Relevant bibliographies by topics / SOD1 gene

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Academic literature on the topic 'SOD1 gene'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "SOD1 gene"

1

Lian, Shanshan, Liang Zhao, Xiaogang Xun, Jiarun Lou, Moli Li, Xu Li, Shi Wang, Lingling Zhang, Xiaoli Hu, and Zhenmin Bao. "Genome-Wide Identification and Characterization of SODs in Zhikong Scallop Reveals Gene Expansion and Regulation Divergence after Toxic Dinoflagellate Exposure." Marine Drugs 17, no. 12 (December 12, 2019): 700. http://dx.doi.org/10.3390/md17120700.

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As filter-feeding animals mainly ingesting microalgae, bivalves could accumulate paralytic shellfish toxins (PSTs) produced by harmful algae through diet. To protect themselves from the toxic effects of PSTs, especially the concomitant oxidative damage, the production of superoxide dismutase (SOD), which is the only eukaryotic metalloenzyme capable of detoxifying superoxide, may assist with toxin tolerance in bivalves. To better understand this process, in the present study, we performed the first systematic analysis of SOD genes in bivalve Chlamys farreri, an important aquaculture species in China. A total of six Cu/Zn-SODs (SOD1-6) and two Mn-SODs (SOD7, SOD8) were identified in C. farreri, with gene expansion being revealed in Cu/Zn-SODs. In scallops exposed to two different PSTs-producing dinoflagellates, Alexandrium minutum and A. catenella, expression regulation of SOD genes was analyzed in the top ranked toxin-rich organs, the hepatopancreas and the kidney. In hepatopancreas, which mainly accumulates the incoming PSTs, all of the six Cu/Zn-SODs showed significant alterations after A. minutum exposure, with SOD1, 2, 3, 5, and 6 being up-regulated, and SOD4 being down-regulated, while no significant change was detected in Mn-SODs. After A. catenella exposure, up-regulation was observed in SOD2, 4, 6, and 8, and SOD7 was down-regulated. In the kidney, where PSTs transformation occurs, SOD4, 5, 6, and 8 were up-regulated, and SOD7 was down-regulated in response to A. minutum feeding. After A. catenella exposure, all the Cu/Zn-SODs except SOD1 were up-regulated, and SOD7 was down-regulated in kidney. Overall, in scallops after ingesting different toxic algae, SOD up-regulation mainly occurred in the expanded Cu/Zn-SOD group, and SOD6 was the only member being up-regulated in both toxic organs, which also showed the highest fold change among all the SODs, implying the importance of SOD6 in protecting scallops from the stress of PSTs. Our results suggest the diverse function of scallop SODs in response to the PST-producing algae challenge, and the expansion of Cu/Zn-SODs might be implicated in the adaptive evolution of scallops or bivalves with respect to antioxidant defense against the ingested toxic algae.
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Ściskalska, Milena, Monika Ołdakowska, Grzegorz Marek, and Halina Milnerowicz. "Changes in the Activity and Concentration of Superoxide Dismutase Isoenzymes (Cu/Zn SOD, MnSOD) in the Blood of Healthy Subjects and Patients with Acute Pancreatitis." Antioxidants 9, no. 10 (October 1, 2020): 948. http://dx.doi.org/10.3390/antiox9100948.

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This study was aimed at evaluating the changes in the concentration and activity of all superoxide dismutase isoenzymes (SOD1, SOD2, SOD3) in the blood of patients with acute pancreatitis (AP) and healthy subjects, taking into account the extracellular (plasma) and intracellular (erythrocyte lysate) compartment. The relationships between the activity/concentration of SODs, metal concentration and the markers of inflammation were evaluated. To assess the pro/antioxidative imbalance, the malonyldialdehyde (MDA) concentration and the value of total antioxidant capacity (TAC) were measured. The impact of single-nucleotide polymorphism (SNP) in the SOD1 gene (rs2070424) on the activity/concentration of SOD1 as the main isoenzyme of the SOD family was also analyzed in this study. The SOD2 activity in erythrocytes was increased compared to plasma: 10-fold in the AP patient group and 5-fold in healthy subjects. The plasma of AP patients showed an increased SOD1 concentration and decreased SOD2 and SOD3 concentrations compared to healthy subjects. The Cu/Zn SOD (SOD1 + SOD3) concentration in plasma of AP patients was elevated compared to healthy subjects, but changes in plasma Cu/Zn SOD (SOD1 + SOD3) activity in the examined groups were not observed. An influence of SNP rs2070424 in the SOD1 gene on the total activity of SOD in AP patients (with AG genotype), accompanied by an increased IL-6 concentration, was observed. In oxidative stress conditions induced by inflammation, the participation of individual forms of plasma SOD isoenzymes in total antioxidative activity of SOD changed. A significant increase in the intracellular SOD1 concentration in plasma of AP patients proves the important role of this isoenzyme in the neutralization of oxidative stress induced by impaired Cu and Zn homeostasis. The presence of increased concentration of SOD2 in erythrocytes of healthy subjects and AP patients confirms the important function of this isoenzyme in the antioxidative defense.
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Tuna, A., G. Ozturk, TB Gerceker, E. Karaca, H. Onay, SM Guvenc, and O. Cogulu. "Superoxide dismutase 1 and 2 gene polymorphism in Turkish vitiligo patients." Balkan Journal of Medical Genetics 20, no. 2 (December 29, 2017): 67–73. http://dx.doi.org/10.1515/bjmg-2017-0033.

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Abstract Vitiligo is an acquired disease of unknown etiology. Several theories have been proposed to understand the pathogenesis. The role of oxidative stress has been getting more important in recent years. One of the primary antioxidant enzymes in vitiligo is the superoxide dismutase (SOD). The aim of this study is to investigate the polymorphisms of the SOD1 and SOD2 in Turkish vitiligo patients. One hundred one vitiligo patients and 99 healthy controls without family history of vitiligo were included into the study. The SOD1 35 A/C and SOD2 A16V (C/T) polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphim (PCR-RFLP). Vitiligo patients and control group of SOD1 35 A/C and SOD2 A16V (C/T) polymorphism allele frequencies were compared by using χ2 tests. The distribution of the SOD1 35 AA and AC genotypes were similar in vitiligo patients and control group. When the patient and the control groups were compared for the SOD2 Ala9Val (C/T) polymorphism, a significant difference was determined for the distribution of the genotypes [p = 0.047, odds ratio (OR) = 2.075, 95% confidence interval (95% CI) = 1.008-4.272]. The relative risk for development of vitiligo was found as a 2-fold increase in the TT genotype. The increase of TT homozygosity in the vitiligo cases creates the problem on the transfer of the enzyme to the mitochondria and thus, the SODs antioxidant effect may decrease in vitiligo but the polymorphism was not determined in all patients, so this study needs to be substantiated by other studies containing a higher number of patients.
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Kim, Sang-Hoon, Sang-Heon Kim, Jae-Hyoung Lee, Byoung-Hoon Lee, Ho Joo Yoon, Dong Ho Shin, Sung Soo Park, Suk Bin Jang, Jae-Seuk Park, and Young-Koo Jee. "Superoxide Dismutase Gene (SOD1, SOD2, and SOD3) Polymorphisms and Antituberculosis Drug-induced Hepatitis." Allergy, Asthma & Immunology Research 7, no. 1 (2015): 88. http://dx.doi.org/10.4168/aair.2015.7.1.88.

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Kotowska, Jadwiga, and Ewa Jówko. "Effect of Gene Polymorphisms in Antioxidant Enzymes on Oxidative-Antioxidative Status in Young Men." Polish Journal of Sport and Tourism 27, no. 4 (December 1, 2020): 7–13. http://dx.doi.org/10.2478/pjst-2020-0020.

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Abstract Introduction. The aim of the study was to evaluate the relationship between SOD1 +35A/C, SOD2 Val16Ala and GPx1 Pro198Leu gene polymorphisms and baseline level of oxidative-antioxidative status in blood. Material and methods.The study included 154 male students of physical education who participated in practical classes included in the study curriculum. Genotyping was carried out on genomic DNA using real-time PCR reaction with TaqMan assays. Also, fasting blood samples were analyzed for biochemical parameters including superoxide dismutase (SOD) activity in erythrocytes and the activity of glutathione peroxidase (GPx) in whole blood, as well as serum concentration of lipid hydroperoxides (LOOHs) and total antioxidant capacity (TAC) of serum. Results. SOD2 polymorphism had a significant effect on serum LOOHs concentration. Individuals with Val/Val genotype presented a significantly higher level of LOOHs than Val/Ala genotype carriers (p < 0.05). In addition, no significant differences in SOD and GPx activity or TAC were found between SOD2 genotypes. Apart from the SOD2 polymorphism, no significant influence of both SOD1 and GPx1 polymorphisms on measured biochemical parameters was found, probably due to the lack of mutant homozygous genotypes in the study group. Conclusions. In young, healthy and physically active men, SOD2 polymorphism has an influence on the resting level of oxidative stress marker in the blood without affecting both enzymatic and non-enzymatic antioxidant defence. In turn, SOD1 and GPx1 polymorphisms do not seem to affect oxidative-antioxidative status. However, the absence of SOD1 CC and GPx1 Leu/Leu may indicate that these genotypes are disadvantageous, and thus underrepresented in young, healthy and physically fit population.
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Cao, Xueli, Yujuan Sun, Yanfei Lin, Yanjun Pan, Umer Farooq, Lan Xiang, and Jianhua Qi. "Antiaging of Cucurbitane Glycosides from Fruits of Momordica charantia L." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/1538632.

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Methanol extracts of Momordica charantia L. fruits are extensively studied for their antiaging activities. A new cucurbitane-type triterpenoid (1) and nine other known compounds (2–10) were isolated, and their structures were determined according to their spectroscopic characteristics and chemical derivatization. Biological evaluation was performed on a K6001 yeast bioassay system. The results indicated that all the compounds extended the replicative lifespan of K6001 yeast significantly. Compound 9 was used to investigate the mechanism involved in the increasing of the lifespan. The results indicated that this compound significantly increases the survival rate of yeast under oxidative stress and decreases ROS level. Further study on gene expression analysis showed that compound 9 could reduce the levels of UTH1 and SKN7 and increase SOD1 and SOD2 gene expression. In addition, it could not extend the lifespan of the yeast mutants of Uth1, Skn7, Sod1, and Sod2. These results demonstrate that compound 9 exerts antiaging effects via antioxidative stress and regulation of UTH1, SKN7, SOD1, and SOD2 yeast gene expression.
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Bonder, Claudine S., Derrice Knight, Daniel Hernandez-Saavedra, Joe M. McCord, and Paul Kubes. "Chimeric SOD2/3 inhibits at the endothelial-neutrophil interface to limit vascular dysfunction in ischemia-reperfusion." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 3 (September 2004): G676—G684. http://dx.doi.org/10.1152/ajpgi.00049.2004.

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After an ischemic episode, reperfusion causes profound oxidative stress in the vasculature of the afflicted tissue/organ. The dysregulated accumulation of reactive oxygen species (ROS), such as superoxide, has been closely linked to the production and release of proinflammatory mediators, a profound increase in adhesion molecule expression by the vascular endothelium, and infiltration of neutrophils during ischemia-reperfusion (I/R). Superoxide dismutase (SOD) has been shown to protect tissues and organs against I/R-induced injury; however, the drug had to be continuously perfused or kidneys had to be occluded to prevent clearance. We used intravital microscopy, a system that allowed us to visualize neutrophil-endothelial interactions within the mesenteric postcapillary venules of cats subjected to I/R and tested the hypothesis that I/R-induced neutrophil recruitment was inhibited by treatment with SOD2/3. SOD2/3 is a chimeric fusion gene product that contains the mature SOD2 as well as the COOH-terminal “tail” of SOD3 and, unlike the three naturally occurring SODs (SOD1, SOD2, and SOD3), which bear a net negative charge at pH 7.4, SOD2/3 is positively charged and physiologically stable. Our results suggest that not only does SOD2/3 have a much greater efficacy in vivo than the native human SOD2, but its administration prevents I/R-induced neutrophil-endothelial cell interactions and microvascular dysfunction. Moreover, our data support the hypothesis that reactive oxidants mediate I/R-induced injury and that the chimeric recombinant SOD2/3 has the potential to be a therapeutic agent against this debilitating illness.
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Lisse, Thomas S. "Vitamin D Regulation of a SOD1-to-SOD2 Antioxidative Switch to Prevent Bone Cancer." Applied Sciences 10, no. 7 (April 8, 2020): 2554. http://dx.doi.org/10.3390/app10072554.

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Superoxide, a form of reactive oxygen species (ROS), is catabolized by superoxide dismutase (SOD) and contributes to carcinogenesis via the oxidative damage it inflicts on cells. The aim of this research was to analyze the potential vitamin D-mediated regulation of the antioxidative “SOD1-to-SOD2 switch” within the human MG-63 osteosarcoma model. For this study, real-time PCR analysis was performed using MG-63 cells exposed to metabolically active 1,25(OH)2D3. First, a sustained statistically significant >2-fold suppression of proliferating cell nuclear antigen (PCNA) transcripts was observed after 10 nM but not at 100 nM of 1,25(OH)2D3 treatment, suggesting a cytostatic effect. In order to assess regulators of mitochondrial oxidative phosphorylation, gene expression of COX2 and COX4l1 of the mitochondrial complex IV and antioxidative enzymes (SOD1, SOD2 and Catalase (CAT)) were monitored. For COX2 and COX4l1, no changes in gene expression were observed. However, a concomitant decrease in CAT and SOD1 mRNA, and increase in SOD2 mRNA after 24 h of 10 nM 1,25(OH)2D3 treatment were observed. A ~8-fold increase in SOD2 mRNA was apparent after 48 ours. The significant increase in SOD2 activity in the presence of vitamin D indicates an antioxidant potential and sensitization of vitamin D during osteosarcoma transformation and mitochondrial detoxification over time.
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Muratet, François, Elisa Teyssou, Aude Chiot, Séverine Boillée, Christian S. Lobsiger, Delphine Bohl, Beata Gyorgy, et al. "Impact of a frequent nearsplice SOD1 variant in amyotrophic lateral sclerosis: optimising SOD1 genetic screening for gene therapy opportunities." Journal of Neurology, Neurosurgery & Psychiatry 92, no. 9 (March 30, 2021): 942–49. http://dx.doi.org/10.1136/jnnp-2020-325921.

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ObjectiveMutations in superoxide dismutase 1 gene (SOD1), encoding copper/zinc superoxide dismutase protein, are the second most frequent high penetrant genetic cause for amyotrophic lateral sclerosis (ALS) motor neuron disease in populations of European descent. More than 200 missense variants are reported along the SOD1 protein. To limit the production of these aberrant and deleterious SOD1 species, antisense oligonucleotide approaches have recently emerged and showed promising effects in clinical trials. To offer the possibility to any patient with SOD1-ALS to benefit of such a gene therapy, it is necessary to ascertain whether any variant of unknown significance (VUS), detected for example in SOD1 non-coding sequences, is pathogenic.MethodsWe analysed SOD1 mutation distribution after SOD1 sequencing in a large cohort of 470 French familial ALS (fALS) index cases.ResultsWe identified a total of 27 SOD1 variants in 38 families including two SOD1 variants located in nearsplice or intronic regions of the gene. The pathogenicity of the c.358–10T>G nearsplice SOD1 variant was corroborated based on its high frequency (as the second most frequent SOD1 variant) in French fALS, the segregation analysis confirmed in eight affected members of a large pedigree, the typical SOD1-related phenotype observed (with lower limb onset and prominent lower motor neuron involvement), and findings on postmortem tissues showing SOD1 misaccumulation.ConclusionsOur results highlighted nearsplice/intronic mutations in SOD1 are responsible for a significant portion of French fALS and suggested the systematic analysis of the SOD1 mRNA sequence could become the method of choice for SOD1 screening, not to miss these specific cases.
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Broom, Wendy J., Kristen E. Auwarter, Jake Ni, Deborah E. Russel, Li-An Yeh, Michele M. Maxwell, Marcie Glicksman, Aleksey G. Kazantsev, and Robert H. Brown. "Two Approaches to Drug Discovery in SOD1-Mediated ALS." Journal of Biomolecular Screening 11, no. 7 (September 14, 2006): 729–35. http://dx.doi.org/10.1177/1087057106290937.

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Familial amyotrophic lateral sclerosis (ALS) accounts for 10% of all ALS cases; approximately 25% of these cases are due to mutations in the Cu/Zn superoxide dismutase gene (SOD1). To date, 105 different mutations spanning all 5 exons have been identified in the SOD1 gene. Mutant SOD1-associated ALS is caused by a toxic gain of function of the mutated protein. Therefore, regardless of the specific mechanism whereby mutant SOD1 initiates motor neuron death, the authors hypothesize that measures that decrease levels of mutant SOD1 protein should ameliorate the phenotype in transgenic mice and potentially in patients with SOD1-mediated disease. They have designed 2 cell-based screening assays to identify small, brain-permeant molecules that inactivate expression of the SOD1 gene or increase the degradation of the SOD1 protein. Here they describe the development and optimization of these assays and the results of high-throughput screening using a variety of compound libraries, including a total of more than 116,000 compounds. The majority of the hit compounds identified that down-regulated SOD1 were shown to be toxic in a cell-based viability assay or were nonselective transcription inhibitors, but work is continuing on a number of nonspecific inhibitors of SOD1 expression. Ultimately, the authors believe that these 2 cell-based assays will provide powerful strategies to identify novel therapies for the treatment of inherited SOD1-associated forms of ALS.
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Dissertations / Theses on the topic "SOD1 gene"

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Kennedy, Zachary C. "Optimizing CRISPR/Cas9 for Gene Silencing of SOD1 in Mouse Models of ALS." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1047.

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Mutations in the SOD1 gene are the best characterized genetic cause of amyotrophic lateral sclerosis (ALS) and account for ~20% of inherited cases and 1-3% of sporadic cases. The gene-editing tool Cas9 can silence mutant genes that cause disease, but effective delivery of CRISPR-Cas9 to the central nervous system (CNS) remains challenging. Here, I developed strategies using canonical Streptococcus pyogenes Cas9 to silence SOD1. In the first strategy, I demonstrate effectiveness of systemic delivery of guide RNA targeting SOD1 to the CNS in a transgenic mouse model expressing human mutant SOD1 and Cas9. Silencing was observed in both the brain and the spinal cord. In the second strategy, I demonstrate the effectiveness of delivering both guide RNA and Cas9 via two AAVs into the ventricles of the brain of SOD1G93A mice. Silencing was observed in the brain and in motor neurons within the spinal cord. For both strategies, treated mice had prolonged survival when compared to controls. Treated mice also had improvements in grip strength and rotarod function. For ICV treated mice, we detected a benefit of SOD1 silencing using net axonal transport assays, a novel method to detect motor neuron function in mice before onset of motor symptoms. These studies demonstrate that Cas9-mediated genome editing can mediate disease gene silencing in motor neurons and warrants further development for use as a therapeutic intervention for SOD1-linked ALS patients.
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Abens, Ryan. "GENE EXPRESSION OF CYTOKINES AND OXIDATIVE STRESS MARKERS IN CTRP3 TRANSGENIC MICE WITH CHRONIC ETHANOL EXPOSURE." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/2.

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Oxidative stress and inflammation are often linked to the prognosis of diseases caused by chronic alcohol consumption. Chronic alcohol consumption plays a key role in brain tissue damage, often leading to the development of cognitive disorders and loss of brain function. In addition to the direct effects of alcohol on brain function, consumption of alcohol can lead to psychosocial stressors such as legal, financial, and interpersonal problems. It has been found that mice that overexpress C1q/Tumor Necrosis Factor-related protein-3 (CTRP3) and exposed to ethanol daily do not die like the mice who did not overexpress CTRP3 and fed the same diet. Although the specific physiological functions regulated by the CTRP family are largely unknown, there is evidence showing that they have diverse biological effects on inflammation, metabolism, and survival signaling in several different types of tissue. Postmortem brain tissue samples were collected from mice that were exposed to ethanol with transgenic overexpression of CTRP3 and from wild type mice that were only exposed to ethanol. Interestingly, previous immunoblotting of the cerebellum and the hippocampus using collected tissue demonstrated that glia activation was present in the CTRP3 overexpressing mice but not in the wild-type ethanol fed mice. This finding suggests that glia cells are either dying in the ethanol fed wild type mice or that CTRP3 protects and prolongs activated glia cells. The current study will determine if markers of oxidative stress and cell viability are altered in the CTRP3 overexpressing mice when compared to wild-type mice at the molecular level. RNA isolation using the Directzol system and cDNA synthesis using punch dissected homogenate tissue collected from the hippocampus was used for this investigation. Gene expression of BDNF, SOD1 and PARP1 in mouse tissue was determined using quantitative PCR. Immunoblotting of a small number of hippocampal tissue using PARP1 was performed. The mice that were CTRP3 overexpressed and fed ethanol will likely exhibit altered gene expression of cytokines and increased oxidative stress gene expression in postmortem hippocampal brain tissue when compared to wild-type ethanol fed mice. The current studies could contribute to the body of knowledge for the development of novel therapies that may alleviate the neuro-inflammatory effects of alcohol use.
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Baker, David. "Gene expression profiling and functional studies of astrocytes in SOD1-related amyotrophic lateral sclerosis." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/9173/.

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Amyotrophic Lateral Sclerosis (ALS) is the most common adult onset motor neuron (MN) disorder, characterised by muscle wasting due to MN death. Astrocytes play an important role in disease progression in the SOD1G93A transgenic mouse model and patients of ALS. Although astrocytes display a selective toxicity to MN, the toxic factor(s) have not been identified. We hypothesise that differential gene expression in SOD1-ALS astrocytes will reveal targets for therapeutic intervention. Microarray analysis was performed upon Laser Capture Microdissected astrocytes isolated from spinal cord of symptomatic (90 day) and late-stage (120 day) SOD1G93A mice and non-transgenic (NTg) littermates, and from post-mortem human SOD1-ALS and control spinal cord. Functional studies were performed using enzymatic activity assays and immunohistochemistry upon spinal cord and in vitro validation studies were performed using murine neonatal cultures of astrocytes, microglia and embryonic MNs and “i-astrocytes” directly converted from human ALS fibroblasts. In murine astrocytes annotation clustering analysis showed increased expression of lysosomal transcripts which were validated by qPCR . Using functional experiments, we have found significantly higher activity of the lysosomal enzyme β hexosamindase in the spinal cord of SOD1G93A mice. Immune response and phagocytic pathways are also enriched within both datasets, and phagocytosis assays using fluorescently labelled NSC34 cell debris show that SOD1G93A astrocytes engulf significantly higher amounts of neuronal debris compared to NTg controls, highlighting an increased reactivity of astrocytes at symptom onset. Human SOD1-astrocytes show down-regulation of transcripts involved in tight junction formation such as ZO-2, Claudin-5 and Occludin, and we hypothesise that ALS-astrocytes contribute to the breakdown in blood-brain-barrier (BBB) integrity seen in ALS. qPCR confirmed differential expression of BBB-influencing genes such as claudin-5, junctional adhesion molecule 2 and transforming growth factor beta-2. Model BBBs made with i-astrocytes from human patients co-cultured with endothelia show significantly lower transendothelial electrical resistance and dextran-permeability values pointing to an astrocyte role in increased BBB permeability during disease. These studies show the breadth of behaviours displayed by astrocytes during ALS disease progression and will provide an important guide for future therapeutic intervention.
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Likhite, Shibi B. "Therapeutic suppression of mutant SOD1 by AAV9-mediated gene therapy approach in Amyotrophic Lateral Sclerosis." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1417394084.

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Stoica, Lorelei I. "Gene Therapy for Amyotrophic Lateral Sclerosis: An AAV Delivered Artifical MicroRNA Against Human SOD1 Increases Survival and Delays Disease Progression of the SOD1G93A Mouse Model: A Dissertation." eScholarship@UMMS, 2015. http://escholarship.umassmed.edu/gsbs_diss/813.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by loss of motor neurons, resulting in progressive muscle weakness, atrophy, paralysis and death within five years of diagnosis. About ten percent of cases are inherited, of which twenty percent are due to mutations in the superoxide dismutase 1 (SOD1) gene. Since the only FDA approved ALS drug prolongs survival by just a few months, new therapies for this disease are needed. Experiments in transgenic ALS mouse models have shown that decreasing levels of mutant SOD1 protein alters and in some cases entirely prevents disease progression. We explored this potential therapeutic approach by using a single stranded AAV9 vector encoding an artificial microRNA against human SOD1 injected bilaterally into the cerebral lateral ventricles of neonatal SOD1G93A mice. This therapy extended median survival from 135 to 206 days (a 50% increase) and delayed hind limb paralysis. Animals remained ambulatory until endpoint, as defined by a sharp drop in body weight. Treated animals had a reduction of mutant human SOD1 mRNA levels in upper and lower motor neurons. As compared to untreated SOD1G93A mice, the AAV9 treated mice also had significant improvements in multiple parameters including the number of motor neurons, diameter of ventral root axons, and degree of neuroinflammation in the spinal cord. These studies clearly show that an AAV9-delivered artificial microRNA is a translatable therapeutic approach for ALS.
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Scarrott, Joseph. "Investigating the specificity of RNAi molecules in human gene therapy for SOD1-linked familial amyotrophic lateral sclerosis." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22558/.

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20% of familial amyotrophic lateral sclerosis (fALS) cases are caused by mutations in the gene encoding the cytosolic protein human Cu/Zn superoxide dismutase 1 (hSOD1). RNA interference (RNAi) technology offers the therapeutic potential for the treatment of SOD-linked fALS by reducing the burden of pathogenic mutant SOD1 protein. Translation of this gene therapy strategy to the clinic requires the development of vectors that are free of significant off-target effects and with reliable biomarkers to determine treatment efficacy, successful target gene reduction, and correct dosing. Using self-complementary adeno-associated virus serotype 9 (scAAV9) to deliver RNAi against hSOD1 in the SOD1G93A mouse model, the work presented in this thesis demonstrates that intrathecal injection of the therapeutic vector via the cisterna magna delayed onset of disease, decreased motor neuron death at end stage by up to 88%, and prolonged the median survival of SOD1G93A mice by up to 42%. Using a panel of purposefully designed RNAi constructs cloned into the scAAV9 backbone this is, to our knowledge, the first study to demonstrate no significant in vitro off-target effects linked to hSOD1 silencing, providing further confidence in the specificity of this approach. This study also reports the measurement of cerebrospinal fluid (CSF) hSOD1 protein levels as a biomarker of effective dosing and efficacy of hSOD1 knockdown. Together, this data provides further confidence in the safety of the clinical therapeutic vector.
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Oliveira, Yonara Monique da Costa. "Avalia??o do status antioxidante, express?o g?nica e polimorfismos dos genes SOD1, SOD2 e GPx1 em crian?as, adolescentes e adultos jovens com diabetes tipo 1." Universidade Federal do Rio Grande do Norte, 2012. http://repositorio.ufrn.br:8080/jspui/handle/123456789/13503.

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Studies report that the pathophysiological mechanism of diabetes complications is associated with increased production of Reactive Oxygen Species (ROS)-induced by hyperglycemia and changes in the capacity the antioxidant defense system. In this sense, the aim of this study was to evaluate changes in the capacity of antioxidant defense system, by evaluating antioxidant status, gene expression and polymorphisms in the genes of GPx1, SOD1 and SOD2 in children, adolescents and young adults with type 1 diabetes. We studied 101 individuals with type 1 diabetes (T1D) and 106 normoglycemic individuals (NG) aged between 6 and 20 years. Individuals with type 1 diabetes were evaluated as a whole group and subdivided according to glycemic control in DM1G good glycemic control and DM1P poor glycemic control. Glycemic and metabolic control was evaluate by serum glucose, glycated hemoglobin, triglycerides, total cholesterol and fractions (HDL and LDL). Renal function was assessed by measurement of serum urea and creatinine and albumin-to-creatinine ratio (ACR) in spot urine. Antioxidant status was evaluate by content of reduced glutathione (GSH) in whole blood and the activity of erythrocyte enzymes glutathione peroxidase (GPx) and superoxide dismutase (SOD). We also analyzed gene expression and gene polymorphisms of GPx1 (rs1050450), SOD1 (rs17881135) and SOD2 (rs4880) by the technique of real-time PCR (Taqman?). Most individuals with DM1 (70.3%) had poor glycemic control (glycated hemoglobin> 8%). Regarding the lipid profile, individuals with type 1 diabetes had significantly elevated total cholesterol (p <0.001) and LDL (p <0.000) compared to NG; for triglycerides only DM1NC group showed significant increase compared to NG. There was an increase in serum urea and RAC of individuals with DM1 compared to NG. Nine individuals with type 1 diabetes showed microalbuminuria (ACR> 30 mg / mg). There was a decrease in GSH content (p = 0.006) and increased erythrocyte GPx activity (p <0.001) and SOD (p <0.001) in DM1 group compared to NG. There was no significant difference in the expression of GPx1 (p = 0.305), SOD1 (.365) and SOD2 (0.385) between NG and DM1. The allele and genotype frequencies of the polymorphisms studied showed no statistically significant difference between the groups DM1 and NG. However, the GPx1 polymorphism showed the influence of erythrocyte enzyme activity. There was a decrease in GPx activity in individuals with type 1 diabetes who had a polymorphic variant T (p = 0.012). DM1 patients with the polymorphic variant G (AG + GG) for polymorphism of SOD2 (rs4880) showed an increase in the RAC (p <0.05). The combined data suggest that glucose control seems to be the predominant factor for the emergence of changes in lipid profile, renal function and antioxidant system, but the presence of the polymorphisms studied may partly contribute to the onset of complications
Estudos relatam que o mecanismo fisiopatol?gico das complica??es do diabetes est? associado ao aumento na produ??o de Esp?cies Reativas de Oxig?nio (ERO) induzido pela hiperglicemia persistente e altera??es na capacidade de defesa do sistema antioxidante. Nesse sentido, o presente estudo teve como objetivo avaliar altera??es na capacidade de defesa do sistema antioxidante, atrav?s da avalia??o do status antioxidante, express?o g?nica e pesquisa de polimorfismos nos genes da GPx1, SOD1 e SOD2 de crian?as, adolescentes e adultos jovens com Diabetes Mellitus tipo 1 (DM1). Foram estudados 101 indiv?duos com diabetes tipo 1 (DM1) e 106 indiv?duos normoglic?micos (NG) com idade entre 6 e 20 anos. Os indiv?duos com DM1 foram avaliados como um grupo total e subdivididos de acordo com o controle glic?mico em DM1NC diab?tico n?o-compensado e DM1C diab?ticos compensados. Para avaliar o controle glic?mico e metab?lico foram realizadas as dosagens de glicose s?rica, hemoglobina glicada, triglicer?deos, colesterol total e fra??es (HDL e LDL). A fun??o renal foi avaliada pelas dosagens de ureia e creatinina s?ricas e a rela??o albumina/creatinina (RAC) urin?ria. Os par?metros antioxidantes avaliados foram o conte?do da glutationa reduzida (GSH) em sangue total e a atividade eritrocit?ria das enzimas glutationa peroxidase (GPx) e super?xido dismutase (SOD). Tamb?m foi avaliada a express?o g?nica e a pesquisa dos polimorfismos dos genes GPx1 (rs1050450), SOD1(rs17881135) e SOD2 (rs4880) pela t?cnica da PCR em tempo real (Taqman?). A maioria dos indiv?duos com DM1 (70,3%) apresentou controle glic?mico insatisfat?rio (hemoglobina glicada >8%). Em rela??o ao perfil lip?dico, indiv?duos com DM1 apresentaram valores significativamente elevados de colesterol total (p<0,001) e LDL (p<0,000) em rela??o ao NG; para os triglicer?deos s? o grupo DM1NC apresentou aumento significante em rela??o ao NG. Observou-se o aumento na ur?ia s?rica e na RAC dos indiv?duos com DM1 em rela??o ao NG. Nove dos indiv?duos com DM1 apresentaram microalbumin?ria (RAC> 30 μg/mg). Houve diminui??o no conte?do de GSH (p=0,006) e aumento na atividade eritrocit?ria da GPx (p<0,001) e SOD (p<0,001) do grupo DM1 em rela??o ao NG. N?o foi observada diferen?a significante na express?o de GPx1 (p=0,305), SOD1 (0,365) e SOD2 (0,385) entre NG e DM1. As freq??ncias genot?picas e al?licas dos polimorfismos estudados n?o mostraram diferen?a estatisticamente significante entre os grupos DM1 e NG. Por?m o polimorfismo da GPx1 mostrou influ?ncia na atividade eritrocit?ria da enzima, observando-se diminui??o da atividade nos indiv?duos com DM1 que possu?am a variante polim?rfica T (p=0,012). J? para o polimorfismo Ala16Val da SOD2 observou-se eleva??o da RAC para aqueles indiv?duos diab?ticos que possu?am o alelo G (p<0,05). O conjunto dos dados sugere que o controle glic?mico parece ser o fator predominante para o surgimento de altera??es no perfil lip?dico, fun??o renal e no sistema antioxidante, por?m a presen?a dos polimorfismos estudados possam, pelo menos em parte, contribuir para o aparecimento de complica??es
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Malaspina, Andrea. "Amyotrophic lateral sclerosis (ALS) : analysis of differential gene expression in spinal cord and study of the Cu/Zn superoxide dismutase gene (SOD1) in familial ALS cases (FALS) of Italian origins." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248425.

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Andrade, Alice Tavares Reis 1977. "Evolução do gene sodC nas bactérias naturalmente transformáveis Neisseria meningitidis e Haemophilus influenzae." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314453.

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Orientador: Marcelo Lancellotti
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Em 1998, foi relatada a transferência lateral do gene sodC do gênero Haemophilus para a espécie Neisseria meningitidis. Sabe-se que, nestes dois grupos a dinâmica deste gene é bastante distinta. Este trabalho tem por objetivo estimar árvores filogenéticas que possam apontar qual a espécie do gênero Haemophilus compartilhou o gene sodC com a espécie N. meningitidis. Testes de seleção positiva foram empregados no intuito de avaliar quais forças evolutivas estão subjacentes ao processo de diversificação molecular do gene nestas espécies ao longo do tempo. Além disso, foi realizada uma modelagem protéica computacional por homogia para avaliar quais substituições de aminoácidos tinham impacto no processo adaptativo da enzima nas espécies consideradas. Ao se reconstruir uma filogenia para o gene sodC, foi constatado que a origem deste gene na espécie H. influenzae é distinta. Um grupo de linhagens recebeu o gene, provavelmente por transferência lateral, da espécie H. haemolyticus, enquanto o outro grupo recebeu o gene da espécie H. parainfluenzae. Neste grupo, o gene sofreu pseudogeneização. Foi observado também que as sequências de N. meningitidis agrupam com as sequências que compartilham um ancestral comum com a espécie H. haemolyticus, porém as sequências do meningococo formam um ramo distinto dentro deste clado. Dada à alta clonalidade das sequências de N. meningitidis, foi constatado que o evento de transferência lateral de genes foi muito recente na escala do tempo. O teste de seleção positiva demonstrou que seleção positiva está atuando especificamente no ramo da árvore que compartilha um ancestral comum com a espécie H. haemolyticus, através da modificação de uma alanina por uma serina na posição 72, embora a nota geral da árvore tenha sido menor que 1. Sabe-se que pseudogenes, por não codificarem uma proteína ativa e, portanto, por não estarem sob nenhum tipo de restrição funcional, estão sob uma ação maior da deriva genética. Portanto, diferentes forças evolutivas estão governando a evolução deste gene nas espécies consideradas. A modelagem protéica concluiu que tal modificação contribuiu para o aumento do potencial redox do sítio ativo. Desta forma, a ação da seleção positiva sob um único resíduo de aminoácido foi benéfica para a função da enzima como um todo
Abstract: In 1998, it was reported the lateral transfer of the sodC gene from the genus Haemophilus to Neisseria meningitidis. It is known that this two groups show a quite distinct dynamics of this gene. This study aims to estimate phylogenetic trees that might point to which species of the genus Haemophilus shared the sodC gene with N. meningitidis. In addition, tests of positive selection were employed in order to assess which evolutionary forces are governing the process of molecular diversification of the gene in these species through time. Moreover, we performed a computational protein modeling by homology to asses which amino acids substitutions had an impact on the adaptative process of the enzyme in the species considered. A phylogeny of the sodC gene was reconstructed and it was found that this gene in H. influenzae has two different origins. A group of lineages has received the gene, probably by lateral transfer, from H. haemolyticus, whereas the other group has received the gene from H. parainfluenzae. In the latter, the gene has become a pseudogene. It was also observed that the sequences from N. meningitides group together with those sequences that share a common ancestor with H. haemolyticus, but they form a distinct branch within this clade. Given the high clonality of the sequences from N. meningitidis, it was found that the lateral gene transfer event is very recent in the time scale. A test of positive selection showed that positive selection is acting specifically in the branch that shares a common ancestor with H. haemolyticus through the substitution of an alanine to a serine at position 72, though the overall score of the tree is less than one. It is known that pseudogenes do not encode active proteins and therefore they are not under any kind of functional constraints, so they are under greater influence of genetic drift. Thus, it was concluded that different forces are driving the evolution of this gene in the species considered here. Protein modeling concluded that this modification contributed to the increase in the redox potencial of the active site. Thus the action of positive selection under a single amino acid residue was beneficial to the function of the enzyme as whole
Mestrado
Bioquimica
Mestra em Biologia Funcional e Molecular
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Turner, Taylor Brian. "Cloning and Characterization of the Salt Overly Sensitive 1 (SOS1) Gene in Chenopodium quinoa WILLD." BYU ScholarsArchive, 2007. https://scholarsarchive.byu.edu/etd/1023.

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Salt tolerance is a commercially important trait that affects plant species around the globe. Cellular response to saline environments is a well studied but complex system that is far from being completely understood. The SALT OVERLY SENSITIVE 1 (SOS1) gene is a critical component of salt tolerance in many species, encoding a plasma membrane Na+/H+ antiporter that plays an important role in germination and growth in saline environments. Here we report a preliminary investigation of salt tolerance in quinoa (Chenopodium quinoa Willd.). Quinoa is a halophytic grain crop of the Chenopodiaceae family with impressive nutritional content and an increasing world-wide market. Many quinoa varieties have impressive salt tolerance characteristics and research suggests quinoa may utilize novel mechanisms to confer salt tolerance. At this time there is no published data on the molecular characteristics of those mechanisms. We report the identification and sequencing of the SOS1 gene in quinoa, including a full length cDNA sequence of 3490 bp and a full length genomic clone of 21314 bp. Sequence analysis predicts the quinoa SOS1 homolog spans 23 exons and is comprised of 3474 bp of coding sequence (excluding the stop codon). Introns comprise 17840 bp of the genomic clone and range in size from 77 to 2123 bp. The predicted protein contains 1158 amino acid residues and aligns closely with SOS1 homologs of other species. The quinoa SOS1 homolog contains two putative domains, a Nhap cation-antiporter domain and a cyclic-nucleotide binding domain. Sequence analyses of both cDNA fragments and intron fragments suggest that two SOS1 loci are present in the quinoa genome that are likely orthologous loci derived from the ancestral diploid genomes of the modern allotetraploid quinoa genome. This report represents the first molecular characterization of a putative salt-tolerance gene in C. quinoa.
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Books on the topic "SOD1 gene"

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Nicholson, Katharine A., and James D. Berry. Amyotrophic Lateral Sclerosis Clinical Trials. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0030.

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The current state of amyotrophic lateral sclerosis (ALS) trial design is best understood within the context of ALS research over the past quarter century. Before the early 1990s, trials in ALS were typically small and clinical trial methodology was less rigorous than it is today. With the discovery of the SOD1 gene mutation in the early 1990s, a new era of excitement and innovation for ALS research began. Since then, the number of ALS trials has steadily increased and trial design and methodology has become increasingly sophisticated.
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Book chapters on the topic "SOD1 gene"

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Tower, John. "Superoxide Dismutase (SOD) Genes and Aging in Drosophila." In Life Extension, 67–81. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18326-8_3.

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Inoue, Masayasu, and Nobukazu Watanabe. "Targeting Sod by Gene and Protein Engineering and Inhibition of Oxidative Stress in Various Diseases." In Advances in Experimental Medicine and Biology, 5–12. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5730-8_2.

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Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "SOD1." In The Gene Knockout FactsBook, 956–57. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50523-8.

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Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "SOD2." In The Gene Knockout FactsBook, 958–59. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50524-x.

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Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "SOD3." In The Gene Knockout FactsBook, 960. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50525-1.

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Logroscino, Giancarlo, and Adriano Chiò. "Amyotrophic lateral sclerosis (ALS) and fronto-temporal dementia (FTD)." In Oxford Textbook of Neurologic and Neuropsychiatric Epidemiology, edited by Carol Brayne, Valery L. Feigin, Lenore J. Launer, and Giancarlo Logroscino, 119–32. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198749493.003.0013.

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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are both progressive neurodegenerative disorders considered part of the same spectrum of overlapping genetic neurological and clinical diseases. ALS involves primarily the motor system, but recent advances consider also the involvement of other parts of the central nervous system (CNS), primarily cognition. FTD presents clinical syndromes with behavioural and language variants, but some subtypes have motor involvement of the motor pathways and/or of some extrapyramidal areas. C9ORF72 is a gene responsible for 7–10% of cases both of sporadic and familial of ALS and FTD as well. Both ALS and FTD are rare diseases with incidence around 3/100,000 for ALS in Europe and FTD probably lower. The data for ALS have been mainly produced in Europe by a system of registries in limited territories. FTD data from populations are sparse. Trauma, smoking, military service, and agricultural occupation are environmental probable risk factors for ALS. No analytic data are available for FTD. FUS, TARDP, SOD 1, and C9ORF72 are the main genes involved in ALS, while C9ORF72, PGR, and TAU have been reported in FTD.
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Wingbermüuhle, Ellen, and Ineke van der Burgt. "Noonan Syndrome." In Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.003.0026.

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Noonan syndrome (NS) is a genetic disorder characterized by short stature, typical facial dysmorphology, and congenital heart defects. Noonan syndrome may occur on a sporadic basis or in a pattern consistent with autosomal dominant inheritance, with a predominance of maternal transmission (Noonan 1994). In approximately 50% of the patients with definite NS, a missense mutation is found in the PTPN11 gene on chromosome 12. PTPN11 is one of the genes of the Ras-MAPK pathway, a signal transduction cascade that has been studied extensively for its role in human oncogenesis. The signaling cascade regulates cell proliferation, differentiation, and survival. PTPN11 encodes the nonreceptor protein tyrosine phosphatase SHP-2. The mutations associated with NS result in a gain of function of SHP-2 (Tartaglia and Gelb 2005). Recently, activating mutations in other genes of the Ras-MAPK pathway (SOS1, KRAS, RAF1) were found as the causative dominant mutations in NS. These findings establish hyperactive Ras as a cause of the developmental abnormalities seen in NS (Schubbert et al. 2007). The diagnosis is made on clinical grounds, by observation of key features. Establishing the diagnosis can be very difficult, especially at an older age. There is great variability in expression, and mild expression is likely to be overlooked. Improvement of the phenotype occurs with increasing age. The age-related change of facial appearance can be subtle, especially at older age. Several scoring systems have been devised to guide the diagnostic process). The most recent scoring system was developed in 1994 (Van der Burgt et al. 1994). The incidence of NS is estimated to be between 1:1,000 and 1:2,500 live births (Mendez and Opitz 1985). Further details on the various medical aspects of NS (e.g., congenital heart defects, skeletal and urethrogenital abnormalities, growth delay) can be found in Van der Burgt (2007). A number of conditions have phenotypes strikingly similar to NS. The first is Turner syndrome (45, X0), a well-known chromosomal abnormality in girls. A group of distinct syndromes with partially overlapping phenotypes also exist in which causative mutations are also found in genes of the RAS-MAPK pathway.
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Lee, Chanjae, Min K. Bae, and Sung-Jae Lee. "An Antioxidant Defense System in Radiation-Resistant Bacterium Deinococcus geothermalis against Oxidative Stress." In Antioxidants - Benefits, Sources, Mechanisms of Action. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95658.

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A radiation-resistant bacterium, Deinococcus geothermalis has various stress response mechanisms, including antioxidation. Features that maintain vitality at high radiation doses include the following: enzymatic scavengers of ROS such as catalase, SOD, and peroxidase; strain-specific DNA repair systems such as Deinococcal unique proteins; non-enzymatic responses such as manganese complexes, carotenoids, and DNA-binding proteins. This chapter summarizes the primary response mechanism by redox balance centered on the cystine transporter. It also reviews action characteristics of DNA-binding protein Dps and a putative LysR family protein, and effects on loss of function of the carotenoid biosynthesis genes by transposition of insertion sequences. Environmental adaptation and molecular evolution of radiation-resistant bacterium are also considered to explain the potentials of molecular behavior induced by oxidative stress.
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Zhan, Xianquan, and Na Li. "The Anti-Cancer Effects of Anti-Parasite Drug Ivermectin in Ovarian Cancer." In Ovarian Cancer - Updates in Tumour Biology and Therapeutics [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95556.

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Ivermectin is an old, common, and classic anti-parasite drug, which has been found to have a broad-spectrum anti-cancer effect on multiple human cancers. This chapter will focus on the anti-cancer effects of ivermectin on ovarian cancer. First, ivermectin was found to suppress cell proliferation and growth, block cell cycle progression, and promote cell apoptosis in ovarian cancer. Second, drug pathway network, qRT-PCR, and immunoaffinity blot analyses found that ivermectin acts through molecular networks to target the key molecules in energy metabolism pathways, including PFKP in glycolysis, IDH2 and IDH3B in Kreb’s cycle, ND2, ND5, CYTB, and UQCRH in oxidative phosphorylation, and MCT1 and MCT4 in lactate shuttle, to inhibit ovarian cancer growth. Third, the integrative analysis of TCGA transcriptomics and mitochondrial proteomics in ovarian cancer revealed that 16 survival-related lncRNAs were mediated by ivermectin, SILAC quantitative proteomics analysis revealed that ivermectin extensively inhibited the expressions of RNA-binding protein EIF4A3 and 116 EIF4A3-interacted genes including those key molecules in energy metabolism pathways, and also those lncRNAs regulated EIF4A3-mRNA axes. Thus, ivermectin mediated lncRNA-EIF4A3-mRNA axes in ovarian cancer to exert its anticancer capability. Further, lasso regression identified the prognostic model of ivermectin-related three-lncRNA signature (ZNRF3-AS1, SOS1-IT1, and LINC00565), which is significantly associated with overall survival and clinicopathologic characteristics in ovarian cancer patients. These ivermectin-related molecular pattern alterations benefit for prognostic assessment and personalized drug therapy toward 3P medicine practice in ovarian cancer.
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"Flachmann (1997) studied the PS II antennae composition under varying light conditions in tobacc o plants transformed with antisense echnique. An increase of P S II antenna size was observed under low irradiance and also higher LHC II content. The results also suggested that LHC II biogenesis is perhaps not controlled by transcription. The foregone account of different studies using transgenics have inmmensely helped by adding new dimension in our understanding of the structure and function of the photosystem core complexes and of the antennae systems related to both PS II and PS I. A fairly larg e number of studies have also been directed using transgenic technology to understand the process of photoinhibition. Tyystjarvi et al., (1999b) have made a study of photoinhibition of PS II in tobacco an d poplar plants. The tobacco cultivars were expressed with bacterial gov gene in the cytosol and Fe SOD gene from Arabidopsis thaliana rather in the chloroplast. The transformations were affected as an overexpression of glutathione reductase in tobacco and superoxide dismutase in poplar. This transformation resulted in the activities of glutathione reductase in tobacco leaves and superoxide dismutase in poplars were five to eight times higher than in the untransformed plants. The experiments of the authors (Tyystjarvi et al., (1999b) with the transformed plants have led to some important clues regarding the identity of Active Oxygen Species and the mechanisms. There was a lack of protection by overproduction of SOD in the stroma, suggesting that superoxide is not accessible to dismutation by the stromal enzymes. Protection by glutathione reductase suggested that a soluble reductant has a limited chance to trap the species before it reacts with PS II RC. It was concluded (Tyystjarvi et al., 1999b) that much further work is required to understand the molecular mechanism of loss of PS II activity. H.Y.Yamamoto and his scholars have made several studies manipulating the levels of the enzymes of the xanthophyll cycle through transgenic techniques. Verhoeven et al., (2001) have investigated the effect of suppression of Z in tobacco plants with an antisense construct of VDE in growth chambers. Under short-term (2 or 3h) high light treatment, antisense plants had a greater reduction in Fv/Fm ratio relative to wild type, which implied a greater susceptibity to photoinhibition. In the long-term highlight stress experiment, the antisense plants had significant reduction in Fv/Fm. The authors concluded that XC-dependent energy dissipiation is critical for photoprotection in tobacco under excess light in the long term." In Photosynthesis, 119–22. CRC Press, 2004. http://dx.doi.org/10.1201/9781482294446-20.

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Conference papers on the topic "SOD1 gene"

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Zhang, Shuyu, Jie Zheng, Jori E. Avery, Jinchang Wu, and Wei-Qun Ding. "Abstract 4194: The superoxide dismutase 1 (SOD1) 3′-UTR maintains high expression of the SOD1 gene in cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4194.

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Erdman, Vera Viktorovna, Timur Ruslanovich Nasibullin, Ilsiar Avkhatovna Tuktarova, Yanina Rimovna Timasheva, Ksenia Vladimirovna Danilko, Alisa Zaurovna Matua, and Tatiana Viktorovna Viktorova. "POLYMORPHISM OF ANTIOXIDANT DEFENSE GENES AND LIFESPAN." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.07.

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In the ethnic group of Russians, residents of the Republic of Bashkortostan, age-dependent changes in the alleles and genotypes frequencies in SOD1, SOD2, PON1, PON2, NQO1, GPX1 genes SNVs were found. Enzymes, encoded by these genes, are involved in the metabolism of reactive oxygen species of the first and second stages, as well as toxic compounds of endogenous and exogenous nature.
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Fomenko, M. P., A. M. Menzheritsky, and G. V. Karantysh. "INFLUENCE OF PINEALON ON EXPRESSION OF GENES OF PRO- AND ANTIOXIDANT ENZYMES AND FREE RADICAL PROCESSES IN RATS IN THE MODEL OF SUGAR DIABETES." In STATE AND DEVELOPMENT PROSPECTS OF AGRIBUSINESS Volume 2. DSTU-Print, 2020. http://dx.doi.org/10.23947/interagro.2020.2.232-234.

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The article presents an analysis of the effect of pinealon on free radical processes and the level of expression of the SOD1, GPX4 and GSR genes in the rat hippocampus in a model of streptozotocininduced diabetes (type I diabetes mellitus). It has been established that when modeling diabetes in the hippocampus, intensification of radically radical processes is observed: the level of prooxidants increases, the level of antioxidants decreases, as well as the level of expression of antioxidant genes. With the introduction of pinealone in dosages of 50 or 100 ng/kg in the model of diabetes mellitus, the pro-antioxidant balance shifts towards a decrease in the production of free radicals and an increase in antioxidant protection. Pinealon at a dosage of 100 ng/kg is more effective.
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Pinkart, Holly C., and Michael C. Storrie-Lombardi. "Diversity, evolution, and horizontal gene transfer (HGT) in soda lakes." In Optical Engineering + Applications, edited by Richard B. Hoover, Gilbert V. Levin, Alexei Y. Rozanov, and Paul C. W. Davies. SPIE, 2007. http://dx.doi.org/10.1117/12.736267.

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Soerheim, I., D. DeMeo, G. Washko, A. Litonjua, D. Sparrow, R. Bowler, P. Bakke, E. Silverman, and C. Hersh. "Polymorphisms in the SOD3 Gene Are Associated with Emphysema in COPD." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3657.

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Luisa Boldim Vaggione, Maria, and Marcondes Cavalcante Franca Junior. "Esclerose Lateral Amiotrófica familiar ligada aos genes SOD1 e VAPB: frequência e correlação genótipo-fenótipo." In XXV Congresso de Iniciação Cientifica da Unicamp. Campinas - SP, Brazil: Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-77828.

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He, Chao, Shubha Murthy, Alan Ryan, and A. Brent Carter. "Overexpression Of Cu,Zn-SOD Augments Proinflammatory Cytokines Gene Expression Via Mitochondrial H2O2 Generation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2693.

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8

Lilja, Andrew, Steven Bozinovski, Bernadette Scott, Elisabetta De Luca, Paul Hertzog, and Gary Anderson. "Embryonic Stem Cell-derived Macrophage-based Gene Replacement Therapy In SOD3-deficient Mice Ameliorates LPS-induced Lung Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5273.

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9

Pharmawati, Made, and Eka Maya Kurniasih. "Characterization of partial DREB and SOD genes from three Bali local rice cultivars." In TOWARDS THE SUSTAINABLE USE OF BIODIVERSITY IN A CHANGING ENVIRONMENT: FROM BASIC TO APPLIED RESEARCH: Proceeding of the 4th International Conference on Biological Science. Author(s), 2016. http://dx.doi.org/10.1063/1.4953511.

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Reports on the topic "SOD1 gene"

1

Li, Chuan-Yaun. Molecular dissection of the roles of the SOD genes in mammalian response to low dose irradiation. Office of Scientific and Technical Information (OSTI), January 2009. http://dx.doi.org/10.2172/946501.

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2

Chuang, Eric Y. Molecular dissection of the roles of the SOD genes in mammalian response to low dose irradiation. Office of Scientific and Technical Information (OSTI), August 2006. http://dx.doi.org/10.2172/928041.

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