Relevant bibliographies by topics / Potentiators

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Academic literature on the topic 'Potentiators'

Author: Grafiati
Published: 20 April 2024

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Journal articles on the topic "Potentiators"

1

Cui, Guiying, and Nael A. McCarty. "Murine and human CFTR exhibit different sensitivities to CFTR potentiators." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 7 (October 1, 2015): L687—L699. http://dx.doi.org/10.1152/ajplung.00181.2015.

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Development of therapeutic molecules with clinical efficacy as modulators of defective CFTR includes efforts to identify potentiators that can overcome or repair the gating defect in mutant CFTR channels. This has taken a great leap forward with the identification of the potentiator VX-770, now available to patients as “Kalydeco.” Other small molecules with different chemical structure also are capable of potentiating the activity of either wild-type or mutant CFTR, suggesting that there are features of the protein that may be targeted to achieve stimulation of channel activity by structurally diverse compounds. However, neither the mechanisms by which these compounds potentiate mutant CFTR nor the site(s) where these compounds bind have been identified. This knowledge gap partly reflects the lack of appropriate experimental models to provide clues toward the identification of binding sites. Here, we have compared the channel behavior and response to novel and known potentiators of human CFTR (hCFTR) and murine (mCFTR) expressed in Xenopus oocytes. Both hCFTR and mCFTR were blocked by GlyH-101 from the extracellular side, but mCFTR activity was increased with GlyH-101 applied directly to the cytoplasmic side. Similarly, glibenclamide only exhibited a blocking effect on hCFTR but both blocked and potentiated mCFTR in excised membrane patches and in intact oocytes. The clinically used CFTR potentiator VX-770 transiently increased hCFTR by ∼13% but potentiated mCFTR significantly more strongly. Our results suggest that mCFTR pharmacological sensitivities differ from hCFTR, which will provide a useful tool for identifying the binding sites and mechanism for these potentiators.
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Fowler, Jill H., Katherine Whalley, Tracey Murray, Michael J. O'Neill, and James McCulloch. "The AMPA Receptor Potentiator LY404187 Increases Cerebral Glucose Utilization and c-fos Expression in the Rat." Journal of Cerebral Blood Flow & Metabolism 24, no. 10 (October 2004): 1098–109. http://dx.doi.org/10.1097/01.wcb.0000138665.25305.7c.

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AMPA receptor potentiators enhance AMPA receptor-mediated glutamatergic neurotransmission and may have therapeutic potential as cognitive enhancers or antidepressants. The anatomical basis for the action of AMPA receptor potentiators is unknown. The aim of this study was to determine the effects of the biarylpropylsulfonamide AMPA receptor potentiator, LY404187 (0.05 to 5 mg/kg subcutaneously), upon cerebral glucose utilization and c-fos expression using 14C-2-deoxglucose autoradiography and c-fos immunocytochemistry. LY404187 (0.5 mg/kg) produced significant elevations in glucose utilization in 28 of the 52 anatomical regions analyzed, which included rostral neocortical areas and the hippocampus, as well the dorsal raphe nucleus, lateral habenula, and locus coeruleus. No significant decreases in glucose utilization were observed in any region after LY404187 administration. The increases in glucose utilization with LY404187 (0.5 mg/kg) were blocked by pretreatment with the AMPA receptor antagonist LY293558 (25 mg/kg), indicating that LY404187 acts through AMPA receptor-mediated mechanisms. LY404187 (0.5 mg/kg) also produced increases in c-fos immunoreactivity in the cortex, locus coeruleus, and the dorsal raphe nucleus. These studies demonstrate neuronal activation in key brain areas that are associated with memory processes and thus provide an anatomical basis for the cognitive enhancing effects of AMPA receptor potentiators.
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Righetti, Giada, Monica Casale, Michele Tonelli, Nara Liessi, Paola Fossa, Nicoletta Pedemonte, Enrico Millo, and Elena Cichero. "New Insights into the Binding Features of F508del CFTR Potentiators: A Molecular Docking, Pharmacophore Mapping and QSAR Analysis Approach." Pharmaceuticals 13, no. 12 (December 4, 2020): 445. http://dx.doi.org/10.3390/ph13120445.

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Cystic fibrosis (CF) is the autosomal recessive disorder most recurrent in Caucasian populations. To combat this disease, many life-prolonging therapies are required and deeply investigated, including the development of the so-called cystic fibrosis transmembrane conductance regulator (CFTR) modulators, such as correctors and potentiators. Combination therapy with the two series of drugs led to the approval of several multi-drug effective treatments, such as Orkambi, and to the recent promising evaluation of the triple-combination Elexacaftor-Tezacaftor-Ivacaftor. This scenario enlightened the effectiveness of the multi-drug approach to pave the way for the discovery of novel therapeutic agents to contrast CF. The recent X-crystallographic data about the human CFTR in complex with the well-known potentiator Ivacaftor (VX-770) opened the possibility to apply a computational study aimed to explore the key features involved in the potentiator binding. Herein, we discussed molecular docking studies performed onto the chemotypes so far discussed in the literature as CFTR potentiator, reporting the most relevant interactions responsible for their mechanism of action, involving Van der Waals interactions and π–π stacking with F236, Y304, F305 and F312, as well as H-bonding F931, Y304, S308 and R933. This kind of positioning will stabilize the effective potentiator at the CFTR channel. These data have been accompanied by pharmacophore analyses, which promoted the design of novel derivatives endowed with a main (hetero)aromatic core connected to proper substituents, featuring H-bonding moieties. A highly predictive quantitative-structure activity relationship (QSAR) model has been developed, giving a cross-validated r2 (r2cv) = 0.74, a non-cross validated r2 (r2ncv) = 0.90, root mean square error (RMSE) = 0.347, and a test set r2 (r2pred) = 0.86. On the whole, the results are expected to gain useful information to guide the further development and optimization of new CFTR potentiators.
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Favia, Maria, Maria T. Mancini, Valentino Bezzerri, Lorenzo Guerra, Onofrio Laselva, Anna C. Abbattiscianni, Lucantonio Debellis, et al. "Trimethylangelicin promotes the functional rescue of mutant F508del CFTR protein in cystic fibrosis airway cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 1 (July 1, 2014): L48—L61. http://dx.doi.org/10.1152/ajplung.00305.2013.

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Cystic fibrosis transmembrane conductance regulator (CFTR) carrying the F508del mutation is retained in endoplasmic reticulum and fails to traffic to the cell surface where it functions as a protein kinase A (PKA)-activated chloride channel. Pharmacological correctors that rescue the trafficking of F508del CFTR may overcome this defect; however, the rescued F508del CFTR still displays reduced chloride permeability. Therefore, a combined administration of correctors and potentiators of the gating defect is ideal. We recently found that 4,6,4′-trimethylangelicin (TMA), besides inhibiting the expression of the IL-8 gene in airway cells in which the inflammatory response was challenged with Pseudomonas aeruginosa, also potentiates the cAMP/PKA-dependent activation of wild-type CFTR or F508del CFTR that has been restored to the plasma membrane. Here, we demonstrate that long preincubation with nanomolar concentrations of TMA is able to effectively rescue both F508del CFTR-dependent chloride secretion and F508del CFTR cell surface expression in both primary or secondary airway cell monolayers homozygous for F508del mutation. The correction effect of TMA seems to be selective for CFTR and persisted for 24 h after washout. Altogether, the results suggest that TMA, besides its anti-inflammatory and potentiator activities, also displays corrector properties.
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Bacalhau, Mafalda, Filipa C. Ferreira, Iris A. L. Silva, Camilla D. Buarque, Margarida D. Amaral, and Miquéias Lopes-Pacheco. "Additive Potentiation of R334W-CFTR Function by Novel Small Molecules." Journal of Personalized Medicine 13, no. 1 (January 1, 2023): 102. http://dx.doi.org/10.3390/jpm13010102.

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The R334W (c.1000C>T, p.Arg334Trp) is a rare cystic fibrosis (CF)-causing mutation for which no causal therapy is currently approved. This mutation leads to a significant reduction of CF transmembrane conductance regulator (CFTR) channel conductance that still allows for residual function. Potentiators are small molecules that interact with CFTR protein at the plasma membrane to enhance CFTR-dependent chloride secretion, representing thus pharmacotherapies targeting the root cause of the disease. Here, we generated a new CF bronchial epithelial (CFBE) cell line to screen a collection of compounds and identify novel potentiators for R334W-CFTR. The active compounds were then validated by electrophysiological assays and their additive effects in combination with VX-770, genistein, or VX-445 were exploited in this cell line and further confirmed in intestinal organoids. Four compounds (LSO-24, LSO-25, LSO-38, and LSO-77) were active in the functional primary screen and their ability to enhance R334W-CFTR-dependent chloride secretion was confirmed using electrophysiological measurements. In silico ADME analyses demonstrated that these compounds follow Lipinski’s rule of five and are thus suggested to be orally bioavailable. Dose–response relationships revealed nevertheless suboptimal efficacy and weak potency exerted by these compounds. VX-770 and genistein also displayed a small potentiation of R334W-CFTR function, while VX-445 demonstrated no potentiator activity for this mutation. In the R334W-expressing cell line, CFTR function was further enhanced by the combination of LSO-24, LSO-25, LSO-38, or LSO-77 with VX-770, but not with genistein. The efficacy of potentiator VX-770 combined with active LSO compounds was further confirmed in intestinal organoids (R334W/R334W genotype). Taken together, these molecules were demonstrated to potentiate R334W-CFTR function by a different mechanism than that of VX-770. They may provide a feasible starting point for the design of analogs with improved CFTR-potentiator activity.
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Pedemonte, Nicoletta, Valeria Tomati, Elvira Sondo, and Luis J. V. Galietta. "Influence of cell background on pharmacological rescue of mutant CFTR." American Journal of Physiology-Cell Physiology 298, no. 4 (April 2010): C866—C874. http://dx.doi.org/10.1152/ajpcell.00404.2009.

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Cystic fibrosis (CF) is caused by mutations in the CFTR chloride channel. Deletion of phenylalanine 508 (F508del), the most frequent CF mutation, impairs the maturation and gating of the CFTR protein. Such defects may be corrected in vitro by pharmacological modulators named as correctors and potentiators, respectively. We have evaluated a panel of correctors and potentiators derived from various sources to assess potency, efficacy, and mechanism of action. For this purpose, we have used functional and biochemical assays on two different cell expression systems, Fischer rat thyroid (FRT) and A549 cells. The order of potency and efficacy of potentiators was similar in the two cell types considered, with phenylglycine PG-01 and isoxazole UCCF-152 being the most potent and least potent, respectively. Most potentiators were also effective on two mutations, G551D and G1349D, that cause a purely gating defect. In contrast, corrector effect was strongly affected by cell background, with the extreme case of many compounds working in one cell type only. Our findings are in favor of a direct action of potentiators on CFTR, possibly at a common binding site. In contrast, most correctors seem to work indirectly with various mechanisms of action. Combinations of correctors acting at different levels may lead to additive F508del-CFTR rescue.
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Mancini, Giulia, Nicoletta Loberto, Debora Olioso, Maria Cristina Dechecchi, Giulio Cabrini, Laura Mauri, Rosaria Bassi, et al. "GM1 as Adjuvant of Innovative Therapies for Cystic Fibrosis Disease." International Journal of Molecular Sciences 21, no. 12 (June 24, 2020): 4486. http://dx.doi.org/10.3390/ijms21124486.

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Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein is expressed at the apical plasma membrane (PM) of different epithelial cells. The most common mutation responsible for the onset of cystic fibrosis (CF), F508del, inhibits the biosynthesis and transport of the protein at PM, and also presents gating and stability defects of the membrane anion channel upon its rescue by the use of correctors and potentiators. This prompted a multiple drug strategy for F508delCFTR aimed simultaneously at its rescue, functional potentiation and PM stabilization. Since ganglioside GM1 is involved in the functional stabilization of transmembrane proteins, we investigated its role as an adjuvant to increase the effectiveness of CFTR modulators. According to our results, we found that GM1 resides in the same PM microenvironment as CFTR. In CF cells, the expression of the mutated channel is accompanied by a decrease in the PM GM1 content. Interestingly, by the exogenous administration of GM1, it becomes a component of the PM, reducing the destabilizing effect of the potentiator VX-770 on rescued CFTR protein expression/function and improving its stabilization. This evidence could represent a starting point for developing innovative therapeutic strategies based on the co-administration of GM1, correctors and potentiators, with the aim of improving F508del CFTR function.
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Basta, Karol, and Chris John. "Combination Correctors and Potentiators for Cystic Fibrosis." Physician 6, no. 1 (November 27, 2019): c7. http://dx.doi.org/10.38192/1.6.1.c7.

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The most common cause of cystic fibrosis (CF) is the Phe508del mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) protein, resulting in CFTR’s reduced trafficking, targeted by correctors, and reduced functioning, targeted by potentiators. For the majority of CF patients, the combination correctors and potentiators (CCPs) lumacaftor/ivacaftor and tezacaftor/ivacaftor, are the only treatments licensed to target the disease origin.
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Cuyx, Senne, and Kris De Boeck. "Treating the Underlying Cystic Fibrosis Transmembrane Conductance Regulator Defect in Patients with Cystic Fibrosis." Seminars in Respiratory and Critical Care Medicine 40, no. 06 (October 28, 2019): 762–74. http://dx.doi.org/10.1055/s-0039-1696664.

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AbstractDetailed knowledge of how mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene disturb the trafficking or function of the CFTR protein and the use of high-throughput drug screens have allowed novel therapeutic strategies for cystic fibrosis (CF). The main goal of treatment is slowly but surely shifting from symptomatic management to targeting the underlying CFTR defect to halt disease progression and even to prevent occurrence of CF complications. CFTR potentiators for patients with class III mutations, mutation R117H (and in United States also for patients with specific residual function mutations) and the combination of a CFTR modulator plus a potentiator for patients homozygous for F508del, are the two classes of modulators that are in use in the clinic. Approval of these therapeutics has progressively expanded to include both younger patients and a wider range of CFTR mutations. For a significant proportion of patients with CF, current treatment is however still insufficient or unavailable.This review provides an overview of the clinical trial results and the real-life efficacy data of approved CFTR modulators. In addition, we discuss the entire pipeline of CFTR modulators: novel potentiators and correctors, amplifiers, stabilizers, and read-through agents. Furthermore, we discuss other strategies to improve CFTR function like nonsense-mediated decay inhibitors, modified transfer ribonucleic acids, antisense oligonucleotides, and genetic therapies.CFTR modulators are already changing the face of CF and the pipeline of new therapies continues to be exciting.
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Mareux, Elodie, Martine Lapalus, Amel Ben Saad, Renaud Zelli, Mounia Lakli, Yosra Riahi, Marion Almes, et al. "In Vitro Rescue of the Bile Acid Transport Function of ABCB11 Variants by CFTR Potentiators." International Journal of Molecular Sciences 23, no. 18 (September 15, 2022): 10758. http://dx.doi.org/10.3390/ijms231810758.

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ABCB11 is responsible for biliary bile acid secretion at the canalicular membrane of hepatocytes. Variations in the ABCB11 gene cause a spectrum of rare liver diseases. The most severe form is progressive familial intrahepatic cholestasis type 2 (PFIC2). Current medical treatments have limited efficacy. Here, we report the in vitro study of Abcb11 missense variants identified in PFIC2 patients and their functional rescue using cystic fibrosis transmembrane conductance regulator potentiators. Three ABCB11 disease-causing variations identified in PFIC2 patients (i.e., A257V, T463I and G562D) were reproduced in a plasmid encoding an Abcb11-green fluorescent protein. After transfection, the expression and localization of the variants were studied in HepG2 cells. Taurocholate transport activity and the effect of potentiators were studied in Madin–Darby canine kidney (MDCK) clones coexpressing Abcb11 and the sodium taurocholate cotransporting polypeptide (Ntcp/Slc10A1). As predicted using three-dimensional structure analysis, the three variants were expressed at the canalicular membrane but showed a defective function. Ivacaftor, GLP1837, SBC040 and SBC219 potentiators increased the bile acid transport of A257V and T463I and to a lesser extent, of G562D Abcb11 missense variants. In addition, a synergic effect was observed when ivacaftor was combined with SBC040 or SBC219. Such potentiators could represent new pharmacological approaches for improving the condition of patients with ABCB11 deficiency due to missense variations affecting the function of the transporter.
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Dissertations / Theses on the topic "Potentiators"

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Voss, Oliver Paul. "AMPA receptor potentiators : mechanisms of neuroplasticity." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/25276.

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The AMPA receptor potentiator LY404187 is able to significantly increase the average length of neuritic processes in the neuroblastoma cell line SH-SY5Y only in the presence of s-AMPA, and this response is dependent on AMPA receptor activation. The compound also increases neurofilament protein levels as well as levels of the BDNF receptor Trk-B. The increase in neuritic length is blocked by addition of an antibody specific for BDNF indicating that this neurotrophin is required for the induction of neurite growth. The ability to induce morphological change in neuronal processes of the compound was then tested in a rodent model of lesions and sprouting. Unilateral ibotenic lesions of the entorhinal cortex in mice produce a progressive and substantial loss of synapses in the molecular layer of the dentate gyrus. Twice daily s.c. injections of LY404187 for 14 and 28 days post-lesion did not produce any significant change in synaptophysin immunoreactivity in the dentate gyrus. There was also no change in the volume of the lesion in the entorhinal cortex. In a secondary study the rate of neurogenesis in the dentate gyrus was also measured. Administration of LY404187 failed to induce a change in the number of BrdU +ve cells within the sub-granular zone of the dentate gyrus. Any long term structural of behavioural change caused by prolonged AMPA receptor potentiation is likely to be underpinned by changes in protein expression. The levels of key proteins involved in the intracellular response to AMPA receptor activation were measured by Western Blot and immunohistochemistry and levels of the neurotransmitters dopamine and serotonin were measured by HPLC. The effect of chronic administration to the AMPA receptor potentiator LY450108 on the rate of neurogenesis and the development of newly born neuron in the hippocampus was also investigated.
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Krishnan, Ramya. "Characterization of Novel Small Molecule Potentiators of Oncolytic Virotherapy." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37551.

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The use of oncolytic viruses (OVs) to selectively destroy cancer cells is poised to make a major impact in the clinic and potentially revolutionize cancer therapy. Pre-clinical and clinical studies have shown that OV therapy is safe, well-tolerated and effective in a broad range of cancers. Still, resistance due to tumour heterogeneity highlights areas for improvement in OV based therapeutics. Combining OVs and small molecules is a promising strategy to selectively enhance OV-mediated anti-tumour effects. To this end, we have previously identified the synthetic compound Viral Sensitizer 1 (VSe1) that enhances the spread of oncolytic vesicular stomatitis virus (VSVΔ51) in resistant cancer cell lines up to 1000-fold, resulting in synergistic cell killing and improved efficacy in vitro and in vivo. The electrophilic nature of VSe1 prompted us to investigate the scaffold to identify active analogs with more favourable physiochemical properties and explore structure-activity relationships (SAR). In vitro assays and a rational approach in the design of VSe1 analogs allowed us to identify functional groups that can be modified without hampering activity. Lead compounds created in this study based on a pyrrole scaffold increase OV growth up to 2000-fold in vitro and demonstrate remarkable selectivity for cancer cells over normal tissue ex vivo and in vivo. Compared to the parental VSe1, these small molecules also possess enhanced stability with reduced electrophilicity and are well-tolerated in animals, leading to reduced tumour burden and prolonged survival in vivo when used in combination with VSVΔ51. It was known from previous studies that VSe1 suppresses the type I interferon response generated by cancer cells to defend against viral infection. In this study, further investigation revealed that VSe1 and its analogs inhibit the nuclear translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), resulting in dampened transcriptional expression and secretion of IFN-β and interferon stimulated genes, thereby increasing viral replication and spread. While these findings further elucidated the effect these compounds have on the innate antiviral response, the molecular mechanisms leading to NFκB inhibition remained unclear. We used the newly generated VSe1 analogs to perform ligand-based affinity capture studies leading to the identification of glutathione-s-transferases as interacting proteins, catalytically inhibited by VSe1 and to a lesser extent by its pyrrole analogs. Further inquiry revealed that VSe1 and its analogs cause an imbalance in cellular glutathione homeostasis and increase oxidative stress, which is associated with inhibition of the nuclear translocation of NFκB. However, further studies are required to assess whether these phenomena are directly or indirectly linked. Overall, this study highlights a novel approach to improving OV therapy by using a previously uncharacterized class of compounds that ultimately alter the innate cellular antiviral response through inhibition of NFκB.
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El-Sayes, Nader. "Small Molecule Potentiators of Oncolytic Virus Therapy Suppress the Innate Antiviral Response." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37115.

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Oncolytic Viruses (OVs) are often attenuated to increase their safety profile, however this can lead to reduced efficacy in heterogeneous malignancies and result in resistance to OV therapy. Our group utilizes small molecule enhancers of OV therapy termed viral sensitizers. These small molecules have been shown to enhance the replication and spread of oncolytic rhabdovirus VSVΔ51 in vitro and prolong survival in tumour-bearing mice. In this study, we evaluate the ef-fect of these viral sensitizers on the innate antiviral response in order to identify the mechanism of action responsible for their viral-sensitizing properties. Our previous data suggest that VSe1 and its structural analogues affect the type I IFN antiviral response and have the potential to af-fect cellular redox homeostasis. We hypothesized that VSe1 and its structural analogues potenti-ate VSV∆51 activity by inhibiting the type I IFN response via redox-mediated dysregulation. In this study, we demonstrate that the viral sensitizers inhibit the nuclear translocation and transcrip-tional activity of NFκB, which in turn dampens the expression of antiviral cytokines IFN-, TNFα and IL-6. We also provide evidence supporting the possibility that the NFκB inhibition may be a result of the formation of ROS intermediates by the viral sensitizers, which leads to re-duced nuclear translocation of NFκB subunits, thereby preventing NFκB-mediated cytokine production. Overall, this work contributes to the identification of the mechanism of action of our viral sensitizers and highlights the finding that oncolytic VSV infection can be enhanced through redox-mediated modulation of the innate antiviral response.
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Kinting, Susanna [Verfasser], and Heinrich [Akademischer Betreuer] Leonhardt. "Functional rescue of mutant ABCA3 by correctors and potentiators / Susanna Kinting ; Betreuer: Heinrich Leonhardt." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1204005281/34.

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Quintela, Varela Hugo [Verfasser], and Dirk [Akademischer Betreuer] Trauner. "Biomimetic synthesis of (−)-PF-1018 and development of photoswitchable GABAA receptor potentiators / Hugo Quintela Varela ; Betreuer: Dirk Trauner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1221960458/34.

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Mareux, Elodie. "Pharmacothérapie ciblée des déficits en ABCB11." Electronic Thesis or Diss., université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL083.

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ABCB11/BSEP (Bile Salt Export Pump) est exprimé à la membrane canaliculaire des hépatocytes. Sa fonction de transport d’acides biliaires dans la bile est essentielle à la sécrétion biliaire. Près de 400 variations du gène ABCB11 ont été identifiées et sont associées à des maladies hépatobiliaires rares, la plus sévère étant la cholestase intrahépatique progressive familiale de type 2 (PFIC2). L’efficacité des traitements médicaux est limitée. Par conséquent, une transplantation hépatique est indiquée avant l’âge adulte pour près de deux tiers des patients. Dans ce contexte, l’identification de thérapies alternatives est un enjeu capital.Cette thèse s’intéresse à la recherche de stratégies thérapeutiques personnalisées permettant de corriger les conséquences pathologiques de certaines variations d’ABCB11 identifiées chez des patients. Dans le cadre d’une stratégie de traitement par des molécules potentiatrices, nous avons étudié les variations A257V, G562D et T463I d’ABCB11 par modélisation moléculaire 3D. L’étude de l’expression et de la fonction de ces variants dans différents modèles cellulaires a confirmé que ces variations étaient responsables d’un défaut de fonction du transporteur Abcb11. L’ivacaftor (VX 770, Kalydeco®), approuvé cliniquement pour le traitement de la mucoviscidose, corrigeait le défaut d’activité de ces trois variants.Des effets similaires ont été observés avec les molécules GLPG1837, SBC040 et SBC219, connues comme potentiateurs de CFTR (Cystic Fibrosis Transmembrane conductance Regulator). Dans une optique de thérapie combinatoire, nous avons également mis en évidence la capacité de ces potentiateurs à corriger le défaut de fonction des variants R1090C et R1090W, produits potentiels de la translecture du variant non-sens R1090X. Nous avons également évalué les molécules correctrices elexacaftor (VX-445) et tezacaftor (VX-661). Ces correcteurs, en monothérapie ou en combinaison, permettaient de restaurer l’adressage du variant R1128C, s’accompagnant d’une augmentation significative du transport de taurocholate. De façon intéressante, l’addition de molécules potentiatrices réduisait ces effets.L’ensemble de ces travaux constitue une preuve de concept que les défauts de certains variants d’ABCB11 peuvent être corrigés par ces molécules potentiatrices à haut potentiel thérapeutique. Ce type de traitements pourrait être envisagé pour les patients atteints de déficit en ABCB11 et permettrait ainsi d’augmenter la pharmacopée disponible pour traiter ce genre de pathologies et ainsi repousser voir palier à la transplantation hépatique pour les cas les plus sévères
ABCB11/BSEP (Bile Salt Export Pump) is expressed at the canalicular membrane of hepatocytes. It ensures bile acids secretion into bile which is essential for biliary secretion. Nearly 400 variations of the ABCB11 gene have been identified and are associated with rare hepatobiliary diseases, the most severe being progressive familial intrahepatic cholestasis type 2 (PFIC2). The effectiveness of medical treatments is limited. Consequently, liver transplantation is required before adulthood for almost 2/3 of PFIC2 patients. In this context, the identification of alternative therapies is a major challenge.This thesis focuses on personalized therapeutic strategies to correct the pathological consequences of some ABCB11 variations identified in patients. The A257V, G562D and T463I variations of ABCB11 were studied by 3D molecular modelling. These variations were responsible for a defect in Abcb11 transport function. Ivacaftor (VX-770, Kalydeco®), a clinically approved cystic fibrosis treatment, corrects the activity defect of the three variants.Similar effects were observed with GLPG1837, SBC040 and SBC219, known as potentiators of CFTR (Cystic Fibrosis Transmembrane Conductance Regulator).From a combinatory therapy perspective, we also demonstrated the ability of these potentiators to correct the transport defect of the R1090C and R1090W variants, potential readthrough products of the R1090X nonsense variant. We also evaluated the ability of Elexacaftor (VX-445) and Tezacaftor (VX 661) correctors of CFTR. These correctors, alone or in combination, restored trafficking of the R1128C missense variant, leading to a significant increase in the transport function. Interestingly, the addition of potentiators abolishes this effect.Altogether, this thesis constitutes a proof of concept that molecules with high therapeutic potential can correct the molecular defects of ABCB11 variants. These treatments could increase the pharmacopoeia available for patients with ABCB11 deficiency and thus delay or even suppress the need for liver transplantation
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Hanoteau, Aurélie. "Chemotherapy potentiates immune responses against murine tumors." Doctoral thesis, Universite Libre de Bruxelles, 2016. https://dipot.ulb.ac.be/dspace/bitstream/2013/231745/5/Thesis.pdf.

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There is increasing evidence that the effect of chemotherapy on tumor rejection is not cell autonomous but relies on the immune system. Indeed, several reports have shown that human and murine tumors respond to chemotherapeutic agents more efficiently when the host immune system is intact. In particular, we have shown that cyclophosphamide treatment of DBA/2 mice bearing P815 mastocytoma induces rejection and long term protection in a CD4- and CD8-dependent manner. We used this tumor model, as it is poorly immunogenic, expresses tumor-associated P1A and tumor-specific P1E antigens, encoded by germline and mutated genes, respectively, and allows the identification of some tumor-specific CD8+ T cells.We have previously reported that tumor regression correlates with selective infiltration of CD8+ T cells specific for P1E/H-2Kd antigen in tumor bed upon cyclophosphamide treatment. Unexpectedly, the proportion of CD8+ T cells specific for the tumor-associated antigen P1A in the context of H-2Ld decreases concomitantly, indicating that cyclophosphamide alters the repertoire of CD8+ T cells recognizing tumor antigens. Using P1A KO mice, we found that preferential activation of CD8+ T cells to P1E is not solely due to thymic negative selection. The major role of “mutated” antigens in tumor resistance has been recently highlighted in humans and raises an interesting question about the immune mechanisms of tumor rejection. Additionally to its effect on the specific immune response, cyclophosphamide promotes tumor infiltration by effector memory (P1E/H-2Kd)+ CD8+ T cells which are characterized by higher expression of KLRG1 and Eomes. Our data point to a role of IL-15 and type 1 IFNs for their development, as increased levels of IL-15 and IRF7 were measured in tumor after cyclophosphamide. IFNAR1 blockade interferes with the tumor rejection in 50% of mice and decreases the (P1E/H-2Kd)+ CD8+ T cell infiltration induced by cyclophosphamide, suggesting a role of this cytokine in the expansion and/or recruitment of (P1E/H-2Kd)+ CD8+ T cells in vivo.Altogether, our results suggest that type 1 IFNs and IL-15 induced after cyclophosphamide promote the reprogramming of CD8+ T cells specific for the “mutated” P1E/H-2Kd antigen into effector memory lymphocytes.
Option Biologie moléculaire du Doctorat en Sciences
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Khalil, Dayekh. "Novel Combination Therapy: Monensin Potentiates Erlotinib-Induced Cytotoxicity." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24405.

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Receptor Tyrosine Kinase (RTK) inhibitors, such as erlotinib/tarceva, have been introduced in the past decade as a promising therapeutic option in Head and Neck Squamous Cell Carcinoma (HNSCC), however, they lack significant efficacy as single agents. As a result, RTK inhibitors require a combination based therapeutic approach with other treatment modalities. To uncover such a combination of agents, we performed a high throughput Prestwick library screen that included 1200 compounds approved by the FDA on HNSCC cell lines and found that monensin, a coccidial antibiotic, synergistically enhanced the cytotoxicity of erlotinib. RT-PCR revealed that monensin induced the expression of Activation of Transcription Factor (ATF) 3 and its downstream target C/EBP homologous protein (CHOP) which are key regulators of apoptosis. Furthermore, RNA-Seq analysis suggests that monensin augments erlotinib cytotoxicity by disturbing lipid and sterol biosynthesis. Therefore, identifying the mechanism of action exerted by monensin may open alternative avenues of cancer treatment.
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Lortie, Karine. "The growth-arrest-specific protein gas7 potentiates neuronal differentiation." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26701.

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The growth-arrest-specific gas7 protein is involved in neuronal development. Its role in neuronal differentiation and its potential neuroprotective activity were investigated in PC 12 and NT2 cells. gas7 overexpression in PC12 cells promoted neurite outgrowth and potentiated nerve growth factor-induced expression of the neuronal markers betaIII-tubulin, synaptotagmin, alpha7 subunit of the acethylcholine receptor, and dihydropyrimidinase related protein-3. This effect was exerted independently of cellular proliferation, as gas7 did not affect cell cycle progression. Endogenous gas7 expression was induced during neuronal differentiation of NT2 cells with retinoic acid, suggesting a role for gas7 in neuronal development. Finally, gas7 overexpression in PC 12 cells did not protect against toxicity triggered by oxygen-glucose deprivation, the calcium ionophore A23187 or sodium nitroprusside. The ability of gas7 to potentiate neuritogenesis and neuronal differentiation makes it a potential therapeutic target to promote re-establishment of neuronal connections in the injured or diseased brain, such as following stroke.
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Seufert, Florian [Verfasser], and Ulrike [Gutachter] Holzgrabe. "Entwicklung von Inhibitoren des „macrophage infectivity potentiator“-Proteins / Florian Seufert. Gutachter: Ulrike Holzgrabe." Würzburg : Universität Würzburg, 2016. http://d-nb.info/1112041222/34.

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Books on the topic "Potentiators"

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Singh, Manmohan, ed. Novel Immune Potentiators and Delivery Technologies for Next Generation Vaccines. Boston, MA: Springer US, 2013. http://dx.doi.org/10.1007/978-1-4614-5380-2.

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Dare, Amos O. Ouabain potentiates kainate neurotoxicity: A new rat model of human temporal lobe epilepsy. [New Haven, Conn: s.n.], 1996.

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Schwartz, Gary K. Combination Cancer Therapy: Modulators and Potentiators. Humana Press, 2014.

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Schwartz, Gary K. Combination Cancer Therapy: Modulators and Potentiators. Humana Press, 2004.

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Singh, Manmohan. Novel Immune Potentiators and Delivery Technologies for Next Generation Vaccines. Springer London, Limited, 2013.

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Singh, Manmohan. Novel Immune Potentiators and Delivery Technologies for Next Generation Vaccines. Springer, 2015.

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Novel Immune Potentiators And Delivery Technologies For Next Generation Vaccines. Springer-Verlag New York Inc., 2012.

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Combination Cancer Therapy: Modulators and Potentiators (Cancer Drug Discovery and Development). Humana Press, 2004.

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The New Superantioxidant-Plus : The Amazing Story of Pycnogenol, Free-Radical Antagonist and Vitamin C Potentiator (Good Health Guide Series). McGraw-Hill, 1998.

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Main, Jeffrey Scott *. Heart failure potentiates the modulatory influence of the endothelium on alpha-adrenergic-mediated responses in canine coronary arteries. 1989.

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Book chapters on the topic "Potentiators"

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Heath, Henry B., and Gary Reineccius. "Flavor Potentiators." In Flavor Chemistry and Technology, 318–31. London: Macmillan Education UK, 1986. http://dx.doi.org/10.1007/978-1-349-09350-2_9.

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Heath, Henry B., and Gary Reineccius. "Flavor Potentiators." In Flavor Chemistry and Technology, 318–31. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-011-9759-5_9.

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Lindenmann, J. "The Use of Viruses as Immunological Potentiators." In Ciba Foundation Symposium 18 - Immunopotentiation, 197–215. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720011.ch10.

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Shikina, Shinya, and Ching-Fong Chang. "Neuropeptides as Potentiators of Coral Polyp Contraction." In Frontiers in Invertebrate Physiology: A Collection of Reviews, 317–41. New York: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003403319-6.

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Garro-Martínez, Emilio, and Albert Adell. "AMPA Receptor Potentiators as Potential Rapid-Acting Antidepressants." In Contemporary Clinical Neuroscience, 85–109. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-79790-4_6.

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Tomai, Mark A., and John P. Vasilakos. "TLR7/8 Agonists as Vaccine Adjuvants." In Novel Immune Potentiators and Delivery Technologies for Next Generation Vaccines, 3–18. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-5380-2_1.

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Andrianov, Alexander K. "Microneedles for Intradermal Vaccination: Immunopotentiation and Formulation Aspects." In Novel Immune Potentiators and Delivery Technologies for Next Generation Vaccines, 217–32. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-5380-2_10.

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Singh, Parminder, Guohua Chen, and Wade Worsham. "MicroCor® Transdermal Delivery System: A Safe, Efficient, and Convenient Transdermal System for Vaccine Administration." In Novel Immune Potentiators and Delivery Technologies for Next Generation Vaccines, 233–44. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-5380-2_11.

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Leenhouts, Kees. "Mimopath™-Based Vaccine Delivery." In Novel Immune Potentiators and Delivery Technologies for Next Generation Vaccines, 245–65. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-5380-2_12.

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Hamouda, Tarek, Jakub Simon, Ali Fattom, and James Baker. "NanoBio™ Nanoemulsion for Mucosal Vaccine Delivery." In Novel Immune Potentiators and Delivery Technologies for Next Generation Vaccines, 269–86. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-5380-2_13.

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Conference papers on the topic "Potentiators"

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Prasetyoputri, Anggia, Mega Ferdina Warsito, Akhirta Atikana, Eko Wahyu Putro, Lutfi Nia Kholida, and Linda Sukmarini. "Antibiotic potentiators to combat resistance in methicillin-resistant Staphylococcus aureus (MRSA): A mini review." In PROCEEDINGS OF THE 9TH INTERNATIONAL SYMPOSIUM ON INNOVATIVE BIOPRODUCTION INDONESIA ON BIOTECHNOLOGY AND BIOENGINEERING 2022: Strengthening Bioeconomy through Applied Biotechnology, Bioengineering, and Biodiversity. AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0185419.

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Heneghan, M., KW Southern, J. Murphy, IP Sinha, and SJ Nevitt. "P70 Corrector therapies (with or without potentiators) for people with cystic fibrosis with class II CFTR gene variants (most commonly F508del)." In British Thoracic Society Winter Meeting 2022, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 23 to 25 November 2022, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2022. http://dx.doi.org/10.1136/thorax-2022-btsabstracts.206.

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Grosche, A., X. Xu, S. Lin, M. Abu-Hassan, S. Prabhakaran, and S. Vidyasagar. "Amino Acids Regulate Defective CFTR Trafficking and Gating in Primary Human F508del-Bronchial Epithelial Cells Similar to Cystic Fibrosis Correctors and Potentiators." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7455.

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Uluata, Sibel, Seymanur Avci, and Gokhan Durmaz. "Comparing Physical Stability of Ultrasound and Pickering Emulsion Fortified with Vitamin D." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/cwoy2387.

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"Vitamin D is one of the important fat-soluble vitamins for human health. The fact that this vitamin is much lower or higher than needed creates some problems. The World Health Organization (WHO) has recognized fortification as the most effective and safest method to meet the daily requirements of Vitamin D, addressing malnutrition. However, it has numerous difficulties such as loss during processing and storage during food fortification. In recent developments in nanotechnology, microencapsulation technique such as emulsion has great potential to design efficient nanomaterials with desired functionality for fortifying potentiators such as vitamin D. In this study, the effect of emulsifier type and different oil types on the formation and stability of emulsions was determined by measuring the changes in droplet properties (size and charge) under pH, salt and temperature conditions. Emulsion fortified with vitamin D was prepare by using oil phase (linseed, sunflower and MCT oil), emulsifier (pea and lentil protein) with ultrasonication and pickering emulsion method. The mean particle diameter of the pea protein-linseed oil-water emulsions formed using the ultrasonication method was 0.21 µm and the droplet charge was -37.3 mV. In the Pickering emulsion method, the mean particle diameter was 0.17 µm and the droplet charge was -26.75 mV. Also, particle size were 0.24, 22.14, 0.15 µm and particle charge were 24.60, -19.65, -27.80 mV at pH 3, 5 and 7, respectively. In addition, the particle size of pickering emulsion did not dramtically change at 30˚C and 90˚C temperatures and at 100 mM and 500 mM salt concentrations. As a result, pickering emulsion was physically more stable than ultrasound emulsion. This study was supported by Inonu University Scientific Research Projects Unit with The Project number :FYL-2021-2355"
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Joseph, S. K., S. Krishnamurthi, and V. V. Kakkar. "R59022, A DIACYLGLYCEROL (DG) KINASE INHIBITOR POTENTIATES THROMBIN-INDUCED PLATELET AGGREGATION AND GRANULE RELEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644504.

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R59022 is a recently described inhibitor of the enzyme DG kinase [1], which converts DG to phosphatidic acid. While R59002 inhibits DG conversion in platelets resulting in enhanced protein kinase C (PrkC) activation [1], little is known on its effect on other platelet responses. In this study, we have examined the effect of R59022 on agonist-induced platelet aggregation and [14C]-5-hydroxytryptamine (5HT) release using washed human platelets. With a sub-maximal concentration of thrombin (T, 0.05U/ml) R59022 (10-30μM) significantly potentiated T-induced platelet aggregation and [14C]-5HT release eg % [14C]-5HT release:- 0.05U/ml T-52±5,30μM R59022+T-76±8. Removal of external Ca2+ (ImM) using EGTA (5mM) reduced T-induced 5HT release but not the potentiation of it by R59022 eg EGTA+ 0.05U/ml T-36±6%, EGTA+R59022+T- 72±5%. These results show that in the presence of EGTA and R59022 the increased DG levels can compensate for the diminished rise in T-induced Ca/2+ mobilisation thus re-emphasizing the importance of DG in promoting granule secretion. In addition to inhibiting DG phosphorylation, R59022 also inhibits the phosphorylation of the DG analogue 1-oleoyl 2-acetylglycerol (OAG) [1]. OAG (63μM) with pre-incubation times of 10-60 sec, significantly potentiated threshold T (0.03U/ml)-induced [l4C]-5HT release, though with longer incubation times, this potentiatory effect was gradually lost eg 0.03U/ml T-l±0.3%, OAG+T (10 sec)- 33±4%, OAG+T (1 min)-11±3%, 0AG+veh.-0%. However, in the presence of R59022 (30μM), OAG retained its potentiatory effect for longer periods eg R59022+0AG+T (1 min)-45+10%, R59022+T-2±l%. With incubation times > 5 min the potentiatory effects of OAG were lost even in the presence of R59022. This is possibly due to the metabolism of OAG by DG lipase. Our results demonstrate that R59022, which has been reported to inhibit DG kinase leading to enhanced PrkC activation, also enhances agonist-induced platelet aggregation and 5HT release. It may therefore be a useful compound in elucidating further the role of DG in terms of both stimulatory and inhibitory effects on platelet activation.[1]. de Chaffoy de Coucelles, D. et al (1985) J Biol Chem 260, 15762.
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Schaible, N., R. Guo, E. Phalen, K. Chmiel, X. Ai, Y. Bai, A. A. Zeki, and R. Krishnan. "Pitavastatin Potentiates Beta2-Agonist Induced Bronchodilation." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5496.

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Sherrill, Taylor P., George Stathopoulos, Fiona E. Yull, Barbara Fingleton, and Timothy S. Blackwell. "Host-Derived Interleukin-5 Potentiates Lung Metastasis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2522.

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Takada, Y., Y. Sugawara, Y. Makino, and A. Takada. "KINETIC ANALYSES OF THE ACTIVATION OF GLU- OR LYS-PLASMINOGEN BY STREPTOKINASE IN THE PRESENCE OF FIBRIN OR ITS DEGRADATION PRODUCTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644419.

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Human plasminogen was activated better by streptokinase (SK) in the presence of fibrin or its degradation products(potentiating agents). Such potentiating agents must be mixed with SK and plasminogen simultaneously. The addition of potentiating agents to the mixture of SK and plasminogen did not result in any enhancement of the activator activity of SK-plasminogen complex. Since potentiating agents such as fibrin bind to lysine binding sites (LBS) of plasminogen, and SK was known to bind to light chain side of plasminogen, it appears that a trimolecular complex of SK, plasminogen and a potentiating agent is a better enzyme than a complex of SK and plasminogen. The effectiveness of the potentiation was in the order of fibrin> SK-potentiator(early FgDP)> fibrinogen >fragment D >fragment E, when Glu-plasminogen was activated by SK. When Lys-plasminogen was used, fragment E was more effective than fragment D, thus in the order of fibrin> SK potentiator> fibrinogen>fragment E >fragment D. Such enhancement of the activation of plasminogen by fibrin or potentiating agents is more significant in the presence of lower concentration of SK. Increase in the concentration of SK did not result in much enhancement of the activation of plasminogen. Kinetic analyses indicated that kcat of the trimolecular complex (SK, plasminogen and potentiating agent) was higher than SK-plasminogen complex, without change in Km. These results suggest that a trimolecular complex of SK, plasminogen and potentiating agent converts plasminogen to plasmin more effectively than a dimole-cular complex of SK and plasminogen. Considering the fact that the plasma concentrations of thrombolytic agents such as SK or UK were low even after drip infusion of their large dose Intravenously, the potentiation of the activation of plasminogen by SK in the presence of fibrin maybe significant in the mechanisms of thrombolytic therapy.
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Hanthazi, Aliénor, Samantha Gomart, Caroline Gaudreau Ménard, Pascale Jespers, Jean-Yves Springael, Robert Naeije, Laurence Dewachter, and Kathleen Mc Entee. "Chemerin potentiates pulmonary artery reactivity to endothelin-1." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2440.

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Kurai, Jun, Rebecca L. Toonkel, Alain Borczuk, and Charles A. Powell. "Oxidative Stress Potentiates Carcinogenesis In Chronic Lung Inflammation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4953.

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Reports on the topic "Potentiators"

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Fisher, Joshua L. Selenium Potentiates Chemotherapeutic Selectivity: Improving Efficacy and Reducing Toxicity. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470578.

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Huacani, Maria R., and D. McDonnell. Analysis of the Mechanism of Action of RPF1: Potentiator of Progesterone Receptor and p53-Dependent Transcriptional Activity. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada398343.

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Green, Lora M. Low Dose Gamma Irradiation Potentiates Secondary Exposure to Gamma Rays or Protons in Thyroid Tissue Analogs. Office of Scientific and Technical Information (OSTI), May 2006. http://dx.doi.org/10.2172/882942.

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Zlotkin, Eliahu, Shizuo G. Kamita, Nor Chejanovsky, and S. Maeda. Targeting of an Expressed Insect Selective Neurotoxin by its Recombinant Baculovirus: Pharmacokinetic and Pharmacodynamic Aspects. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7571354.bard.

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Objectives: 1) Clarification of the mode of potentiation of an expressed insect selective neurotoxin (AaIT) by its recombinant baculovirus. 2) In vitro formation and/or modification of neuroactive polypeptides for the design of new improved recombinant baculoviruses. Results: 1) A combined utilization of bioassays, LM-cytochemistry, the highly resolutive EM immunogold and electrical recording from the CNS of baculovirus and AaIT - expressing – recombinant baculovirus infected larvae it has been shown that the recombinant virus potentiates the effect of the toxin. Potentiation is achieved through its continuous expression in the infected tracheal epithelia thus providing a: a) Local supply of freshly produced toxin in the vicinity of its traget sites; b) Translocation of the expressed toxin to the insect CNS. The latter exposes the recombinant toxin to new, critical, target sites which are inaccessible through the natural route of scorpion envenomation. 2) Subjecting a recombinant AaIT toxin to a newly designed system of random mutagenesis results in large numbers of new AaIT genes with amino acid substitutions. The new or modified toxin genes were inserted into a linear BmNPV expressed in silkworm cell culture and assayed on blowfly and silkworm larvae. Thus a system for mass formation and screening of neuroactive agents was developed. Contribution to agriculture: 1) Demonstration of the insecticidal mechanism, capacity and utility of the combination of neuroactive polypeptides and recombinant pathogens. 2) Development of a simple in vitro system for the formation and selection of new neuroactive polypeptides.
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Yaron, Zvi, Martin P. Schreibman, Abigail Elizur, and Yonathan Zohar. Advancing Puberty in the Black Carp (Mylopharyngodon Piceus) and the Striped Bass (Morone Saxatilis). United States Department of Agriculture, August 1993. http://dx.doi.org/10.32747/1993.7568102.bard.

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The black carp (bc)GtH IIb cDNA was amplified and isolated, cloned and sequenced. Comparison of the bcGtH IIb deduced a.a. sequence with that of GtH IIb from other teleosts revealed high homology to cyprinid species and a lower homology to salmonid or perciform fish. The gene coding for the GtH IIb was isolated and sequenced. Three bc recombinant phages which hybridized to the goldfish GtH Ib cDNA probe were isolated and are currently being characterized. The region coding for the mature GtH IIb was expressed in a bacterial expression vector resulting in the production of a recombinant protein. In vitro folding resulted in a protein only 1.3% of which displaced the native common carp GtH II in a RIA. Therefore, the common carp GtH RIA was utilized for the physiological studies at the current phase of the project. Two non-functional sites were identified along the brain-pituitary gonadal axis in the immature black carp. The pituitary is refractory to GnRH stimulation due to a block proximal to the activation of PKA and PKC probably at the level of GnRH receptors. The gonads, although capable of producing steroids, are refractory to gonadotropic stimulation but do respond to cAMP antagonists, indicating a block at the GtH receptor level. Attempts to advance puberty in 2 and 3 y old black carp showed that testosterone (T) stimulates GtH synthesis in the pituitary and increases its sensitivity to GnRh. A 2 month treatment combining T+GnRH increased the circulating GFtH level in 3 y old fish. Addition of domperidone to such a treatment facilitated both the accumulation of GtH in the pituitary and its response to GnRH. The cDNA of striped bass GtH a, Ib and IIb subunits were amplified, isolated, cloned and sequenced, and their deduced a.a. sequences were compared with those of other teleosts. A ribonuclease protection assay was developed for a sensitive and simultaneous determination of all GtH subunits, and of b-actin mRNAs of the striped bass. GnRH stimulated dramatically the expression of the a and GtH IIb subunits but the level of GtH Ib mRNA increased only moderately. These findings suggest that GtH-II, considered in salmonids to be involved only in final stages of gametogenesis, can be induced by GnRH to a higher extent than GtH-I in juvenile striped bass. The native GtH II of the striped bass was isolated and purified, and an ELISA for its determination was developed. The production of all recombinant striped bass GtH subunits is in progress using the insect cell (Sf9) culture and the BAC-TO-BAC baculovirus expression system. A recombinant GtH IIb subunit has been produced already, and its similarity to the native subunit was confirmed. The yield of the recombinant glycoprotein can reach 3.5 mg/ml after 3 days culture. All male striped bass reach puberty after 3 y. However, precocious puberty was discovered in 1 and 2 y old males. Females become vitellogenic during their 4th year. In immature 2 y old females, T treatment elevates the pituitary GtH II content while GnRH only potentiates the effect. However, in males GnRH and not T affects GtH accumulation in the pituitary. Neither GnRH, nor T treatment resulted in gonadal growth in 2 y old striped bass, indicating that either the accumulated GtH II was not released, or if released, the gonads were refractory to GtH stimulation, similar to the situation in the immature black carp. In 3 y old female striped bass, 150 day GnRHa treatment resulted in an increase in GSI, while T treatment, with or without GnRHa, resulted in a decrease in oocyte diameter, similar to the effect seen in the black carp. Further attempts to advance puberty in both fish species should take into account the positive effect of T on pituitary GtH and its negative effect of ovarian growth.
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