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Littérature scientifique sur le sujet « PRX6 »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "PRX6"

Kim, Yosup, et Ho Hee Jang. « Role of Cytosolic 2-Cys Prx1 and Prx2 in Redox Signaling ». Antioxidants 8, n^o 6 (10 juin 2019) : 169. http://dx.doi.org/10.3390/antiox8060169.

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Peroxiredoxins (Prxs), a family of peroxidases, are reactive oxygen species scavengers that hydrolyze H2O2 through catalytic cysteine. Mammalian Prxs comprise six isoforms (typical 2-Cys Prxs; Prx1–4, atypical 2-Cys Prx; Prx5, and 1-Cys Prx; Prx6) that are distributed over various cellular compartments as they are classified according to the position and number of conserved cysteine. 2-Cys Prx1 and Prx2 are abundant proteins that are ubiquitously expressed mainly in the cytosol, and over 90% of their amino acid sequences are homologous. Prx1 and Prx2 protect cells from ROS-mediated oxidative stress through the elimination of H2O2 and regulate cellular signaling through redox-dependent mechanism. In addition, Prx1 and Prx2 are able to bind to a diversity of interaction partners to regulate other various cellular processes in cancer (i.e., regulation of the protein redox status, cell growth, apoptosis, and tumorigenesis). Thus, Prx1 and Prx2 can be potential therapeutic targets and it is particularly important to control their level or activity. This review focuses on cytosolic 2-Cys Prx1 and Prx2 and their role in the regulation of redox signaling based on protein-protein interaction.

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Lankin, V. Z., M. G. Sharapov, R. G. Goncharov, A. K. Tikhaze et V. I. Novoselov. « Natural dicarbonyls inhibit peroxidase activity of peroxiredoxins ». Доклады Академии наук 485, n^o 3 (21 mai 2019) : 377–80. http://dx.doi.org/10.31857/s0869-56524853377-380.

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It has been established that the activity of recombinant human peroxiredoxins (Prx1, Prx2, Prx4 and Prx6) inhibits by natural dicarbonyls formed during free radical peroxidation of unsaturated lipids (malonic dialdehyde) and oxidative transformations of glucose (glyoxal, methylglyoxal). The possible role of peroxiredoxins activity decreasing under oxidative and carbonyl stress is discussed as an important factor that includes molecular mechanisms of vascular wall damage in atherosclerosis and diabetes mellitus.

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Chen, Jun, Dong-Nan Cui, Hidayat Ullah, Shuang Li, Fan Pan, Chao-Min Xu, Xiong-Bing Tu et Ze-Hua Zhang. « The Function of LmPrx6 in Diapause Regulation in Locusta migratoria Through the Insulin Signaling Pathway ». Insects 11, n^o 11 (5 novembre 2020) : 763. http://dx.doi.org/10.3390/insects11110763.

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Peroxiredoxins (Prxs), which scavenge reactive oxygen species (ROS), are cysteine-dependent peroxide reductases that group into six structurally discernable classes: AhpC-Prx1, BCP-PrxQ, Prx5, Prx6, Tpx, and AhpE. A previous study showed that forkhead box protein O (FOXO) in the insulin signaling pathway (ISP) plays a vital role in regulating locust diapause by phosphorylation, which can be promoted by the high level of ROS. Furthermore, the analysis of transcriptome between diapause and non-diapause phenotypes showed that one of the Prxs, LmPrx6, which belongs to the Prx6 class, was involved. We presumed that LmPrx6 might play a critical role in diapause induction of Locusta migratoria and LmPrx6 may therefore provide a useful target of control methods based on RNA interference (RNAi). To verify our hypothesis, LmPrx6 was initially cloned from L. migratoria to make dsLmPrx6 and four important targets were tested, including protein-tyrosine phosphorylase 1B (LmPTP1B), insulin receptor (LmIR), RAC serine/threonine-protein kinase (LmAKT), and LmFOXO in ISP. When LmPrx6 was knocked down, the diapause rate was significantly reduced. The phosphorylation level of LmPTP1B significantly decreased while the phosphorylation levels of LmIR, LmAKT, and LmFOXO were significantly increased. Moreover, we identified the effect on two categories of genes downstream of LmFOXO, including stress tolerance and storage of energy reserves. Results showed that the mRNA levels of catalase and Mn superoxide dismutase (Mn-SOD), which enhanced stress tolerance, were significantly downregulated after silencing of LmPrx6. The mRNA levels of glycogen synthase and phosphoenolpyruvate carboxy kinase (PEPCK) that influence energy storage were also downregulated after knocking down of LmPrx6. The silencing of LmPrx6 indicates that this regulatory protein may probably be an ideal target for RNAi-based diapause control of L. migratoria.

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Otero-Losada, Matilde, Canepa L, Lucas Udovin, Tamara Kobiec, Nicolás Toro-Urrego, Kölliker-Frers Rodolfo A. et Francisco Capani. « Long-Term Effects of Hypoxia-Reoxygenation on Thioredoxins in Rat Central Nervous System ». Current Pharmaceutical Design 25, n^o 45 (10 janvier 2020) : 4791–98. http://dx.doi.org/10.2174/1381612825666191211111926.

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Background: Oxidative stress induced by the oxidative pathway dysregulation following ischemia/ reperfusion has been proposed as an important cause of neuronal death and brain damage. The proteins of the thioredoxin (Trx) family are crucial mediators of protein function regulating the intracellular hydrogen peroxide levels and redox-sensitive post-translational protein changes. Aim: To analyze the expression and distribution of fourteen members of the Trx family, potentially essential for the regeneration upon long-term brain damage, in a perinatal hypoxia-ischemia rat model induced by common carotid artery ligation. Methods: The right common carotid artery (CCA) was exposed by an incision on the right side of the neck, isolated from nerve and vein, and permanently ligated. Sham-surgery rats underwent right CCA surgical exposure but no ligation. Euthanasia was administered to all rats at 30, 60, and 90 days of age. Protein expression and distribution of fourteen members of the Trx family and related proteins (Grx1, Grx2, Grx3, Grx5, Prx1, Prx2, Prx3, Prx4, Prx5, Prx6, Trx1, Trx2, TrxR1, TrxR2) was examined in the most hypoxia susceptible rat brain areas, namely, cerebellum, corpus striatum, and the hippocampus. Results: The thioredoxin proteins displayed a complex, cell-type, and tissue-specific expression pattern following ischemia/reperfusion. Even 60 days after ischemia/reperfusion, Western blot analysis showed a persistent expression of Trx1 and Grx2 in several brain areas. Conclusion: The Trx family of proteins might contribute to long-term survival and recovery supporting their therapeutic use to curtail ischemic brain oxidative damage following an ischemia/reperfusion insult. Characterization of ischemia/reperfusion oxidative brain damage and analysis of the involved mechanisms are required to understand the underneath processes triggered by ischemia/reperfusion and to what extent and in what way thioredoxins contribute to recovery from brain hypoxic stress.

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Nelson, Kimberly J., Terri Messier, Stephanie Milczarek, Alexis Saaman, Stacie Beuschel, Uma Gandhi, Nicholas Heintz, Terrence L. Smalley, W. Todd Lowther et Brian Cunniff. « Unique Cellular and Biochemical Features of Human Mitochondrial Peroxiredoxin 3 Establish the Molecular Basis for Its Specific Reaction with Thiostrepton ». Antioxidants 10, n^o 2 (20 janvier 2021) : 150. http://dx.doi.org/10.3390/antiox10020150.

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A central hallmark of tumorigenesis is metabolic alterations that increase mitochondrial reactive oxygen species (mROS). In response, cancer cells upregulate their antioxidant capacity and redox-responsive signaling pathways. A promising chemotherapeutic approach is to increase ROS to levels incompatible with tumor cell survival. Mitochondrial peroxiredoxin 3 (PRX3) plays a significant role in detoxifying hydrogen peroxide (H2O2). PRX3 is a molecular target of thiostrepton (TS), a natural product and FDA-approved antibiotic. TS inactivates PRX3 by covalently adducting its two catalytic cysteine residues and crosslinking the homodimer. Using cellular models of malignant mesothelioma, we show here that PRX3 expression and mROS levels in cells correlate with sensitivity to TS and that TS reacts selectively with PRX3 relative to other PRX isoforms. Using recombinant PRXs 1–5, we demonstrate that TS preferentially reacts with a reduced thiolate in the PRX3 dimer at mitochondrial pH. We also show that partially oxidized PRX3 fully dissociates to dimers, while partially oxidized PRX1 and PRX2 remain largely decameric. The ability of TS to react with engineered dimers of PRX1 and PRX2 at mitochondrial pH, but inefficiently with wild-type decameric protein at cytoplasmic pH, supports a novel mechanism of action and explains the specificity of TS for PRX3. Thus, the unique structure and propensity of PRX3 to form dimers contribute to its increased sensitivity to TS-mediated inactivation, making PRX3 a promising target for prooxidant cancer therapy.

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Forshaw, Tom E., Julie A. Reisz, Kimberly J. Nelson, Rajesh Gumpena, J. Reed Lawson, Thomas J. Jönsson, Hanzhi Wu et al. « Specificity of Human Sulfiredoxin for Reductant and Peroxiredoxin Oligomeric State ». Antioxidants 10, n^o 6 (11 juin 2021) : 946. http://dx.doi.org/10.3390/antiox10060946.

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Human peroxiredoxins (Prx) are a family of antioxidant enzymes involved in a myriad of cellular functions and diseases. During the reaction with peroxides (e.g., H2O2), the typical 2-Cys Prxs change oligomeric structure between higher order (do)decamers and disulfide-linked dimers, with the hyperoxidized inactive state (-SO2H) favoring the multimeric structure of the reduced enzyme. Here, we present a study on the structural requirements for the repair of hyperoxidized 2-Cys Prxs by human sulfiredoxin (Srx) and the relative efficacy of physiological reductants hydrogen sulfide (H2S) and glutathione (GSH) in this reaction. The crystal structure of the toroidal Prx1-Srx complex shows an extended active site interface. The loss of this interface within engineered Prx2 and Prx3 dimers yielded variants more resistant to hyperoxidation and repair by Srx. Finally, we reveal for the first time Prx isoform-dependent use of and potential cooperation between GSH and H2S in supporting Srx activity.

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Carvalho, Larissa A. C., Rodrigo G. Queijo, Alexandre L. B. Baccaro, Ádamo D. D. Siena, Wilson A. Silva, Tiago Rodrigues et Silvya Stuchi Maria-Engler. « Redox-Related Proteins in Melanoma Progression ». Antioxidants 11, n^o 3 (22 février 2022) : 438. http://dx.doi.org/10.3390/antiox11030438.

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Melanoma is the most aggressive type of skin cancer. Despite the available therapies, the minimum residual disease is still refractory. Reactive oxygen and nitrogen species (ROS and RNS) play a dual role in melanoma, where redox imbalance is involved from initiation to metastasis and resistance. Redox proteins modulate the disease by controlling ROS/RNS levels in immune response, proliferation, invasion, and relapse. Chemotherapeutics such as BRAF and MEK inhibitors promote oxidative stress, but high ROS/RNS amounts with a robust antioxidant system allow cells to be adaptive and cooperate to non-toxic levels. These proteins could act as biomarkers and possible targets. By understanding the complex mechanisms involved in adaptation and searching for new targets to make cells more susceptible to treatment, the disease might be overcome. Therefore, exploring the role of redox-sensitive proteins and the modulation of redox homeostasis may provide clues to new therapies. This study analyzes information obtained from a public cohort of melanoma patients about the expression of redox-generating and detoxifying proteins in melanoma during the disease stages, genetic alterations, and overall patient survival status. According to our analysis, 66% of the isoforms presented differential expression on melanoma progression: NOS2, SOD1, NOX4, PRX3, PXDN and GPX1 are increased during melanoma progression, while CAT, GPX3, TXNIP, and PRX2 are decreased. Besides, the stage of the disease could influence the result as well. The levels of PRX1, PRX5 and PRX6 can be increased or decreased depending on the stage. We showed that all analyzed isoforms presented some genetic alteration on the gene, most of them (78%) for increased mRNA expression. Interestingly, 34% of all melanoma patients showed genetic alterations on TRX1, most for decreased mRNA expression. Additionally, 15% of the isoforms showed a significant reduction in overall patient survival status for an altered group (PRX3, PRX5, TR2, and GR) and the unaltered group (NOX4). Although no such specific antioxidant therapy is approved for melanoma yet, inhibitors or mimetics of these redox-sensitive proteins have achieved very promising results. We foresee that forthcoming investigations on the modulation of these proteins will bring significant advances for cancer therapy.

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Peskin, Alexander V., Nina Dickerhof, Rebecca A. Poynton, Louise N. Paton, Paul E. Pace, Mark B. Hampton et Christine C. Winterbourn. « Hyperoxidation of Peroxiredoxins 2 and 3 ». Journal of Biological Chemistry 288, n^o 20 (29 mars 2013) : 14170–77. http://dx.doi.org/10.1074/jbc.m113.460881.

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Typical 2-Cys peroxiredoxins (Prxs) react rapidly with H2O2 to form a sulfenic acid, which then condenses with the resolving cysteine of the adjacent Prx in the homodimer or reacts with another H2O2 to become hyperoxidized. Hyperoxidation inactivates the Prx and is implicated in cell signaling. Prxs vary in susceptibility to hyperoxidation. We determined rate constants for disulfide formation and hyperoxidation for human recombinant Prx2 and Prx3 by analyzing the relative proportions of hyperoxidized and dimeric products using mass spectrometry as a function of H2O2 concentration (in the absence of reductive cycling) and in competition with catalase at a fixed concentration of H2O2. This gave a second order rate constant for hyperoxidation of 12,000 m−1 s−1 and a rate constant for disulfide formation of 2 s−1 for Prx2. A similar hyperoxidation rate constant for Prx3 was measured, but its rate of disulfide formation was ∼10-fold higher, making it is more resistant than Prx2 to hyperoxidation. There are two active sites within the homodimer, and at low H2O2 concentrations one site was hyperoxidized and the other present as a disulfide. Prx with two hyperoxidized sites formed progressively at higher H2O2 concentrations. Although the sulfenic acid forms of Prx2 and Prx3 are ∼1000-fold less reactive with H2O2 than their active site thiols, they react several orders of magnitude faster than most reduced thiol proteins. This observation has important implications for understanding the mechanism of peroxide sensing in cells.

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Suzuki, Yuichiro J., Lucia Marcocci, Takashi Shimomura, Yuki Tatenaka, Yuya Ohuchi et Tinatin I. Brelidze. « Protein Redox State Monitoring Studies of Thiol Reactivity ». Antioxidants 8, n^o 5 (22 mai 2019) : 143. http://dx.doi.org/10.3390/antiox8050143.

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Protein cysteine thiol status is a major determinant of oxidative stress and oxidant signaling. The -SulfoBiotics- Protein Redox State Monitoring Kit provides a unique opportunity to investigate protein thiol states. This system adds a 15-kDa Protein-SHifter to reduced cysteine residues, and this molecular mass shift can be detected by gel electrophoresis. Even in biological samples, Protein-SHifter Plus allows the thiol states of specific proteins to be studied using Western blotting. Peroxiredoxin 6 (Prx6) is a unique one-cysteine peroxiredoxin that scavenges peroxides by utilizing conserved Cysteine-47. Human Prx6 also contains an additional non-conserved cysteine residue, while rat Prx6 only has the catalytic cysteine. In cultured cells, cysteine residues of Prx6 were found to be predominantly fully reduced. The treatment of human cells with hydrogen peroxide (H2O2) formed Prx6 with one cysteine reduced. Since catalytic cysteine becomes oxidized in rat cells by the same H2O2 treatment and treating denatured human Prx6 with H2O2 results in the oxidation of both cysteines, non-conserved cysteine may not be accessible to H2O2 in human cells. We also found that untreated cells contained Prx6 multimers bound through disulfide bonds. Surprisingly, treating cells with H2O2 eliminated these Prx6 multimers. In contrast, treating cell lysates with H2O2 promoted the formation of Prx6 multimers. Similarly, treating purified preparations of the recombinant cyclic nucleotide-binding domain of the human hyperpolarization-activated cyclic nucleotide-modulated channels with H2O2 promoted the formation of multimers. These studies revealed that the cellular environment defines the susceptibility of protein cysteines to H2O2 and determines whether H2O2 acts as a facilitator or a disrupter of disulfide bonds.

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Aón Bertolino, Ma Laura, Christopher Horst Lillig et Capani Francisco. « The Thioredoxin Family Proteins : Histopathological Time Course Study in the Asphyctic Male Rat Brain ». Microscopy and Microanalysis 26, S1 (mars 2020) : 183–84. http://dx.doi.org/10.1017/s1431927620001130.

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Summary:Thioredoxin Family of proteins as Thioredoxin (Trxs), Glutaredoxins (Grxs) and Peroxiredoxins (Prxs) are one of the most important agents in the defense of oxidative stress and redox regulation. Perinatal asphyxia (AP) a disorder generated at the expense of the deficit of oxygen associated or not to ischemia, affects 5 to 10 of every 1,000 live births in developing country and is a serious health problem worldwide. Alterations in antioxidant protection systems are involved in the pathogenesis of hypoxic-ischemic insult and neuronal death. For these reasons it is proposed that the AP can cause changes in the distribution and expression of antioxidant proteins and enhance their deleterious or neuroprotective effects on the CNS. Methods: to determine the implication of the proteins role induced in the hypoxic brain injury, an animal model in vivo of PA was used in this work. In the first instance, the identification of the distribution of Trxs family proteins Trx1, Trx2, TrxR1, TrxR2, Txnip, Grx1, Grx2, Grx3, Grx5, γ-GCS, Prx1, Prx2, Prx3, Prx4, Prx5 and Prx6 was performed by immunohistochemistry on areas most sensitive to a hypoxia-ischemia insult: cerebellum, striatum, hippocampus, spinal cord, sustantia nigra, cortex and retina. Previous studies suggest that these proteins have an extensive and characteristic distribution in various cell types and regions of the CNS, although we observed significant differences in labeling intensity and distribution with conventional and fluorescence optical microscopy. After determining the cellular localization of Trxs, their behavior was studied by during a hypoxic- ischemic event by setting a time course at different times (2, 4, 6, 12, 24 and 72 hours post AP). Results: Trx1, Trx2, Grx1 and Grx2 proteins constitutes the main oxidoreductases in the cytosol and mitochondria, both in physiological and pathological conditions. Thus, for the short asphyxia times in which they were studied, Trx1 was detected with increased expression at 2 hours and up to 4 hours post-AP, arguing a probable neuroprotective effect, although not enough, if taken into account tissue liability and high levels of free radicals detected at initial hours and the presence of structural damage at 7 days post-AP. Trx2 shows its increase at 6 and 12 hours and Grx1 at 24 hours. For Grx2, values elicited with the ELISA technique in the initial time curve were not representative in their expression in the hippocampus, contrary to the findings in the distribution in the striatum, where Grx2 was observed to be increased. Although at 7 hours post-AP levels begin to decline, these redoxins appears to be essential in the initial response to injury. Conclusions: by demonstrating of the presence of these enzymes in different cell types and specific regions of the brain in rats subjected to AP provided us with important morphological evidence base to study later some of the molecular mechanisms involved in the pathogenesis of cerebral ischemia that will help to generate new therapeutic tools to mitigate a disease whose neurological complications have no definitive solution.

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Thèses sur le sujet "PRX6"

STUCCHI, SIMONE. « Role of glucose and peroxiredoxin 6 in human chondrocytes and novel biomaterial for in vitro three-dimensional chondrocytes culture ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/261927.

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L’osteoartrite (OA) è una delle malattie reumatiche con più alta incidenza nel mondo moderno e rappresenta la pricipale cause di disabilità. L’OA è data da un disquilibrio tra degradazione e riparazione della cartilagine, a favore della degradazione, con un incremento dell’attivita degli enzimi catabolici come le matrici metalloproteinasiche. I condrociti sono responsabili della riparazione e della biosintesi degli elementi che compongono la ECM. Diversi studi supportano l’ipotesi che il diabete è uno dei fattori che causano l’osteoartrite. Sebbene non si conoscono ancor ai meccanismi molecolari che permettano l’associazione tra diabete e OA. Abbiano analizzato la crescita cellulare, i livelli dei ROS e l’apoptosi di condrociti posti in terreno con differenti concentrazioni di glucosio. I risultati mostrano che i condrociti preferiscono la concentrazione 2.5 mM di glucosio che è stata utilizzata come concentrazione normoglicemica; mentre 25 mM di glucosio è stata utilizzata come concentrazione iperglicemica. I livelli di ROS e la morte cellulare aumentano in condrociti cresciuti in alto glucosio, anche il citoscheletro si presenta disorganizzato in cellule C28/I2 cresciute in queste condizioni. Questo correla con lo stato di attivazione della GTPasi RalA, la cui attivazione è ridotta in condizioni iperglicemiche. Infatti questa GTPasi è coinvolta nella regolazione della riorganizzazione citoscheletrica. Inoltre sono stati effettuati esperimenti utilizzando medium contenenti ITS (Insulina, transferrina e selenio) che pruomuove il differenziamento a condrocita; mentre l’interleuchina-1β per simulare l’ambiente osteoartritico. Anche in uesto caso i livelli di RalA GTP diminuiscono in cellule cresciute in 25 mM glucosio e stimolate con IL-1β. Inoltre in queste condizioni diminuiscono ache i livelli di p-ERK1/2. Sono stati valutati anche i livelli di NF-κB, iNOS e LC3II. I risultati dimostrano che l’alto glucosio blocca l’autofagia nei condrociti. Inoltre sono stati valutati anche i pathways attivati dall’alto glucosio in condrociti primari umani dopo 24 h di trattamento. I risultati mostrano che la fosforilazione di ERK1/2, p38, Akt e p65 è alterata in condrociti cresciuti in condizioni iperglicemiche tale evento è correlato con un aumento di MMP-13. Per analizzare meglio il ruolo dei ROS nei condrociti ho lavorato per 6 mesi nel laboratorio del Dr. Loeser alla scuola di medicina presso l’università della north Carolina a Chapel Hill. Ho lavorato su PRX6 che è coinvolto nella detossificazione dai ROS. Lo stato di ossidazione di PRX6 è stato valutato nei condrociti trattati con diversi stimoli come H2O2, Fn-f, menadione (men) and DMNQ. Dopo questi esperimenti abbiamo voluto osservare se PRX6 potesse influenzare i pathway delle MAPK in cellule trattate con IGF-1, menadione, combinazione tra IGF-1 e menadione e con Fn-f. è stata valutata la localizzazione di PRX6 che si è visto essere sia nucleare che citoplasmatico. Inoltre ho lavorato in collaborazione con Prof. Laura Cipolla e Prof. Maddalena Collini per sviluppare e caratterizzare nuovi idrogel fatti di gelatina usando come agente cross-linkante lo squarato.
Osteoarthritis (OA) is the most common rheumatic disease in the world and represents the first cause of disability in the world. OA results from the loss of balance between degradation and repair inside cartilage, in favor of degradation, with increased activity of catabolic enzymes such as matrix metalloproteinases and decreased production of ECM proteins. Chondrocytes are responsible for the repair and biosynthesis of elements of the extracellular matrix. Experimental findings support the hypothesis that diabetes is an independent risk factors for OA. However, correct molecular mechanisms underlying the diabetes-associated OA phenotype is still largely unknown. Firstly chondrocytes cell growth, ROS levels and apoptosis were analyzed using different glucose concentration. Results shown that chondrocytes prefer 2.5 mM of glucose which was used as normal glucose concentration and 25 mM of glucose was used as high glucose concentration. ROS levels and cell death increase in chondrocytes growth in high glucose environment. Also cytoskeletal network is more disorganized in C28/I2 cells growth at high glucose concentration, this correlates with different RalA-GTP levels which is involved in the regulation of cytoskeletal organization. Experiments were performed even using medium supplemented by ITS (Insulin-transferrin-selenium) to promote chondrocyte differentiation and IL-1β was used to simulate osteoarthritic cartilage environment. Ral A-GTP levels are lower in cells grown in 25 mM of glucose and stimulated with IL1β. Levels of p-ERK1/2 decrease in cells grown at high glucose concentration and in cells stimulated with IL1β. Furthermore, NF-κB, iNOS and LC3II levels were evaluated. Results demonstrate that high glucose media block autophagic process in chondrocytes. Effect of glucose concentration on human primary chondrocytes cells was evaluated after only 24 h to understand which signaling pathways is activated by high glucose environment. Phosphorylation of ERK1/2, p38, Akt and p65 is altered in chondrocytes growth at high glucose concentration and this correlates with an increase secretion of MMP-13. To better analyze the role of ROS levels in the chondrocytes I worked for 6 months in the Dr. Loeser Lab at the School of Medicine in the University of North Carolina at Chapel Hill; one of the best lab in the cartilage biology field. I worked on PRX6 which is involved in the recovery from H2O2. Oxidation state of PRX6 was evaluated in chondrocytes treated with different stimuli, like H2O2, Fn-f, menadione (men) and DMNQ. After this experiment, we wanted to see if PRX6 could impact the MAPK signaling pathways in cells treated with IGF-1, menadione, combination of menadione and IGF-1 and with Fn-f. Localization of PRX6 was analyzed using nuclear and cytoplasm extraction. Then I worked in collaboration with Prof. Laura Cipolla and Prof. Maddalena Collini to develop and characterized a new gelatin-based hydrogel using Diethylsquarate as crosslinker.

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Norman, Per-Gustaf. « Cloning, Purification and Crystallization of Low PSII Accumultation 19 (LPA19) and Peroxiredoxin-6 (Prx6) : A Thorny Road to Diffracting Crystals ». Thesis, Umeå universitet, Kemiska institutionen, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-111548.

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Mishra, Murli. « EXPLORATION OF THE SRX-PRX AXIS AS A SMALL-MOLECULE TARGET ». UKnowledge, 2016. http://uknowledge.uky.edu/toxicology_etds/14.

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Lung cancer is a leading cause of cancer-related mortality irrespective of gender. The Sulfiredoxin (Srx) and Peroxiredoxin (Prx) are a group of thiol-based antioxidant proteins that plays an essential role in non-small cell lung cancer. Understanding the molecular characteristics of the Srx-Prx interaction may help design the strategies for future development of therapeutic tools. Based on existing literature and preliminary data from our lab, we hypothesized that the Srx plays a critical role in lung carcinogenesis and targeting the Srx-Prx axis or Srx alone may facilitate future development of targeted therapeutics for prevention and treatment of lung cancer. First, we demonstrated the oncogenic role of Srx in urethane-induced lung carcinogenesis in genetically modified FVB mice. The Srx-null mice showed resistance to urethane-induced lung cancer. Second, we demonstrated the Srx and Prx sites important for Srx-Prx interaction. The orientation of this arm is demonstrated to cause some steric hindrance for the Srx-Prx interaction as it substantially reduces the rate of association between Srx and Prx. Finally, we carried out virtual screening to identify molecules that can successfully target Srx-Prx interaction. Multiple in-silico filters were used to minimize the number of chemicals to be tested. We identified ISO1 as an inhibitor of the Srx-Prx interaction. KD value for Srx-ISO1 interaction is calculated to be 42 nM. Together, these data helps to identify an inhibitor (ISO1) of the Srx-Prx interaction that can be further pursued to be developed as a chemotherapeutic tool.

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Cao, Zhenbo. « Structure-function studies of Prx III, a mitochondrial typical 2-Cys peroxiredoxin ». Thesis, University of Glasgow, 2006. http://theses.gla.ac.uk/39024/.

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The peroxiredoxuis (Prxs) are a ubiquitous family of antioxidant enzymes that regulate intracellular levels of H2O2 where they are implicated in both tissue protection against oxidative stress and H2O2-niediated signalling pathways (Wood et al., 2003). This thesis describe our results on the structure-function studies of PrxIII, a mitochondrial typical 2-Cys peroxiredoxin. Bovine PrxIII was cloned previously in our laboratory; however PrxIII requires its cognate partners, mammalian mitochondrial thioredoxin (Trx2) and mammalian mitochondrial thioredoxin reductase (TRR2), to reconstitute the complete antioxidant defence system. To establish a direct in vitro assay for PrxIII, Trx2 and TRR2 were cloned, overexpressed and purified in this study. As TRR2 is a selenocysteine (SeCys) protein, a suitable selenocysteine insert sequence (SECIS) for the translation of its penultimate SeCys codon was introduced by incorporating it into the reverse primer for PCR. A combination of different approaches was used for the successful overexpression of active TRR2. Overexpression in modified rich LB media at 15°C in the presence of low IPTG concentrations gave good overexpression of soluble enzyme. Moreover, the addition of the SECIS at the C-terminal of the insert, in the presence of 1 nM Na2SeO3 and co-expression of the SelABC plasmid ensured an optimal supply of the relevant tRNA, tRNA synthase and elongation factor for translation of the UGA SeCys codon. Assays showed that NADPH-linked oxidation needed the presence of all three enzymes to reduce H2O2. PrxIII was also shown to reduce other organic peroxides, although with lower activity. Cys47 and Cysl68, but not Cys66, proved to be crucial for peroxiredoxin activity. Interestingly, at high H2O2 concentrations in the non- physiological range, TRR2 also had the capacity to reduce H2O2 directly in an NADPH-dependent manner. PrxIII is also shown to be susceptible to overoxidation and loses peroxidase activity at increased H2O2 levels in the range 50μM to 1mM. This was monitored by SDS-PAGE analysis of partially or fully overoxidised forms of H2O2-mediated PrxIII and PrxIII pathway assays. Gel filtration chromatography was used to determine under which conditions the PrxIII dodecamer would dissociate into dimers. The results show that redox state, protein concentration and the N-terminal His-tag all affect the oligomerization of PrxIII. The crystal structure of the PrxIII C168S mutant from bovine mitochondria has been determined at a resolution of 3.3 angstroms. The structure reveals that the toroid is composed of 12 (not 10) monomers with a 6(2,2) symmetry. Each ring has an external diameter of 150 angstroms and encompasses a central cavity 70 angstroms in width. Surprisingly, two PrxIII rings are mechanically interlocked in the crystal to form a protein catenane. Interestingly, the catenated form represents only a small proportion (3-5%) of the total PrxIII population, as observed by electronic microscopy studies at dilute concentration (10-50μg/ml). Preliminary analytical ultracentrifugation data suggest that 2-ring catenane formation is concentration dependent. A general model illustrating catenane formation arising from polar contacts between two basic dimeric units is described. It is not clear whether the catenated form of PrxIII has any physiological function. However, the observation that Prxs can protect cells from heat shock in a peroxidase-independent process might provide new insights into possible novel functions.

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Huang, Yang. « Analysis of NMR Spin-lattice Relaxation Dispersion on Complex Systems ». Doctoral thesis, Umeå universitet, Kemiska institutionen, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-110721.

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This thesis focus on the analysis of spin-lattice NMRD relaxation profilesmeasured in various complex systems such as proteins, zeolites and ionicliquids. Proton, deuterium and fluoride T1-NMRD relaxation profiles wereobtained from a fast-field cycling (FFC) instrument. It is found that alsopossible to obtain NMRD profiles from the molecular dynamics (MD)simulation trajectories. NMRD Profiles were analyzed by using differentrelaxation models, such as the Solomon-Bloembergen-Morgan (SBM) theoryand the Stochastic Liouville (SL) theory. Paper I described the hydration of protein PrxV obtained from a MDsimulation, and compared with the picture emerges from an analysis byusing a generally accepted relaxation model [appendix C]. The result showsthat the information from NMRD analysis is an averaged picture of watermolecules with similar relaxation times; and the MD simulations containsinformation of all types of interested water molecules with differentresidence times. In paper II NMRD profiles have been used to characterize the hydration ofthe oxygen-evolving complex in state S1 of photosystem II. NMRDexperiments were performed on both intact protein samples and Mndepletedsamples, and characteristic dispersion difference were foundbetween 0.03 MHz to 1 MHz; approximately. Both the SBM theory and theSL theory have been used to explain this dispersion difference, and it isfound that this is due to a paramagnetic enhancement of 1-2 water moleculesnearby ~10 Å from the spin center of the Mn4CaO5 cluster. The result showsthe reorientation of the molecular cluster is in μs time interval. Whencompare these two theories, the SL theory presented a better interpretationbecause parameters obtained from the SBM theory shows they didn’t fulfilthe presupposed perturbation criterion (the Kubo term). Paper III deals with the water dynamics in the restricted/confined spaces inthe zeolite samples (H-ZSM-5 and NH4-ZSM-5) and obtained by proton anddeuterium spin-lattice NMRD profiles. The results show that the spin-latticeNMRD can be used to characterize various zeolites. The temperature has aweak effect on the relaxation rate R1, but the change of different counter ionsmay change the hydration and the translational diffusion pores and givedifferent R1. Proton and fluoride NMRD profiles and MD simulations were both used tostudy the dynamics of BMIM[PF6] in paper IV. Results indicate the reorientation of the molecules are in the ns time regime, and the effectivecorrelation time obtained from 1H and 19F are the same. From the MDsimulation it is found the reorientation of [PF6]- ions is much faster (in ps)compare with BMIM+ ion which moves in the ns time range. With previous results, the FFC NMRD profiles are indeed very informativetools to study the molecular dynamics of complex systems. The MDsimulation can be used as a complementary method to obtain detailedinformation. By combine these two methods, it provide a more colorfulpicture in the study of protein hydration and liquid molecular dynamics.

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Lamichhane, Suman. « Physiological and Molecular Dissection of Salinity Tolerance in Arabidopsis and Maize and Nitrogen Uptake in Wheat ». Diss., Virginia Tech, 2020. http://hdl.handle.net/10919/97843.

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The PROTEOLYSIS 6 (PRT6) branch of the N-end rule pathway is a well-characterized negative regulator of flooding and low oxygen tolerance in plants. This study investigated the role of this pathway in adaptation to salinity stress in Arabidopsis and maize via physiological and molecular characterization of Arabidopsis prt6-1 and maize prt6 MU insertion mutants, respectively. Our study demonstrated that the loss of function mutation of prt6 in Arabidopsis activated hormonal and transcriptional responses associated with adaptation to salinity stress, enhancing high salt tolerance at seed germination, seedling, and adult plant stages. Our data also indicated that salinity tolerance conferred by the prt6 mutation is attributed to increased mRNA abundance of key transcriptional factors in ABA-dependent (AREB/ABFs) and independent (DREBs) pathways, together with the dominant expression of downstream dehydrins. Furthermore, this study revealed that the prt6 mutation enhances ethylene and brassinosteroid responses, resulting in restricted Na+ accumulation in roots and shoots as well as increased expression of dehydrin genes such as RD29A and RD29B. Maize prt6 mutant plants, contrary to our observation in Arabidopsis, showed lower seed germination, primary root elongation, and shoot biomass growth along with increased malondialdehyde (MDA) accumulation under high salt. Moreover, maize prt6 mutants exhibited reduced grain yield and yield-related components under high salt. These results indicate that PRT6 functions as a negative regulator for salinity tolerance in Arabidopsis, whereas this gene plays a positive role in salinity tolerance in maize. In wheat, we compared two genotypes with contrasting nitrogen-use-efficiency (NUE), VA08MAS-369 and VA07W-415, to dissect physiological and molecular mechanisms underlying NUE regulation. Our agronomic data revealed that line 369 maintained yield and yield-related parameters and exhibited greater NUE indexes relative to line 415 under N deficient conditions. Furthermore, our analyses suggested that the significantly higher nitrogen use efficiency (NUE) in line 369 could be attributed to the greater N uptake efficiency in this genotype. In fact, line 369 was able to maintain the development of root systems under N limitation. Consistently, genes encoding high-affinity nitrate transporters such as TaNRT2.1 and TaNRT2.2 were expressed more abundantly in the roots of line 369 than line 415 at limited N. Overall, the results of this study characterized physiological and molecular phenotypes associated with high N uptake efficiency in line 369. This is useful information for the development of new wheat accessions with improved NUE.
Doctor of Philosophy
In coastal areas, sea-level rise increases the chances of saltwater intrusion into cultivable lands, making a hostile environment for crop growth and production by imposing flooding and salinity stresses simultaneously. Identification of central regulators that regulate the adaptation to both flooding and salinity is a critical step for the development of new crop genotypes with enhanced tolerance to these stresses. Previous studies have characterized the function of the PROTEOLYSIS 6 (PRT6) gene in adaptation to flooding stress in plants. This study assessed whether this gene is involved in adaptation to salinity stress in Arabidopsis and maize by evaluating the growth and survival of their respective prt6 mutants under high salt. Consistent with the flooding tolerance data, our study showed that the PRT6 gene also functions as a negative regulator of salinity stress tolerance in Arabidopsis. The prt6 mutation in Arabidopsis activated the key transcriptional and hormone response pathways associated with adaptation to both salinity/osmotic stress and sodium toxicity, expressed as enhanced tolerance to excess salt at seed germination, seedling, and adult plant stages. In maize, disruption of the PRT6 gene decreased seed germination, primary root elongation, and shoot biomass growth under high salt, which is opposite to our observations in Arabidopsis. Additionally, the maize mutant plants encountered more oxidative stress, as demonstrated by the higher accumulation of malondialdehyde (MDA) under high salt. Moreover, maize prt6 mutants exhibited reduced grain yield under high salt. Overall, these results indicate that disruption of the PRT6 gene confers increased tolerance to high salt in Arabidopsis, whereas it conversely reduced salinity tolerance in maize. In wheat, we compared two genotypes with distinct nitrogen use efficiency (NUE), VA08MAS-369 and VA07W-415, to determine critical traits involved in NUE regulation. Our study showed that grain yield and yield-related parameters were significantly higher in line 369 than line 415 under low N. Moreover, high NUE in line 369 was attributed to efficient N uptake in this genotype under limited N. Our root architecture analysis demonstrated that line 369 was able to maintain root depth, volume, and thickness even under N limitation. Consistently, line 369 highly induced expression of genes associated with nitrogen transport at low N. Altogether, this study identified key traits involved in high NUE in wheat, facilitating the breeding of new wheat genotypes with enhanced NUE.

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Ruiz, Marion. « Etude de la réponse au stress oxydatif chez la cyanobactérie Anabaena sp PCC 7120 : mise en évidence d'une peroxiredoxine PrxQ-A et de la cystéine défulfurase Scdb ». Aix-Marseille 2, 2009. http://theses.univ-amu.fr.lama.univ-amu.fr/2009AIX22015.pdf.

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La photosynthèse oxygénique peut être le lieu de formation des Formes Réactives de l’Oxygène (FROs). Ces espèces réactives peuvent altérer toutes les macromolécules de la cellule, générant ainsi un stress oxydatif. Les cyanobactéries étant les premiers organismes à avoir émis de l’oxygène sur terre, elles ont développé très tôt au cours de l’évolution des mécanismes de défense pour lutter contre le stress oxydatif. Nous nous sommes intéressés à l’étude de la réponse de la cyanobactérie filamenteuse Anabaena sp. PCC 7120 à ce stress. Nous avons mis en évidence l’implication d’un opéron, dit pkn, dans cette réponse adaptative. Nous avons notamment caractérisé la fonction de la peroxiredoxine PrxQ-A dans la réduction des FROs de type peroxyde. Nous avons également caractérisé une protéine codée par le dernier gène de cet opéron comme étant une cystéine désulfurase. Cette classe d’enzymes est impliquée dans la mobilisation du soufre dans divers processus comme la biosynthèse de la thiamine, la biosynthèse de la molybdoptérine, la thiolation des ARNt ou encore la biogénèse des centres [Fe-S]. L’éventuelle relation fonctionnelle entre les différentes protéines codées par l’opéron pkn et le rôle qu’elles jouent dans la réponse de ce micro-organisme au stress oxydatif offrent de nouvelles perspectives à ce travail
Oxygenic photosynthesis may generate of reactive oxygen species(ROS). These reactive species can damage all the macromolecules of the cell, inducing an oxidative stress. Cyanobacteria were the first organisms producing oxygen on earth, they have developed very early in the evolution various defenses to protect themselves against deleterious effects of ROS. We are interested in studying the response of the filamentous cyanobacterium Anabaena sp. PCC7120 to oxidative stress. During this wrok, we have highlighted the involvement of an operon, the pkn operon, in this adaptive response. We have characterized the function of peroxiredoxin Prx QA in reducing peroxide. We also characterized a protein encoded by the last gene of this operon as a cysteine desulfurase. They are pyridoxal phosphate-depending enzymes involved into the mobilization of sulfur to various processes such as biosynthesis of thiamine, the biosynthesis of molybdopterin, tRNA thiolation and also the biogenesis of [Fe-S] clusters. The possible relationship between the different proteins encoded by this operon and their role in the response of Anabaena sp. PCC 7120 to oxidative stress offer interesting perspectives

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Patel, Maryam. « Cerebral autoregulation in children with traumatic brain injury : Comparing the autoregulatory index (ARI) to pressure reactivity index (PRx) and their associations with cerebral physiological parameters ». Master's thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/27399.

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As an important hemodynamic mechanism, pressure autoregulation protects the brain against inappropriate fluctuations in cerebral blood flow subject to changing cerebral perfusion pressures. In acute neurological illnesses, including traumatic brain injury in children, impaired autoregulation is associated with a worse prognosis. It also has important clinical implications for managing blood pressure and intracranial pressure. Two common methods of measuring pressure autoregulation reported in the adult literature have been rarely reported in children. This pilot study aimed to examine the relationship between two autoregulatory indices, namely PRx (pressure reactivity index) and ARI (autoregulatory index) in children with severe TBI. The study also examined their relationship with the response of clinically relevant variables such as intracranial pressure (ICP), brain oxygenation (PbtO2) and local cerebral blood flow (loCBF) to dynamic testing. The study is a retrospective cohort study of prospectively collected data conducted at the Red Cross Children Hospital. We analyzed the results of 18 patients in 28 tests of autoregulation to determine the static state of autoregulation by calculating the autoregulatory index (ARI). These tests were done by controlled elevation of blood pressure to evaluate changes in transcranial Doppler-derived flow velocity of the middle cerebral artery. Concomitant recordings were made of ICP, PbtO2, and loCBF. Secondly, we also calculated the PRx as a moving correlation co-efficient between slow changes in blood pressure and ICP. Two time epochs of PRx were examined in relation to the static tests: 1 hour before and after the test, and 12 hours before and after the test. The results included 28 tests done for ARI and 27 calculations for PRx epochs; all tests had ICP and PbtO2 data and 23 had loCBF. PRx and ARI showed no significant relationship between them. However, there was a significant relationship between ARI and ΔICP (p=0.04), i.e. when autoregulation was weak the change in ICP with a change in blood pressure was greater; and between PRx and ΔPbtO2 (p=0.04). There was a trend in correlation analysis between loCBF and PRx but not in the linear mixed effects model In conclusion, the study showed no correlation between the two autoregulatory indices, PRx and ARI, probably because they assess different aspects of autoregulation. However, significant relationships exist between ARI and ΔICP as well as PRx and ΔPbtO2, which generate interesting hypotheses about autoregulation and have clinical implications. Both autoregulatory indices have benefits and limitations. Further studies on such relationships, taking into consideration a larger sample group, inclusion of unstable patients, and utilization of the same range in BP for calculating the indices, are recommended.

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Wang, Xu. « The role of ethylene and the N-end rule pathway in the regulation of Arabidopsis seed dormancy ». Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS421.

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L'éthylène comme la stratification au froid et le GA3, stimule la germination des graines d'Arabidopsis thaliana (Col-0) ayant une dormance primaire, à 25 °C et à l'obscurité. L'élimination de la dormance au froid n'exige pas ETR1, EIN4 et EIN2, alors que l'effet du GA3 nécessite ETR1. L'effet stimulateur de l'éthylène est associé à une réduction de l'expression des gènes impliqués dans les voies de signalisation des GAs (DELLAs) et de l'ABA (ABI5). Les graines du mutant prt6 affectées dans la voie "N-end rule" de la protéolyse, sont insensibles à l'éthylène, montrant que PRT6 intervient dans l'action de l'éthylène, et cette insensibilité résulte aussi d'une interrelation avec la balance ABA/GAs. D'autre part, les facteurs de transcription de la réponse à l'éthylène du groupe VII, (ERF VIIs), substrats de la voie "N-end rule", interviennent dans cette insensibilité. La sensibilité à l'éthylène de prt6rap2.2rap2.3rap2.12 et l'insensibilité de prt6hre1hre2, permet de montrer que les 3 RAPs et les 2 HREs interviennent respectivement en aval et en amont de PRT6. L'éthylène induit une diminution de l'expression des 3 RAPs dans Col, mais maintient ou induit celle-ci dans prt6. De plus, l'expession de HRE2 augmente dans prt6, mais diminue dans prt6rap2.2rap2.3rap2.12, suggérant que les 3 RAPs peuvent réguler l'expression de HRE2. De plus, l'éthylène modifie différentiellement le protéome de Col et de prt6 avec respectivement 587 et 30 protéines significatives. L'analyse des classes fonctionnelles a permis d'identifier la réponse à hypoxie comme processus biologique spécifique de prt6, mais leur insensibilité à l'éthylène est indépendante des ROS et de l'intensité respiratoire
Ethylene as chilling and GA3, was able to improve the germination of primary dormant seeds of Arabidopsis thaliana (Col-0) at 25 °C in darkness. Chilling did not require EIN4, ETR1 and EIN2 involved in ethylene signaling to break seed dormancy while GA required ETR1.The improving effect of ethylene in seed germination is EIN4 independent, and is associated with a decrease in ABA/GA ratio and a down-regulation of DELLAs and ABI5 genes related to GA and ABA signaling, respectively. The mutant affected in the proteolytic N-end rule pathway, prt6, was insensitive to ethylene in seed germination evidenced that PRT6 was involved in dormancy release by ethylene, and this insensitivity was related to a crosstalk with ABA/GAs. The substrates of the N-end rule pathway, ERFVIIs (HRE1, HRE2, RAP2.2, RAP2.3, and RAP2.12), might result in the insensitivity with an increased germination in prt6rap2.2rap2.3rap2.12 rather than in prt6hre1hre2, which also indicated that the 3 RAPs acted downstream of PRT6, while the 2 HREs acted upstream of PRT6. Ethylene reduced the transcript expression of the 3 RAPs in Col-0, but the 3 RAPs were maintained or induced by ethylene in prt6. Besides, HRE2 was up-regulated in prt6 seeds, but it was down-regulated in prt6rap2.2rap2.3rap2.12, suggesting that the 3 RAPs might stimulate the expression of HRE2. Ethylene differently changed the seed proteome of Col and prt6 with 587 and 30 significant proteins, respectively. The functional class scoring analysis identified one biological process, response to hypoxia, which was distinct in prt6, however the insensitivity of prt6 to ethylene was independent of ROS production or respiration intensity

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Beers-Mulroy, Blaire. « Visualisation of osteoprogenitor cells in a Prx1 murine fracture model ». Thesis, 2015. https://hdl.handle.net/2144/16282.

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Understanding the recruitment of multipotent skeletal progenitor cells and the factors that influence their differentiation would be helpful in providing a means for harnessing the regenerative capacity of skeletal progenitor cells in bone tissue engineering. In order to track the recruitment of skeletal stem cells in fracture healing, transgenic mice containing a Tamoxifen-inducible Cre recombinase that had been placed under the control of a 2.4 kb Prx1 promotor were used to induce conditional expression in periosteal skeletal stem cells that express the Prx1 gene. In order to initially see the cells expressing Prx1, a green fluorescent protein gene (GFP) had also been put downstream to the Prx1 promotor. We then crossed these Prx1CreER-GFP transgenic mice with a second strain containing the Beta-galactosidase gene that becomes constitutively expressed after recombination by the Cre recombinase. The enzymatic activity of Beta-galactosidase was then used to generate a colormetric staining reaction that was used to visualize the cells in which recombination had occurred based on a blue staining product. The recombination activity should only be present in Prx1 expressing cells and their progeny. The goal of the present study was to assess several different approaches to optimize the Beta-galactosidase enzymatic staining protocol and to visualize the Prx1-expressing cells during fracture healing. These studies further examined those populations of cells in the fracture calluses that became labeled and arose from the stem cell populations that had expressed Prx1 at post-operative day 7 and 14. The optimization of a staining method for histology will allow this study to track Prx1 cell fates in a fracture model both in response to specific drug treatments, mechanical loading of the fracture during healing and under pathological conditions that effect healing.

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Livres sur le sujet "PRX6"

Shaikhali, Jehad. Transcription of 2-Cys PrxA gene from Arabidopsis thaliana : Redox and ABA regulation. Bielefeld : [s.n.], 2006.

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Britain, Great. Non-Woven Products (Product Sales & Trade : PRQ6). Stationery Office Books, 1997.

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Non-woven Products (Product Sales and Trade : PRQ6). The Stationery Office Books (Agencies), 1997.

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Non-woven Products (Product Sales and Trade : PRQ6). The Stationery Office Books (Agencies), 1998.

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Non-woven Products (Product Sales and Trade : PRQ6). The Stationery Office Books (Agencies), 1997.

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Non Woven Products (Product Sales and Trade : PRQ6). The Stationery Office Books (Agencies), 1997.

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EBERT. Bus Ess and Bb Crd and Pln and Pro6. Pearson Education, Limited, 2004.

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Hats and Other Accessories (Product Sales and Trade : PRQ6). The Stationery Office Books (Agencies), 1997.

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Grain Mill & Starch 1996 (Product Sales and Trade : PRA6). The Stationery Office Books (Agencies), 1997.

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Armstrong, Gary, et Philip Kotler. PRIN MARKETG and MARKETG PLAN HDBK and PLAN PRO6. 0. Pearson Education, Limited, 2004.

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Chapitres de livres sur le sujet "PRX6"

Gharesi-Fard, Behrouz. « Preoxiredoxin Family Members (Prx3 and Prx4) and Pregnancy Disorder (Recurrent Pregnancy Loss) ». Dans Advanced Protocols in Oxidative Stress III, 299–311. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1441-8_22.

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Choksi, Nishaant. « Pragmatics of script ». Dans Handbook of Pragmatics, 181–98. Amsterdam : John Benjamins Publishing Company, 2020. http://dx.doi.org/10.1075/hop.22.pra6.

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AL-Barakati, Hussam, Robert H. Newman, Dukka B. KC et Leslie B. Poole. « Bioinformatic Analyses of Peroxiredoxins and RF-Prx : A Random Forest-Based Predictor and Classifier for Prxs ». Dans Methods in Molecular Biology, 155–76. New York, NY : Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2317-6_8.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk et I. Savysyuk. « Cs4[Pr6(C2)]I13 ». Dans Structure Types. Part 9 : Space Groups (148) R-3 - (141) I41/amd, 822. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02702-4_595.

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Niimura, Youichi. « The NADH Oxidase-Prx System in Amphibacillus Xylanus ». Dans Subcellular Biochemistry, 195–205. Dordrecht : Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-6051-9_8.

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Kelly, Sophie, Steven M. Bishop et Ari Ercole. « Statistical Signal Properties of the Pressure-Reactivity Index (PRx) ». Dans Acta Neurochirurgica Supplement, 317–20. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-65798-1_62.

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Schaudy, G., T. Holubar, M. Forsthuber, G. Hilscher, E. Holland-Moritz, V. Nekvasil et P. Rogl. « On the Valency of Pr in (Y1−x Prx)Ba2Cu3O7 ». Dans Springer Series in Solid-State Sciences, 113–18. Berlin, Heidelberg : Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84865-0_20.

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Beqiri, Erta, Ken M. Brady, Jennifer K. Lee, Joseph Donnelly, Frederick A. Zeiler, Marek Czosnyka et Peter Smielewski. « Lower Limit of Reactivity Assessed with PRx in an Experimental Setting ». Dans Acta Neurochirurgica Supplement, 275–78. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-59436-7_51.

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Franck, J. P., S. Gygax, J. Jung, M. A.-K. Mohamed et G. I. Sproule. « The Oxygen Isotope Effect in (Y1-x-y Prx Cay) Ba2Cu307-δ ». Dans High-Temperature Superconductivity, 411–16. Boston, MA : Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3338-2_43.

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Chen, J. M., R. S. Liu, M. J. Kramer, K. W. Dennis et R. W. McCallum. « Superconductivity Suppression in (Nd1.05-x-Prx)Ba1.95Cu3O7 Studied By X-Ray Absorption Spectroscopy ». Dans High-Temperature Superconductors and Novel Inorganic Materials, 211–16. Dordrecht : Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4732-3_36.

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Actes de conférences sur le sujet "PRX6"

Holden, Jeffrey K., et Christian N. Cunningham. « Abstract PR06 : Mechanistic insights for TEAD/YAP activation ». Dans Abstracts : AACR Special Conference on the Hippo Pathway : Signaling, Cancer, and Beyond ; May 8-11, 2019 ; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-pr06.

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Kothari, Vishal, Wei Iris, Sunita Shankar, Shanker Kalyana-Sundaram, Lidong Wang, Linda W. Ma, Pankaj Vats et al. « Abstract PR16 : Targeting cancer-specific kinase dependency for precision therapy ». Dans Abstracts : AACR Precision Medicine Series : Synthetic Lethal Approaches to Cancer Vulnerabilities - May 17-20, 2013 ; Bellevue, WA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.pms-pr16.

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De La Fuente, Adriana, Jimmy Caroli, Dimitri Van Simaeys, Serena Zilio, Emilia Mazza, Vincenzo Bronte, Silvio Bicciato et Paolo Serafini. « Abstract PR16 : RNA aptamers specific for tumor-infiltrating myeloid cells ». Dans Abstracts : AACR Special Conference on Tumor Immunology and Immunotherapy ; November 27-30, 2018 ; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-pr16.

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Nabbi, Arash, Pengbo Sun, Sudhaman Sumedha, Kelsey Zhu, S. Y. Cindy Yang, Joseph N. Paulson, Marcel Kool et al. « Abstract PR06 : The immunogenomic landscape of pediatric primary solid tumors ». Dans Abstracts : AACR Special Conference on the Advances in Pediatric Cancer Research ; September 17-20, 2019 ; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-pr06.

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Abraham, Brian J., Nicholas Kwiatkowski, Abraham S. Weintraub, Denes Hnisz, Nancy Hannett et Richard A. Young. « Abstract PR06 : Nucleation of transcriptional super-enhancers at tumor oncogenes ». Dans Abstracts : AACR Special Conference : Computational and Systems Biology of Cancer ; February 8-11, 2015 ; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.compsysbio-pr06.

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KRUEGER, RONALD, et NELSON V. DE CARVALHO. « DEVELOPMENT OF A C-ELS SPECIMEN-BASED NUMERICAL BENCHMARK FOR MODE II DELAMINATION AND ASSESSMENT OF TWO VCCT-BASED PROPAGATION STRATEGIES ». Dans Proceedings for the American Society for Composites-Thirty Seventh Technical Conference. Destech Publications, Inc., 2022. http://dx.doi.org/10.12783/asc37/36366.

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A finite element (FE) benchmark example inspired by the calibrated end-loaded split (C-ELS) specimen is developed and used to assess the performance of delamination propagation capabilities based on linear elastic fracture mechanics (LEFM). The C-ELS specimen has the advantage of a longer region of stable delamination propagation compared to the existing mode II benchmark case. The new benchmark example may therefore provide a better assessment tool by enabling more stable crack growth in regions further away from the boundary conditions or load application. First, a benchmark result is created manually using two-dimensional finite element models of the C-ELS specimen with different delamination lengths. Second, the performance of the virtual crack closure technique (VCCT) delamination propagation capabilities in the Abaqus/Standard®1 FE code and the recently developed Progressive Release eXplicit-VCCT (PRX-VCCT) method are assessed by comparing the results to the benchmark case. Two examples with different starter delamination lengths are studied. A shorter starter length is chosen to create a scenario with unstable delamination propagation. A longer delamination encourages stable delamination propagation. Detailed results from three-dimensional analyses with aligned and misaligned meshes and two levels of mesh refinement are provided. In general, good agreement can be achieved between the results obtained from the quasi-static propagation analysis and the benchmark analysis. Numerical artifacts including anomalous unreleased nodes in the crack wake and zig-zag crack fronts occur for propagation analyses using Abaqus/Standard VCCT. In comparison, continuous, smooth, delamination fronts are observed for PRX-VCCT. The use of the benchmark case to assess different VCCT-based propagation strategies illustrates the value of establishing benchmark cases.

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Wang, Kai, et Suet Yi Leung. « Abstract PR06 : Genomic characterization of immune escape pathways in gastric cancer ». Dans Abstracts : AACR Special Conference : Tumor Immunology and Immunotherapy : A New Chapter ; December 1-4, 2014 ; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-pr06.

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Cook, David N., Jonathan Peled, Marcel van den Brink et Lata Jayaraman. « Abstract PR06 : Drugging the human microbiome for combination with tumor immunotherapy ». Dans Abstracts : AACR Special Conference on Tumor Immunology and Immunotherapy ; October 1-4, 2017 ; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-pr06.

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Bar-Peled, Liron, Esther Kemper et Benjamin Cravatt. « Abstract PR16 : A druggable transcriptional vulnerability in NRF2-dependent lung cancer ». Dans Abstracts : AACR Precision Medicine Series : Opportunities and Challenges of Exploiting Synthetic Lethality in Cancer ; January 4-7, 2017 ; San Diego, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-8514.synthleth-pr16.

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Jones, Dennis, Han-sin Jeong, Shan Liao et Timothy P. Padera. « Abstract PR06 : Formation of lymph node metastases is not angiogenesis dependent ». Dans Abstracts : AACR Special Conference : Tumor Angiogenesis and Vascular Normalization : Bench to Bedside to Biomarkers ; March 5-8, 2015 ; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.tumang15-pr06.

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Rapports d'organisations sur le sujet "PRX6"

Park, Young-Mee. Hypoxia and Prx1 in Malignant Progression of Prostate Cancer. Fort Belvoir, VA : Defense Technical Information Center, septembre 2007. http://dx.doi.org/10.21236/ada474756.

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