiens	45-50
21855229-10	2011	If the superoxide production is not effectively controlled by mitochondrial superoxide dismutase (Mn-SOD), then superoxide leads to OxS and lipid peroxidation.	Superoxides	7-17	superoxide dismutase 2	Homo sapiens	62-96
21899432-1	2011	Gene therapy-mediated overexpression of superoxide dismutases (SOD) appears to be a promising strategy for modulating radiosensitivity based on detoxification of superoxide radicals and suppression of apoptosis.	Superoxides	162-181	superoxide dismutase 2	Homo sapiens	63-66
21899432-5	2011	A six- to eightfold increase in SOD activity was observed after transduction, rendering MnSOD-overexpressing TK6 cells significantly more resistant to paraquat-induced superoxide radical production than controls.	Paraquat	151-159	superoxide dismutase 2	Homo sapiens	32-35
21899432-5	2011	A six- to eightfold increase in SOD activity was observed after transduction, rendering MnSOD-overexpressing TK6 cells significantly more resistant to paraquat-induced superoxide radical production than controls.	Paraquat	151-159	superoxide dismutase 2	Homo sapiens	88-93
21899432-5	2011	A six- to eightfold increase in SOD activity was observed after transduction, rendering MnSOD-overexpressing TK6 cells significantly more resistant to paraquat-induced superoxide radical production than controls.	Superoxides	168-186	superoxide dismutase 2	Homo sapiens	32-35
21899432-5	2011	A six- to eightfold increase in SOD activity was observed after transduction, rendering MnSOD-overexpressing TK6 cells significantly more resistant to paraquat-induced superoxide radical production than controls.	Superoxides	168-186	superoxide dismutase 2	Homo sapiens	88-93
22009531-6	2011	Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	12-16	superoxide dismutase 2	Homo sapiens	53-58
22009531-6	2011	Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	12-16	superoxide dismutase 2	Homo sapiens	121-126
22009531-6	2011	Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas.	Tetradecanoylphorbol Acetate	21-24	superoxide dismutase 2	Homo sapiens	53-58
22009531-6	2011	Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas.	Tetradecanoylphorbol Acetate	21-24	superoxide dismutase 2	Homo sapiens	121-126
21940907-11	2011	CONCLUSIONS AND IMPACT: Previously unreported associations of SNPs in ALDH2, CYP2E1, GPX2, SOD1, and SOD2 with SCCHN and subsite tumors provide evidence that alterations in alcohol and oxidative stress pathways influence SCCHN carcinogenesis and warrant further investigation.	Alcohols	173-180	superoxide dismutase 2	Homo sapiens	101-105
21855229-10	2011	If the superoxide production is not effectively controlled by mitochondrial superoxide dismutase (Mn-SOD), then superoxide leads to OxS and lipid peroxidation.	Superoxides	7-17	superoxide dismutase 2	Homo sapiens	98-104
21855229-10	2011	If the superoxide production is not effectively controlled by mitochondrial superoxide dismutase (Mn-SOD), then superoxide leads to OxS and lipid peroxidation.	Superoxides	76-86	superoxide dismutase 2	Homo sapiens	98-104
21749277-0	2011	Hydrogen peroxide contributes to the manganese superoxide dismutase promotion of migration and invasion in glioma cells.	Hydrogen Peroxide	0-17	superoxide dismutase 2	Homo sapiens	37-67
21982398-11	2011	Exploratory analyses of variations in OGG1 and MnSOD genes indicate that hypotheses about patterns of exposure to selenium and smoking combined with data on genetic variation in genes involved in DNA repair can be valuable to pursue.	Selenium	114-122	superoxide dismutase 2	Homo sapiens	47-52
21749277-7	2011	Collectively, our study indicated that H(2)O(2) would contribute to the MnSOD-promoted migration/invasion in glioma cells through activation of AKTs and ERKs.	Hydrogen Peroxide	39-47	superoxide dismutase 2	Homo sapiens	72-77
21640155-3	2011	In mitochondria, the manganese superoxide dismutase (MnSOD) is a scavenger of reactive oxygen species, and the 8-oxoguanine DNA glycosylase (OGG1) is the major DNA glycosylase for the repair of 8-oxoG lesions.	Reactive Oxygen Species	78-101	superoxide dismutase 2	Homo sapiens	21-51
21750867-6	2011	Curcumin enhanced manganese superoxide dismutase (MnSOD) protein expression in the MCF-10F and Alpha3 cell lines.	Curcumin	0-8	superoxide dismutase 2	Homo sapiens	18-48
21750867-6	2011	Curcumin enhanced manganese superoxide dismutase (MnSOD) protein expression in the MCF-10F and Alpha3 cell lines.	Curcumin	0-8	superoxide dismutase 2	Homo sapiens	50-55
20712406-4	2011	p53 orchestrates mitochondrial redox signaling by the coordinated control of at least two key effectors: the superoxide scavenger MnSOD, and the ROS generator p66shc.	Superoxides	109-119	superoxide dismutase 2	Homo sapiens	130-135
21640155-3	2011	In mitochondria, the manganese superoxide dismutase (MnSOD) is a scavenger of reactive oxygen species, and the 8-oxoguanine DNA glycosylase (OGG1) is the major DNA glycosylase for the repair of 8-oxoG lesions.	Reactive Oxygen Species	78-101	superoxide dismutase 2	Homo sapiens	53-58
21262583-5	2011	Moreover, we observed reactive oxygen species evoked damage to mitochondrial proteins and reduced MnSOD levels.	Reactive Oxygen Species	22-45	superoxide dismutase 2	Homo sapiens	98-103
21536589-6	2011	In response to oxidative stress, LCs from SCA3 patients show a specific impairment to upregulate SOD2 expression in correlation with a significantly increased formation of reactive oxygen species and cytotoxicity.	oxygen species	181-195	superoxide dismutase 2	Homo sapiens	97-101
21705328-0	2011	Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively.	Tetradecanoylphorbol Acetate	43-79	superoxide dismutase 2	Homo sapiens	94-124
21705328-0	2011	Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively.	Tetradecanoylphorbol Acetate	43-79	superoxide dismutase 2	Homo sapiens	126-131
21705328-0	2011	Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively.	Tetradecanoylphorbol Acetate	81-84	superoxide dismutase 2	Homo sapiens	94-124
21705328-0	2011	Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively.	Tetradecanoylphorbol Acetate	81-84	superoxide dismutase 2	Homo sapiens	126-131
21705328-1	2011	12-O-tetradecanoylphorbol-13-acetate (TPA) has been shown to induce transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA in human lung carcinoma cells, A549, mediated by a protein kinase C (PKC)-dependent activation of cAMP-responsive element-binding protein (CREB)-1/ATF-1-like factors.	Tetradecanoylphorbol Acetate	0-36	superoxide dismutase 2	Homo sapiens	104-134
21705328-1	2011	12-O-tetradecanoylphorbol-13-acetate (TPA) has been shown to induce transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA in human lung carcinoma cells, A549, mediated by a protein kinase C (PKC)-dependent activation of cAMP-responsive element-binding protein (CREB)-1/ATF-1-like factors.	Tetradecanoylphorbol Acetate	0-36	superoxide dismutase 2	Homo sapiens	136-141
21705328-1	2011	12-O-tetradecanoylphorbol-13-acetate (TPA) has been shown to induce transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA in human lung carcinoma cells, A549, mediated by a protein kinase C (PKC)-dependent activation of cAMP-responsive element-binding protein (CREB)-1/ATF-1-like factors.	Tetradecanoylphorbol Acetate	38-41	superoxide dismutase 2	Homo sapiens	104-134
21705328-1	2011	12-O-tetradecanoylphorbol-13-acetate (TPA) has been shown to induce transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA in human lung carcinoma cells, A549, mediated by a protein kinase C (PKC)-dependent activation of cAMP-responsive element-binding protein (CREB)-1/ATF-1-like factors.	Tetradecanoylphorbol Acetate	38-41	superoxide dismutase 2	Homo sapiens	136-141
21705328-2	2011	In this study, we showed that MnSOD protein expression was elevated in response to TPA or TNF-alpha, but not to hydrogen peroxide treatment.	Tetradecanoylphorbol Acetate	83-86	superoxide dismutase 2	Homo sapiens	30-35
21705328-4	2011	Small interfering RNA (siRNA) experiments indicated that knocking down the NADPH oxidase components e.g. Rac1, p22(phox), p67(phox), and NOXO1 in A549 cells impaired TPA-induced MnSOD expression.	Tetradecanoylphorbol Acetate	166-169	superoxide dismutase 2	Homo sapiens	178-183
21705328-5	2011	To identify the PKC isozyme involved, we used a sod2 gene response reporter plasmid, pSODLUC-3340-I2E-C, capable of sensing the effect of TNF-alpha and TPA, to monitor the effects of PKC isozyme-specific inhibitors and siRNA-induced knockdown of specific PKC isozyme.	Tetradecanoylphorbol Acetate	152-155	superoxide dismutase 2	Homo sapiens	48-52
21705328-6	2011	Our data indicate that TPA-induced MnSOD expression was independent of p53 and most likely mediated by PKC-alpha-, and -epsilon-dependent signaling pathways.	Tetradecanoylphorbol Acetate	23-26	superoxide dismutase 2	Homo sapiens	35-40
21705328-7	2011	Furthermore, siRNA-induced knock-down of CREB and Forkhead box class O (FOXO) 3a led to a reduction in TPA-induced MnSOD gene expression.	Tetradecanoylphorbol Acetate	103-106	superoxide dismutase 2	Homo sapiens	115-120
21705328-8	2011	Together, our results revealed that TPA up-regulates, in part, two PKC-dependent transcriptional pathways to induce MnSOD expression.	Tetradecanoylphorbol Acetate	36-39	superoxide dismutase 2	Homo sapiens	116-121