Publication for Sod1 and Park7

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Sod1	superoxide dismutase 1, soluble	20655			[link]
mmu	Park7	Parkinson disease (autosomal recessive, early onset) 7	57320

Pubmed ID	Priority	Text
25822630	0.98	SOD1 transgenic mice, there are significant changes in DJ-1 expression and in its acidic isoforms.
	0.98	SOD1 and SOD1 DJ-1 KO mice showed significantly increased astrogliosis in the lumbar spinal cord.
	0.98	SOD1 mice compared to WT and DJ-1 KO mice (Fig. 7A, B).
	0.98	DJ-1 expression levels and oxidized isoforms in brains and spinal cords of SOD1 transgenic mice.
	0.98	DJ-1 acidic isoforms in diseased mice, indicating the presence of oxidized forms of DJ-1 in the CNS of SOD1 mice.
	0.97	DJ-1 KO mice, the levels of HO-1 in SOD1 DJ-1-KO mice is elevated since as in SOD1 mice, the oxidative and inflammatory insults are greater in ALS mice.
	0.97	DJ-1 resulted in an increase in cell viability and a reduction in cell toxicity in mutant SOD1-transfected neuronal cell lines.
	0.97	DJ-1 in the CNS of young SOD1 mice offers protection aimed to counteract the ongoing detrimental disease process, since a more severe and aggressive disease process was observed in DJ-1 knockout mice.
	0.96	DJ-1 is needed for activation of the defensive Nrf2 system, lack of DJ-1 in SOD1 DJ-1 KO mice resulted in a blunted response and increased their vulnerability to the disease process and led to augmented clinical deterioration.
	0.96	SOD1 formed complexes with DJ-1 in the cell lysates.
	0.96	DJ-1 function augmented the impairment of Nrf2 system activation and that the double transgenic SOD1 DJ-1 KO mice showed decreased spinal Nrf2 and HO-1 expression levels as compared to SOD1 mice.
	0.95	SOD1 DJ-1 KO as compared to SOD1 mice.
	0.95	SOD1 DJ-1 KO decreased compared to those of SOD1 mice at the early symptomatic stage (day 90, Fig. 6A).
	0.94	DJ-1, as in the double transgenic DJ-1 KO SOD1 mice, resulted in accelerated damage to the CNS, an accelerated disease course and shortened survival time.
	0.93	SOD1 and SOD1 DJ-1 KO mice there is elevation of HO-1 levels, yet in SOD1 DJ-1 KO mice the elevation is more modest (Fig. 7B).
	0.93	SOD1 and SOD1 DJ-1 KO mice as compared to WT or DJ-1 KO mice (to 45+-2.6% and 52+-5%, respectively).
	0.93	DJ-1 accelerates disease, augments disease severity and shortens survival of SOD1 mice, an animal model of ALS.
	0.89	SOD1 increased the expression of Nrf2 and HO-1 while SOD1 DJ-1 KO demonstrated reduction.
	0.89	SOD1 DJ-1 KO and SOD1 mice as compared to WT and to DJ-1 KO mice (53%+-12.9 vs. 36.5%+-11.31 of WT numbers, respectively.
	0.82	SOD1 DJ-1 KO- mice lost weight significantly earlier and faster than the SOD1 mice, in both the male and female groups (Fig. 1A, B).
	0.81	SOD1 DJ-1 KO mice demonstrated an accelerated disease course.
	0.81	SOD1 model of the disease These results imply that DJ-1 is a possible therapeutic target in ALS(at least with mutated SOD1) and encourage further research on the mechanisms involved in the neuroprotective properties of DJ-1 in this devastating disease.
	0.71	SOD1 DJ-1 KO mice demonstrated earlier motor deterioration as compared to SOD1 mice.
	0.71	SOD1 DJ-1 KO
	0.70	SOD1 DJ-1 KO mice had augmented loss of motor neurons as compared to SOD1 mice (p<0.001.
	0.63	SOD1 DJ-1 KO
	0.62	SOD1 DJ-1 KO mice showed reduced survival
	0.61	SOD1 DJ-1 KO mice demonstrated significantly reduced survival compared to SOD1 mice (Fig. 4).
	0.55	SOD1 DJ-1 KO mice demonstrated shortened survival.
28442712	0.98	DJ-1, which also acts as a copper chaperone, enhancing cytosolic superoxide dismutase-1 (SOD1) function.
	0.98	DJ-1 has been demonstrated to act as a Cu(II) chaperone, which has been directly associated with an increase in its association with SOD1 and its enzyme activity.
	0.98	DJ-1 is not only involved in the induction of Nrf2-regulated antioxidant enzymes, but can also enhance SOD1 association with DJ-1 following acute Cu(II)ATSM treatment.
	0.98	SOD1 activity through DJ-1 association and antioxidant enzyme expression via DJ-1/Nrf2 signaling.
	0.98	SOD1 and DJ-1, we also observed a 2-fold increase in SOD1 activity (Fig. 6E), providing further evidence that acute Cu(II)ATSM activates SOD1 activity, thereby acutely reducing superoxide generation.
	0.98	DJ-1 has been shown to directly regulate SOD1 activity.
	0.98	SOD1 activity in the brain, but to date, only experiments without the use of cells have established that copper enriched DJ-1 directly increases SOD1 activity.
	0.97	DJ-1 with superoxide dismutase-1 (SOD1), paralleled by significant increases in intracellular Cu(II) levels and SOD1 activity.
	0.97	DJ-1 with SOD1 and increasing SOD1 activity, Cu(II)ATSM may confer cardiovascular protection through activation of antioxidant defenses mediated by the Nrf2/DJ-1 axis.
	0.97	DJ-1 may mediate both SOD1 and Nrf2 activation.
	0.97	DJ-1 and SOD1 suggests that DJ-1 was enriched with Cu(II) through an increase in intracellular Cu(II) levels.
	0.97	DJ-1 and SOD1 protein interactions in HCASMC treated with Cu(II)ATSM, providing a possible mechanism by which SOD1 activity may be increased acutely.
	0.96	DJ-1 with SOD1 and intracellular Cu(II) levels
	0.96	DJ-1 with SOD1, intracellular Cu(II) levels and SOD activity in HCASMC.
	0.96	DJ-1 with SOD1 (Fig. 6A).
	0.92	DJ-1 with SOD1 in HCASMC.
31487745	0.98	DJ-1 can regulate Sod1 expression through the ERK1/2-ELK1 pathways, and that there is an upregulation of DJ-1 protein levels in mutant Sod1 transgenic mice.
	0.97	superoxide dismutase 1 (Sod1), DJ-1 (Park-7), and Parkin (Prkn) (triple knock out, TKO) would have an increased level of chronic oxidative stress in the retina, with anatomic and functional consequences just with aging.
	0.97	superoxide dismutase 1 (Sod1 gene), Parkin (Prkn or Park2 gene), and DJ-1 (Park7 gene).
	0.97	DJ-1 forms complexes with mutant Sod1 molecules and reduces the toxicity of the latter to tissues.
	0.97	Sod1/DJ-1/Parkin (here referred to as Sod1/Park7/Prkn) TKO mice have increased susceptibility to light-induced retinal damage.
	0.97	Sod1-/-, DJ-1-/-, Parkin-/-) demonstrate increased susceptibility to acute oxidative stress in a light injury model.
	0.97	SOD-1, Parkin, and DJ-1 are multifunctional proteins that play important roles in the oxidative stress response in neurodegenerative diseases, such as amyotrophic lateral sclerosis, Parkinson's disease, and Alzheimer's disease.
	0.97	Sod1, DJ-1 can also compensate for Sod1 when it is mutated, demonstrating the complex interplay between these pathways.
	0.96	Sod1/Park7/Prkn (triple KO [TKO] mice).
	0.96	Sod1/Park7/Prkn TKO mice will demonstrate early development of AMD-like features under normal aging conditions.
	0.93	DJ-1 and Sod1 interact with the Nrf2 pathway.
	0.89	Sod1 KO mice, DJ-1 [Park7] KO mice, and Parkin [Prkn] KO mice) have been shown to develop retinal changes with aging, we wanted to determine if mice simultaneously deficient in all three genes would represent an additional model for oxidative stress-related retinal disease that would add to our current models.
	0.87	Sod1/Park7/Prkn TKO Mice
	0.87	Sod1, Park7, and Prkn (TKO mice) to try to circumvent the compensatory effects of these proteins.
	0.86	Superoxide Dismutase 1 (Sod1), DJ-1 (Park7), and Parkin (Prkn) Develop Spontaneous Retinal Degeneration With Aging
	0.84	Sod1/Park7/Prkn (TKO).
23983902	0.98	DJ-1 and SOD1 are both tightly connected with Nrf2 protein, a transcriptional factor and master regulator of the expression of many antioxidant/detoxification genes.
	0.98	DJ-1 directly protects from PD and activates ERK1/2-ELK1 pathway thus upregulating WT-SOD1 expression.
	0.97	DJ-1 and SOD1: the two proteins interacted in GST pull-down assays and formed complexes that colocalized in mice primary motor neuron culture.
	0.97	DJ-1 and SOD1 are critical in PD and ALS pathogenesis and are also major players in the association between the neurodegenerative process and redox homeostasis.
	0.97	DJ-1 and SOD1 have a remarkable connection with the antioxidant Nrf2/ARE pathway, with DJ-1 being an upstream activator and SOD1 a target.
	0.97	DJ-1 and Nrf2/ARE inhibit the toxicity of mutSOD1 that causes ALS, and vice versa, Nrf2/ARE pathway is inhibited by mutSOD1.
	0.96	DJ-1 mRNA and protein levels in the brains and spinal cords of SOD1-G93A transgenic mice, a widely employed model of ALS.
	0.94	DJ-1 in stably mutSOD1-expressing cells reduced cell toxicity and OS markers as compared to cells expressing control vector protein.
	0.88	DJ-1 and SOD1 proteins, which are involved in PD and ALS and also exert a prominent role in the interaction between redox homeostasis and neurodegeneration.
	0.86	DJ-1 and SOD1 Involvement in Oxidative Stress and Neurodegeneration
	0.84	DJ-1 Modulates MutSOD1 Motor Neuron Degeneration Processes in ALS
	0.83	SOD1 and DJ-1 Converge at Nrf2 Pathway: A Clue for Antioxidant Therapeutic Potential in Neurodegeneration
	0.79	DJ-1 and mutSOD1 in ALS (Figure 1).
	0.63	DJ-1 and SOD1 Proteins
24386432	0.98	DJ-1 -/- SOD1 -/- mice but not Parkin -/- DJ-1 -/- mice or SOD1 -/- mice had significantly increased levels of dopamine in the striatum.
	0.97	DJ-1 -/- SOD1 -/- mice were significantly higher compared to wild type mice (p<0.05).
	0.96	DJ-1-/-SOD1-/- mice indicates functional abnormalities within the nigrostriatal pathway.
	0.96	DJ-1 -/- SOD1 -/- mice were significantly higher compared to wild type mice (p<0.05, Table 1).
	0.95	DJ-1 -/- SOD1 -/- mice either have dopamine autoreceptor signaling defects or that the increased dopamine compensates for other defects in dopaminergic signaling.
	0.94	DJ-1-/-SOD1-/- triple mutant mice had increased striatal dopamine levels and Parkin-/-DJ-1-/- mice showed improved rotarod performance.
	0.94	DJ-1-/-SOD1-/- mice.
	0.94	DJ-1 -/- SOD1 -/- mice compared to wild type mice.
	0.94	DJ-1 -/-, Parkin -/- DJ-1 -/- SOD1 -/-, and Parkin -/- DJ-1 -/- SOD2 +/- mice, showed a significant decrease in startle response in Parkin -/- DJ-1 -/- and Parkin -/- DJ-1 -/- SOD1 -/- (p < 0.001) compared to wild type (Figure 6B).
	0.94	DJ-1 -/- and Parkin -/- DJ-1 -/- SOD1 -/- indicate impairment of reflexes and/or sensory functions compared to wild type mice.
	0.94	DJ-1 -/- SOD1 -/- mice is consistent with the increased striatal dopamine we identified in mice deficient for Parkin, DJ-1 and another antioxidant protein, glutathione peroxidase 1 and consistent with previously published results indicating an increase in striatal dopamine in aged Parkin -/- DJ-1 -/- PINK1 -/- mice.
	0.91	DJ-1 -/- SOD1 -/- mice is likely due to a loss of hearing in mice deficient for SOD1.
	0.64	DJ-1 -/- SOD1 -/- mice, but not in Parkin -/- DJ-1 -/- SOD2 +/- mice, compared to wild type mice (Figure 2) and no differences in the levels of dopamine or serotonin between wild type and Parkin -/- DJ-1 -/- mice (Table 1).
28336262	0.98	SOD1/DJ-1/Parkin-deficient mice (TKO mice) compared to C57BL/6J mice.
	0.97	SOD1/DJ1/Parkin deficient mice.
	0.97	SOD1, DJ-1 and Parkin (proteins that are important in the retinal response to oxidative stress), does increase the level of retinal and RPE damage after FCD-LIRD, as demonstrated in clinical photos, OCT outer retinal volume, and on analysis of RPE cell morphology.
	0.97	SOD1/DJ-1/Parkin-deficient mice (TKO) compared to C57BL/6J mice (B6J).
	0.97	SOD1/DJ-1/Parkin-deficient (TKO, B) mice.
	0.97	SOD1/DJ-1/Parkin-deficient (TKO) eyes relative to C57BL/6J (B6J) eyes.
	0.96	SOD1, DJ-1 and Parkin (triple KO, TKO) have a marked increase in retinal injury after exposure to the fundus camera-delivered light induced retinal degeneration (FCD-LIRD) models, when compared to C57BL/6J mice.
	0.96	SOD1/DJ1/Parkin-deficient mice (TKO mice) compared to C57BL/6J (B6J).
	0.95	SOD1/DJ-1/Parkin deficient mice compared to C57BL/6J.
	0.91	SOD1, DJ1 and Parkin (TKO mice) demonstrate increased susceptibility to FCD-LIRD
	0.74	SOD1/DJ-1/Parkin triple KO mice.
	0.65	SOD1/DJ-1/Parkin-deficient mice are indeed more susceptible to light-induced retinal degeneration, we plan to start dissecting the pathways involved.
18769717	0.98	Sod1, Ercc6, Prdx6, Als2, Txnrd2, Park7, Srxn1, and Epas1 all undergo enhanced upregulation after CS exposure only in the presence of the Nrf2 gene.
	0.98	Sod1, Ercc6, Prdx6, Als2, Txnrd2, Park7, Srxn1 and Epas1 mRNA were induced selectively more in Nrf2+/+ mouse lungs after CS exposure.
	0.98	Sod1, Ercc6, Prdx6, Als2, Txnrd2, Park7, Srxn1, and Epas1 in wild-type but not Nrf2-knockout mice.
	0.98	Sod1, Ercc6, Prdx6, Als2, Txnrd2, Park7, Srxn1, and Epas1 genes in the mouse lung (Figure 5).
	0.88	Sod1, Als2, Srxn1, and Park7, and the expression of Nfe2l2 (the Nrf2 gene) in the mouse lung.
	0.76	Sod1, Srxn1, Txnrd2, Prdx1, Prdx2, Prdx6, Atf1, Park7, or Als2) and the edge between X and Nqo1 represent a number of possible transcriptional regulatory relationships, with one gene serving as a final target, and the other two genes functioning as activators or repressors of mRNA expression.
25950469	0.98	DJ-1, Sod1, 14-3-3e, Prdx2 and Prdx6) are connected to the mitogen-activated protein kinase p38 pathway.
	0.98	DJ-1, Sod1, 14-3-3e, Prdx2 and Prdx6) were reported to be connected to the mitogen-activated protein kinase p38 pathway, which mediates a wide variety of cellular behaviors ranging from response to stress stimuli and cell cycle.
	0.95	DJ-1 and Sod1) and development of nervous system (e.g., NADH dehydrogenase [ubiquinone] flavoprotein 2, Nduv2) (Supplementary Table 2).
	0.94	DJ-1, Sod1 and Prdx2 were mainly localized in the EGL and PCs layer, with poor staining in IGL (Figure 3a).
	0.90	DJ-1, reduced forms of Prdx2 and Prdx6, Sod1, Pfdn5, Tctp and Pebp1 in cerebella from Ugt1 mutant mice, and an increased representation therein of Dpysl2, Dpysl3, 14-3-3e, Vat1, Atp6v1a and Eno2.
	0.80	Dj-1 and Sod1 in the samples from Ugt1 mutant mice, and an increased representation therein of dihydropyrimidinase-like 3 (Dpysl3), 14-3-3e and Eno2.
23622116	0.98	SOD-1 and SOD-2 was increased in saline-treated DJ-1-/- mice compared to saline-treated wild-type mice (Figure 7), which may reflect compensatory upregulation of certain anti-oxidants in the absence of DJ-1 and may have contributed to the attenuated expression of oxidative stress genes in response to LPS.
	0.97	SOD-1 and SOD-2 mRNA in the midbrain of saline-treated DJ-1-/- mice compared to wild-type saline animals (Figure 7).
	0.96	DJ-1-/- mice resulted in a significant reduction in SOD-1 and in SOD-2 mRNA relative to saline treatment.
	0.96	DJ-1-/- mouse midbrain is attributed to other cell types in the brain, such as astrocytes or neurons which also express SOD-1 and SOD-2, for example.
22792356	0.98	SOD1, SOD2), glutathione and catalase are essential defense mechanisms against oxidative stress in the cell, and DJ-1 has been reported to be involved in the glutathione metabolism and SOD1 expression.
	0.96	SOD1 and SOD2 is normal in DJ-1-/- MEFs (Fig. 8).
	0.80	SOD1, SOD2, catalase, and G6PDH between DJ-1-/- and +/+ MEFs (Fig. 8A and 8B).
22954895	0.98	DJ-1 is thought to be an oxidative stress sensor modulating different cellular defense pathways such as Akt and Cu-Zn superoxide dismutase 1 (SOD1) to mediate protection.
27766037	0.98	DJ-1 can also modulate the expression of superoxide dismutase1 (SOD1), a well-known enzyme for dismutating superoxide, through Erk1/2-Elk1 pathway.
30596094	0.96	Park7, Gpx1, Prdx6, and Sod1) and lipid metabolism proteins (Fabp4, Acaa2, apoA4, and ApoA1).
	0.96	Sod1 or Park7 (Figures 6(a)-6(d)).
	0.79	Park7, Gpx1, Prdx6, and Sod1) as well as a lipid metabolism cluster (yellow nodes: Acaa2, Echs1, Apoa4, ApoA1, and Fapb4A).
28088625	0.86	DJ-1 KO mice are comparable to findings in several mouse models that attempt to recapitulate AMD pathology by increasing retinal oxidative stress with systemic iron overload, by knocking out Sod1, Sod-2, or inserting the human apoB100 transgene in mice.