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Title: Investigation of the oxygen transfer properties of molybdenum-oxide(Et(2)dtc)(2)(THF)(2)I(2).
Creator: Falzone, Samuel, Florida Atlantic University, Baird, Donald M.
Abstract/Description: Mo2o3 (Et2dtc) 2 (THF) 2I2, readily reduces various oxides. The Mo vio2+2 product of this reaction oxidizes TPP to triphenylphosphine oxide. The transient Mo(iv) species formed in the later reaction rapidly and irreversibly reacts with excess Mo vio2+2 to form the original Mo2 o3 4+ complex. These reactions can be also be coupled to provide catalytic oxygen transfer from PNO to TPP. This catalytic cycle can be monitored using a reverse phase high pressure liquid chromatography method that...
Show moreMo2o3 (Et2dtc) 2 (THF) 2I2, readily reduces various oxides. The Mo vio2+2 product of this reaction oxidizes TPP to triphenylphosphine oxide. The transient Mo(iv) species formed in the later reaction rapidly and irreversibly reacts with excess Mo vio2+2 to form the original Mo2 o3 4+ complex. These reactions can be also be coupled to provide catalytic oxygen transfer from PNO to TPP. This catalytic cycle can be monitored using a reverse phase high pressure liquid chromatography method that will also be discussed. The oxides chosen ranged from pyridine-N-oxide to the biological substrates: diphenylsufoxide, DMSO, nicotinamide-N-oxide, and biotin-S-oxide. Since Mo2o3 (Et2dtc) 2 (THF) 2I2 has the ability to abstract oxygen from these biologically significant substrates, it may result in the reconsideration of the role of Mo(V) complexes in catalytic cycles.
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Date Issued: 1989
PURL: http://purl.flvc.org/fcla/dt/14537
Subject Headings: Molybdenum, Oxidation-reduction reaction
Format: Document (PDF)

Title: Methionine sulfoxide reductase deficiency leads to mitochondrial dysfunction in Drosophila melanogaster.
Creator: Verriotto, Jennifer., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Mitochondria are a major source of reactive oxygen species and are particularly vulnerable to oxidative stress. Mitochondrial dysfunction, methionine oxidation, and oxidative stress are thought to play a role in both the aging process and several neurodegenerative diseases. Two major classes of methionine sulfoxide reductases, designated MsrA and MsrB are enzymes that function to repair the enatiomers of methionine sulfoxide, met-(o)-S and met-(o)- R, respectively. This study focuses on the...
Show moreMitochondria are a major source of reactive oxygen species and are particularly vulnerable to oxidative stress. Mitochondrial dysfunction, methionine oxidation, and oxidative stress are thought to play a role in both the aging process and several neurodegenerative diseases. Two major classes of methionine sulfoxide reductases, designated MsrA and MsrB are enzymes that function to repair the enatiomers of methionine sulfoxide, met-(o)-S and met-(o)- R, respectively. This study focuses on the effect of Msr deficiencies on mitochondrial function by utilizing mutant alleles of MsrA and MsrB. The data show that loss of only one form of Msr in the mitochondria does not completely impair the function of the mitochondria. However, loss of both Msr proteins within the mitochondria leads to an increased ROS production and a diminished energy output of the mitochondria. These results support the hypothesis that Msr plays a key role in proper mitochondrial function.
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Date Issued: 2011
PURL: http://purl.flvc.org/FAU/3174310
Subject Headings: Oxidation-reduction reaction, Proteins, Chemical modification, Genetic regulation
Format: Document (PDF)

Title: Protective Mechanisms of Granulocyte-Colony Stimulating Factor Against Experimental Models of Stroke.
Creator: Menzie-Suderam, Janet, Wu, Jang-Yen, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biomedical Science
Abstract/Description: Ischemic stroke has a multiplicity of pathophysiological mechanisms. Granulocyte-colony stimulating factor (G-CSF) is an endogenous growth factor that exerts a diverse range of neuroprotection against ischemic stroke. Several lines of evidence demonstrated the contribution of endoplasmic reticulum (ER) in apoptotic cell death involving ischemia. Cell culture of undifferentiated PC12 cells were subjected to 10mM glutamate and selected doses of G-CSF (25ng/ml, 50ng/ml, 100ng/ml and 250ng/ml)...
Show moreIschemic stroke has a multiplicity of pathophysiological mechanisms. Granulocyte-colony stimulating factor (G-CSF) is an endogenous growth factor that exerts a diverse range of neuroprotection against ischemic stroke. Several lines of evidence demonstrated the contribution of endoplasmic reticulum (ER) in apoptotic cell death involving ischemia. Cell culture of undifferentiated PC12 cells were subjected to 10mM glutamate and selected doses of G-CSF (25ng/ml, 50ng/ml, 100ng/ml and 250ng/ml) for 24 hours. Cell viability, expression of the G-CSF receptor and expression level of CHOP were assessed in vitro. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO). Rats were subcutaneously injected with G-CSF (n= 15; 50ug/kg body weight) 24 hours post-MCAO for 4 days. Vehicle treated rats were administered 5% dextrose for 1 day (n=4) or 4 days (n=16). Sham-operated rats (n=9) were not subjected to MCAO. Neurological deficit and infarct volume were measured while expression levels of pAKT, Bcl2, Bax, Bak, cleaved caspase-3, GRP78, ATF4, ATF6, p-p38MAPK, pJNK, CHOP and HSP27 were analyzed by western blotting. In vitro G-CSF receptor was expressed on undifferentiated PC12 cell, and an optimal dose of 50 ng/ml G-CSF significantly protected these cells against glutamate-induced cytotoxicity (P < 0.05). G-CSF significantly down-regulated (P < 0.01) the ER stressinduced pro-apoptotic marker CHOP in vitro. In vivo, G-CSF reduced infarct volume to 50% while significantly improved neurological deficit compared to vehicle rats. G-CSF significantly (P < 0.05) up-regulated pro-survival proteins pAKT and Bcl2 while downregulating pro-apoptotic proteins Bax, Bak and cleaved caspase 3 in the ischemic brain. It also significantly (P < 0.05) downregulated the ER intraluminal stress sensor GRP78, proteins of ER stress induced intracellular pathway; ATF4, ATF6, p-p38MAPK, pJNK and the ER stress induced apoptotic marker CHOP, which suggests that ER stress is being ameliorated by G-CSF treatment. G-CSF also reduced the level of HSP27, providing additional evidence of cellular stress reduction. G-CSF treatment increased cell survival by attenuating both general pro-apoptotic proteins and specific effector proteins in the ER stress induced apoptotic pathways. Our data has provided new insight into the anti-apoptotic mechanism of G-CSF, especially as it relates to ER stress induced apoptosis in ischemia.
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FA00004795, http://purl.flvc.org/fau/fd/FA00004795
Subject Headings: Cerebral ischemia--Protection., Apoptosis., Rats as laboratory animals., Cellular signal transduction., Oxidation-reduction reaction.
Format: Document (PDF)

Title: Protective mechanism of Sulindac against animal model of ischemic stroke.
Creator: Modi, Jigar P., Charles E. Schmidt College of Medicine, Department of Biological Sciences
Abstract/Description: The Effect of Sulindac was studied on an animal model of ischemic stroke. Sulindac, a non steroid anti inflammatory drug (NSAID) could protect cell death due to hypoxia/reoxygenation. This drug was given 2 days before and 24 hrs after ischemia until animals were sacrificed on 3rd or 11th day. Infarct size was measured for these animals. Sulindac induced Hsp 27 in ischemic penumbra and core on Day 3 & 11 with uncoated nylon suture which shows its cell-survival and anti-apoptotic activity. Also...
Show moreThe Effect of Sulindac was studied on an animal model of ischemic stroke. Sulindac, a non steroid anti inflammatory drug (NSAID) could protect cell death due to hypoxia/reoxygenation. This drug was given 2 days before and 24 hrs after ischemia until animals were sacrificed on 3rd or 11th day. Infarct size was measured for these animals. Sulindac induced Hsp 27 in ischemic penumbra and core on Day 3 & 11 with uncoated nylon suture which shows its cell-survival and anti-apoptotic activity. Also, it increased expression of cell survival markers such as Akt, Bcl2 & Grp 78 in ischemic penumbra and core. With silicon suture it reduced expression of Hsp 27 in ischemic penumbra and core, alleviating cell stress and having pro-survival and anti-stress effects. In conclusion sulindac may have excellent potential as neuro protective agent against oxidative stress in cerebral ischemia.
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Date Issued: 2011
PURL: http://purl.flvc.org/FAU/3333056
Subject Headings: Apoptosis, Biochemical markers, Diagnostic use, Oxidation reduction reaction, Cerebral ischemia, Prevention
Format: Document (PDF)

Title: Methionine sulfoxide reductases: studies on the reducing requirements and role in the metabolism of sulindac.
Creator: Brunell, David J., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: The methionine sulfoxide reductase (Msr) enzymes catalyze the reduction of methionine sulfoxide (Met(O)) to methionine. The Msr enzymes protect cells against oxidative stress and may have a role in aging. The MsrA family of enzymes reduces stereospecifically the S epimer of free and protein-bound Met(O) while the MsrB family reduces the R epimer of Met(O) in proteins. It has been generally accepted, primarily from studies on MsrA, that the biological reductant for the Msr enzymes is...
Show moreThe methionine sulfoxide reductase (Msr) enzymes catalyze the reduction of methionine sulfoxide (Met(O)) to methionine. The Msr enzymes protect cells against oxidative stress and may have a role in aging. The MsrA family of enzymes reduces stereospecifically the S epimer of free and protein-bound Met(O) while the MsrB family reduces the R epimer of Met(O) in proteins. It has been generally accepted, primarily from studies on MsrA, that the biological reductant for the Msr enzymes is thioredoxin (Trx), although high levels of dithiothreitol (DTT) can be used as the reductant in vitro. In contrast, certain MsrB enzymes show less than 10% of the activity with Trx as compared to DTT. This raises the possibility that in animal cells Trx may not be the direct hydrogen donor for the MsrB enzymes. Studies with bovine liver extracts have shown that thionein, the apoprotein of metallothionein, can function as a reductant for the Msr proteins. Certain selenium compounds such as selenocystamine and selenocystine can also serve as potent reducing agents for the Msr enzymes. Since an increased activity of Msr enzymes can reduce the level of oxidative damage in tissues, compounds that could activate Msr may have therapeutic potential. A high-throughput screening assay has been developed to screen large chemical libraries to find activators of MsrA, as well as specific inhibitors that could be useful research tools. This study will be done in collaboration with The Scripps Florida Research Institute. Sulindac was originally developed as a non-steroidal anti-inflammatory drug but has also shown efficacy in the treatment of certain cancers. The S epimer of sulindac is known to be reduced by MsrA, but the enzymes responsible for reduction of the R epimer are not known., An activity has been purified from rat liver which is capable of reducing the R epimers of sulindac, free Met(O) and a dabsylated Met(O) substrate, the latter suggesting that this enzyme may have properties similar t o the MsrB enzymes. The oxidation of the epimers of sulindac to sulindac sulfone has also been characterized, and the members of the cytochrome P450 family involved in the oxidation have been identified.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/227979
Subject Headings: Cellular signal transduction, Proteins, Chemical modification, Biochemical markers, Oxidation-reduction reaction
Format: Document (PDF)

Title: Role of Methionine Sulfoxide Reductase (MsrA) on Aging and Oxidative Stress in Drosophila.
Creator: Foss, Katie, Binninger, David, Florida Atlantic University
Abstract/Description: Oxidative damage is an inevitable consequence of aerobic respiration. Methionine sulfoxide reductases (Msr) are a group of enzymes that function to repair oxidized methionine residues in both free methionine and methionine in proteins. MsrA was the first of these enzymes to be discovered and is the most thoroughly studied. It is thought to play a role in both the aging process and probably several neurodegenerative diseases. I recently obtained a strain of Drosophila that was reported to have...
Show moreOxidative damage is an inevitable consequence of aerobic respiration. Methionine sulfoxide reductases (Msr) are a group of enzymes that function to repair oxidized methionine residues in both free methionine and methionine in proteins. MsrA was the first of these enzymes to be discovered and is the most thoroughly studied. It is thought to play a role in both the aging process and probably several neurodegenerative diseases. I recently obtained a strain of Drosophila that was reported to have a P-element transposon located within Exon 2 (part of the open reading frame) of the eip71cd gene, which is the Drosophila homolog of MsrA. Thus, the transposon insertion should disrupt expression of the msrA gene. I did a series of experiments to "jump out" the P-element in an effort to recover two types of isogenic strains. The first would be a null mutation of the MsrA gene created by deletion of flanking genomic DNA when the P-element excised from the chromosome. The second would be a precise excision of the P-element, which would restore the genetic locus to its original structure. This study looks at the effect of a null mutant of the MsrA gene on aging and resistance to oxidative stress.
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Date Issued: 2006
PURL: http://purl.flvc.org/fau/fd/FA00000772
Subject Headings: Genetic regulation, Oxidation-reduction reaction, Antioxidants, Oxygen--Physiological effect, Proteins--Chemical modification
Format: Document (PDF)

Title: Methionine sulfoxide reductase A (MsrA) and aging in the anoxia-tolerant freshwater turtle (Trachemys scripta).
Creator: Bruce, Lynsey Erin., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: The enzyme Methionine sulfoxide reductase A (MsrA) repairs oxidized proteins, and may act as a scavenger of reactive oxygen species (ROS), making it a potential therapeutic target for age-related neurodegenerative diseases. The anoxia-tolerant turtle offers a unique model to observe the effects of oxidative stress on a system that maintains neuronal function following anoxia and reoxygenation, and that ages without senescence. MsrA is present in both the mitochondria and cytosol, with protein...
Show moreThe enzyme Methionine sulfoxide reductase A (MsrA) repairs oxidized proteins, and may act as a scavenger of reactive oxygen species (ROS), making it a potential therapeutic target for age-related neurodegenerative diseases. The anoxia-tolerant turtle offers a unique model to observe the effects of oxidative stress on a system that maintains neuronal function following anoxia and reoxygenation, and that ages without senescence. MsrA is present in both the mitochondria and cytosol, with protein levels increasing respectively 3- and 4-fold over 4 hours of anoxia, and remaining 2-fold higher than basal upon reoxygenation. MsrA was knocked down in neuronally-enriched cell cultures via RNAi transfection. Propidium iodide staining showed no significant cell death during anoxia, but this increased 7-fold upon reoxygenation, suggesting a role for MsrA in ROS suppression during reperfusion. This is the first report in any system of MsrA transcript and protein levels being regulated by oxygen levels.
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Date Issued: 2010
PURL: http://purl.flvc.org/FAU/2683139
Subject Headings: Oxidation-reduction reaction, Proteins, Chemical modification, Turtles, Physiology, Oxygen, Physiological effect, Aging, Molecular aspects
Format: Document (PDF)

Title: Molecular and phenotypic characterization of MsrA MsrB mutants of Drosophila melanogaster.
Creator: Robbins, Kelli., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Aging is a multifactoral biological process of progressive and deleterious changes partially attributed to a build up of oxidatively damaged biomolecules resulting from attacks by free radicals. Methionine sulfoxide reductases (Msrs) are enzymes that repair oxidized methionine (Met) residues found in proteins. Oxidized Met produces two enantiomers, Met-S-(o) and Met-R-(o), reduced by MsrA and MsrB respectively. Unlike other model organisms, our MsrA null fly mutant did not display increased...
Show moreAging is a multifactoral biological process of progressive and deleterious changes partially attributed to a build up of oxidatively damaged biomolecules resulting from attacks by free radicals. Methionine sulfoxide reductases (Msrs) are enzymes that repair oxidized methionine (Met) residues found in proteins. Oxidized Met produces two enantiomers, Met-S-(o) and Met-R-(o), reduced by MsrA and MsrB respectively. Unlike other model organisms, our MsrA null fly mutant did not display increased sensitivity to oxidative stress or shortened lifespan, suggesting that in Drosophila, having either a functional copy of either Msr is sufficient. Here, two Msr mutant types were phenotypically assayed against isogenic controls. Results suggest that only the loss of both MsrA and MsrB produces increased sensitivity to oxidative stress and shortened lifespan, while locomotor defects became more severe with the full Msr knockout fly.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/359920
Subject Headings: Genetic regulation, Oxidation-reduction reaction, Proteins, Chemical modification, Aging, Molecular aspects, Mutation (Biology), Cell metabolism, Mitochondrial DNA
Format: Document (PDF)

Title: Studies on the mechanism by which sulindac sensitizes cancer cells to oxidative stress.
Creator: Kreymerman, Alexander, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Sulindac is a known NSAID that has also been shown to have anti-cancer activity that is not related to its ability to inhibit COX 1 and 2. During the past 15 years there have been a large number of studies attempting to elucidate its mechanism of action. Our laboratory has shown that sulindac can both protect normal cells and enhance the killing of cancer cells under oxidative stress from H2O2 and TBHP. However, except for mitochondrial dysfunction and ROS production, the mechanism by which...
Show moreSulindac is a known NSAID that has also been shown to have anti-cancer activity that is not related to its ability to inhibit COX 1 and 2. During the past 15 years there have been a large number of studies attempting to elucidate its mechanism of action. Our laboratory has shown that sulindac can both protect normal cells and enhance the killing of cancer cells under oxidative stress from H2O2 and TBHP. However, except for mitochondrial dysfunction and ROS production, the mechanism by which sulindac sensitized the cancer cells to oxidative stress remains unknown. Results of this research project suggest that the effect of sulindac and oxidative stress not only involves mitochondrial ROS production, but also aspects of the preconditioning response. In normal cells this leads to survival by a preconditioning pathway, likely involving PKCε. . However, cancer cells react by initiating a pathway leading to apoptosis involving PKCδ.
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Date Issued: 2011
PURL: http://purl.flvc.org/FAU/3183124
Subject Headings: Proteins, Chemical modification, Cellular signal transduction, Biochemical markers, Diagnostic use, Drug resistance in cancer cells, Oxidation-reduction reaction
Format: Document (PDF)

Title: Role of methionine sulfoxide reductase in thermal-induced spreading depression coma in Drosophila melanogaster.
Creator: Schey, Karin., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Drosophila melanogaster encounter periods of increased temperature or decreased oxygen in its native environment. One consequence of these environmental stresses is increased production of reactive oxygen species that damage major molecules within cells. Another consequence is that flies fall into a protective coma where biological functions are minimized to conserve energy expenditures. This biological phenomenon is called spreading depression. The overarching aim of this project is to...
Show moreDrosophila melanogaster encounter periods of increased temperature or decreased oxygen in its native environment. One consequence of these environmental stresses is increased production of reactive oxygen species that damage major molecules within cells. Another consequence is that flies fall into a protective coma where biological functions are minimized to conserve energy expenditures. This biological phenomenon is called spreading depression. The overarching aim of this project is to determine if methionine sulfoxide reductases affect entrance or exit from the protective coma induced by acute thermal stress. The data revealed that complete deficiency of Msr in young flies causes a faster induction of the coma. In both young and old flies, Msr does not affect average recovery time but does affect the pattern of recovery from coma. Entrance into the coma is age dependent with young flies maintaining activity longer than before entering into the coma as compared to old flies.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3355873
Subject Headings: Cellular signal transduction, Proteins, Chemical modification, Spreading cortical depression, Oxidation-reduction reaction, Aging, Molecular aspects, Mutation (Biology)
Format: Document (PDF)

Title: Mechanism of neuroprotection in stroke-related models.
Creator: Pan, Chunliu., Charles E. Schmidt College of Science, Department of Chemistry and Biochemistry
Abstract/Description: Stroke is the third leading cause of mortality in the United States, and so far, no clinical interventions have been proved truly effective in stroke treatment. Stroke my result in hypoxia, glutamate release and oxidative stress, etc. The purpose of this dissertation study is to evaluate the neuroprotective effects of four drugs (taurine, G-CSF sulindac and DETC-MeSO) on PC12 cell line or primary cortical neuronal cell culture, and to understand the protective mechanisms underlying in three...
Show moreStroke is the third leading cause of mortality in the United States, and so far, no clinical interventions have been proved truly effective in stroke treatment. Stroke my result in hypoxia, glutamate release and oxidative stress, etc. The purpose of this dissertation study is to evaluate the neuroprotective effects of four drugs (taurine, G-CSF sulindac and DETC-MeSO) on PC12 cell line or primary cortical neuronal cell culture, and to understand the protective mechanisms underlying in three stroke-related models : hypoxia, excessive glutamtate and oxidative stress. In the first part of this dissertation, we studied the neuroprotection of taurine against oxidative stress induced by H2O2 in PC12 cells. Our results show that extracellular taurine exerts a neuroprotective function by restoring the expression of Bcl-2 and downregulation of the three Endoplasmic Reticulum (ER) stress markers : GRP78, Bim and CHOP/GADD153, suggesting that ER stress can be provoked by oxidative stress and can be suppressed by taurine. In the second part, glutamate excitotoxicity-induced ER stress was studied with dose and time as variables in primary cortical neurons. The results demonstrate that glutamate excitotoxicity leads to the activation of three ER stress pathways (PERK, ATF6 and IRE1) by initiating PERK first, ATF6 second and IRE1 pathway last. The third part of this dissertation studied the robust and beneficial protection of taurine in cortical neurons under hypoxia/reoxygenation or glutamate toxicity condition. We found that taurine suppresses the up-regulation of GRP778, Bim, caspase-12 and GADD153/CHOP induced by excessive glutamate or hypoxia/reoxygenation, suggesting that taurine may exert a protective function against hypoxia/regeneration by reducing the ER stress., Moreover, taurine can down-regulate the ratio of cleaved ATF6 and full length ATF6, and p-IRE1 expresssion, indicating that taurine inhibits the ER stress induced by hypoxia/reoxygenation or glutamate through suppressing ATF6 and IRE1 pathways. In the fourth part, the synergistic benefits of the combination of taurine and G-CSF, and the neuroprotective effects of G-CSF, sulindac or DETC-MeSO are studied in cortical neurons. Our results show that G-CSF, sulindac or DETC-MeSO can highly increase the neuron visibility by inhibiting ER stress induced by hypoxia/reoxygenation or glutamate toxicity. Furthermore, we proved that G-CSF or sulindac can significantly inhibit the activation of ATF6 or IRE1 pathway stimulated by hypoxia/reoxygenation, and DETC-MeSO can suppress the activation of both PERK and IRE1 pathways in primary neuron cultures. These findings provide promising and rational strategies for stroke therapy.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3352284
Subject Headings: Sulindac, Physiological effect, Taurine, Physiological effect, Cerebral ischemia, Prevention, Biochemical markers, Diagnostic use, Apoptosis, Oxidation reduction reaction
Format: Document (PDF)

Title: Phenotypic and behavioral effects of methionine sulfoxide reductase deficiency and oxidative stress in Drosophila melanogaster.
Creator: Mulholland, Kori., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Harman's theory of aging proposes that a buildup of damaging reactive oxygen species (ROS) is one of the primary causes of the deleterious symptoms attributed to aging. Cellular defenses in the form of antioxidants have evolved to combat ROS and reverse damage; one such group is the methionine sulfoxide reductases (Msr), which function to reduce oxidized methionine. MsrA reduces the S enantiomer of methionine sulfoxide, Met-S-(o), while MsrB reduces the R enantiomer, Met-R-(o). The focus of...
Show moreHarman's theory of aging proposes that a buildup of damaging reactive oxygen species (ROS) is one of the primary causes of the deleterious symptoms attributed to aging. Cellular defenses in the form of antioxidants have evolved to combat ROS and reverse damage; one such group is the methionine sulfoxide reductases (Msr), which function to reduce oxidized methionine. MsrA reduces the S enantiomer of methionine sulfoxide, Met-S-(o), while MsrB reduces the R enantiomer, Met-R-(o). The focus of this study was to investigate how the absence of one or both forms of Msr affects locomotion in Drosophila using both traditional genetic mutants and more recently developed RNA interference (RNAi) strains. Results indicate that lack of MsrA does not affect locomotion. However, lack of MsrB drastically reduces rates of locomotion in all age classes. Furthermore, creation of an RNAi line capable of knocking down both MsrA and MsrB in progeny was completed.
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Date Issued: 2013
PURL: http://purl.flvc.org/fcla/dt/3362558
Subject Headings: Drosophila melanogaster, Genetics, Aging, Molecular aspects, Oxidative stress, Mitochondrial pathology, Cellular signal transduction, Oxidation-reduction reaction, Biochemical markers, Mutation (Biology)
Format: Document (PDF)

Title: Reduced Reproductivity and Larval Locomotion in the Absence of Methionine Sulfoxide Reductase in Drosophila.
Creator: Singkornrat, Diana, Binninger, David, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: The inevitable aging process can be partially attributed to the accumulation of oxidative damage that results from the action of free radicals. Methionine sulfoxide reductases (Msr) are a class of enzymes that repair oxidized methionine residues. The two known forms of Msr are MsrA and MsrB which reduce the R- and S- enantiomers of methionine sulfoxide, respectively. Our lab has created the first genetic animal model that is fully deficient for any Msr activity. Previously our lab showed that...
Show moreThe inevitable aging process can be partially attributed to the accumulation of oxidative damage that results from the action of free radicals. Methionine sulfoxide reductases (Msr) are a class of enzymes that repair oxidized methionine residues. The two known forms of Msr are MsrA and MsrB which reduce the R- and S- enantiomers of methionine sulfoxide, respectively. Our lab has created the first genetic animal model that is fully deficient for any Msr activity. Previously our lab showed that these animals exhibit a 20 hour delay in development of the third instar larvae (unpublished data). My studies have further shown that the prolonged third-instar stage is due to a reduced growth rate associated with slower food intake and a markedly slower motility. These Msr-deficient animals also exhibit decreased egg-laying that can be attributed to a lack of female receptivity to mating.
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FA00004777, http://purl.flvc.org/fau/fd/FA00004777
Subject Headings: Proteins--Chemical modification., Oxidative stress., Oxidation-reduction reaction., Drosophila melanogaster--Genetics., Mitochondrial pathology., Cellular signal transduction., Mutation (Biology), Aging--Molecular aspects.
Format: Document (PDF)

Title: Identification of a truncated form of methionine sulfoxide reductase a expressed in mouse embryonic stem cells.
Creator: Jia, Pingping, Zhang, Chi, Jia, Yuanyuan, Webster, Keith A., Huang, Xupei, Kochegarov, Andrei A., Lemanski, Sharon L., Lemanski, Larry F.
Date Issued: 2011-06-22
PURL: http://purl.flvc.org/fcla/dt/3327268
Subject Headings: Cell nucleus -- metabolism, Cloning, Molecular, Cytosol --metabolism, Embryonic Stem Cells --metabolism, Methionine --metabolism, Methionine Sulfoxide Reductases, Methionine Sulfoxide Reductases --metabolism, Methionine Sulfoxide Reductases --genetics, Mitochondria --metabolism, Molecular Sequence Data, Oxidation --Reduction, Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Methionine
Format: Document (PDF)

FAU Theses and Dissertations (13)	+ -
FAU College Collections (1)	+ -

Oxidation-reduction reaction (9)	+ -
Chemical modification (6)	+ -
Proteins (6)	+ -
Biochemical markers (5)	+ -
Aging (4)	+ -

Cellular signal transduction (4)	+ -
Molecular aspects (4)	+ -
Mutation (Biology) (4)	+ -
Diagnostic use (3)	+ -
Genetic regulation (3)	+ -
Apoptosis (2)	+ -
Cellular signal transduction. (2)	+ -
Cerebral ischemia (2)	+ -
Oxidation reduction reaction (2)	+ -
Oxidation-reduction reaction. (2)	+ -
Physiological effect (2)	+ -
Prevention (2)	+ -
Aging--Molecular aspects. (1)	+ -
Antioxidants (1)	+ -
Apoptosis. (1)	+ -
Cell metabolism (1)	+ -
Cell nucleus -- metabolism (1)	+ -
Cerebral ischemia--Protection. (1)	+ -
Cloning, Molecular (1)	+ -
Cytosol --metabolism (1)	+ -
Drosophila melanogaster (1)	+ -
Drosophila melanogaster--Genetics. (1)	+ -
Drug resistance in cancer cells (1)	+ -
Embryonic Stem Cells --metabolism (1)	+ -
Genetics (1)	+ -

Charles E. Schmidt College of Science (10)	+ -
Department of Biological Sciences (9)	+ -
Florida Atlantic University (4)	+ -
Binninger, David (2)	+ -
Baird, Donald M. (1)	+ -

Bruce, Lynsey Erin. (1)	+ -
Brunell, David J. (1)	+ -
Charles E. Schmidt College of Medicine (1)	+ -
Department of Biomedical Science (1)	+ -
Department of Chemistry and Biochemistry (1)	+ -
Falzone, Samuel (1)	+ -
Foss, Katie (1)	+ -
Huang, Xupei (1)	+ -
Jia, Pingping (1)	+ -
Jia, Yuanyuan (1)	+ -
Kochegarov, Andrei A. (1)	+ -
Kreymerman, Alexander (1)	+ -
Lemanski, Larry F. (1)	+ -
Lemanski, Sharon L. (1)	+ -
Menzie-Suderam, Janet (1)	+ -
Modi, Jigar P. (1)	+ -
Mulholland, Kori. (1)	+ -
Pan, Chunliu. (1)	+ -
Robbins, Kelli. (1)	+ -
Schey, Karin. (1)	+ -
Singkornrat, Diana (1)	+ -
Verriotto, Jennifer. (1)	+ -
Webster, Keith A. (1)	+ -
Wu, Jang-Yen (1)	+ -
Zhang, Chi (1)	+ -

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