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Artykuły w czasopismach na temat "Soluble epoxide hydrolase subdomains"
Gupta, Nandita C., Catherine M. Davis, Jonathan W. Nelson, Jennifer M. Young i Nabil J. Alkayed. "Soluble Epoxide Hydrolase". Arteriosclerosis, Thrombosis, and Vascular Biology 32, nr 8 (sierpień 2012): 1936–42. http://dx.doi.org/10.1161/atvbaha.112.251520.
Pełny tekst źródłaSontakke, Pooja M., Suraj G. Malpani, Pooja R. Tange, MD Rayees Ahmad i Vishweshwar M. Dharashive. "Soluble Epoxide Hydrolase". Asian Journal of Pharmaceutical Research and Development 12, nr 2 (15.04.2024): 87–95. http://dx.doi.org/10.22270/ajprd.v12i2.1369.
Pełny tekst źródłaYu, Zhigang, Benjamin B. Davis, Christophe Morisseau, Bruce D. Hammock, Jean L. Olson, Deanna L. Kroetz i Robert H. Weiss. "Vascular localization of soluble epoxide hydrolase in the human kidney". American Journal of Physiology-Renal Physiology 286, nr 4 (kwiecień 2004): F720—F726. http://dx.doi.org/10.1152/ajprenal.00165.2003.
Pełny tekst źródłaBorhan, Babak, A. Daniel Jones, Franck Pinot, David F. Grant, Mark J. Kurth i Bruce D. Hammock. "Mechanism of Soluble Epoxide Hydrolase". Journal of Biological Chemistry 270, nr 45 (10.11.1995): 26923–30. http://dx.doi.org/10.1074/jbc.270.45.26923.
Pełny tekst źródłaWang, Yi-Xin Jim, Arzu Ulu, Le-Ning Zhang i Bruce Hammock. "Soluble Epoxide Hydrolase in Atherosclerosis". Current Atherosclerosis Reports 12, nr 3 (13.04.2010): 174–83. http://dx.doi.org/10.1007/s11883-010-0108-5.
Pełny tekst źródłaMa, Liang, Hailing Zhao, Meijie Yu, Yumin Wen, Tingting Zhao, Meihua Yan, Qian Liu i in. "Association of Epoxide Hydrolase 2 Gene Arg287Gln with the Risk for Primary Hypertension in Chinese". International Journal of Hypertension 2020 (28.02.2020): 1–7. http://dx.doi.org/10.1155/2020/2351547.
Pełny tekst źródłaHe, Xin, Wen-Yu Zhao, Bo Shao, Bao-Jing Zhang, Tian-Tian Liu, Cheng-Peng Sun, Hui-Lian Huang, Jia-Rong Wu, Jia-Hao Liang i Xiao-Chi Ma. "Natural soluble epoxide hydrolase inhibitors from Inula helenium and their interactions with soluble epoxide hydrolase". International Journal of Biological Macromolecules 158 (wrzesień 2020): 1362–68. http://dx.doi.org/10.1016/j.ijbiomac.2020.04.227.
Pełny tekst źródłaAnita, Natasha Z., i Walter Swardfager. "Soluble Epoxide Hydrolase and Diabetes Complications". International Journal of Molecular Sciences 23, nr 11 (2.06.2022): 6232. http://dx.doi.org/10.3390/ijms23116232.
Pełny tekst źródłaBellevik, Stefan, Jiaming Zhang i Johan Meijer. "Brassica napus soluble epoxide hydrolase (BNSEH1)". European Journal of Biochemistry 269, nr 21 (17.10.2002): 5295–302. http://dx.doi.org/10.1046/j.1432-1033.2002.03247.x.
Pełny tekst źródłaPrzybyla-Zawislak, Beata D., Punit K. Srivastava, Johana Vázquez-Matías, Harvey W. Mohrenweiser, Joseph E. Maxwell, Bruce D. Hammock, J. Alyce Bradbury, Ahmed E. Enayetallah, Darryl C. Zeldin i David F. Grant. "Polymorphisms in Human Soluble Epoxide Hydrolase". Molecular Pharmacology 64, nr 2 (17.07.2003): 482–90. http://dx.doi.org/10.1124/mol.64.2.482.
Pełny tekst źródłaRozprawy doktorskie na temat "Soluble epoxide hydrolase subdomains"
Sellers, Kathleen Walworth. "Role of brain soluble epoxide hydrolase in cardiovascular function". [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0008356.
Pełny tekst źródłaTypescript. Title from title page of source document. Document formatted into pages; contains 156 pages. Includes Vita. Includes bibliographical references.
Davis, Benjamin Boyce. "Novel treatments for atherosclerosis with inhibitors of soluble epoxide hydrolase /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2005. http://uclibs.org/PID/11984.
Pełny tekst źródłaSandberg, Martin. "Mammalian soluble epoxide hydrolase : studies on gene structure and expression /". Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 2000. http://epsilon.slu.se/avh/2000/91-576-5747-5.pdf.
Pełny tekst źródłaVarennes, Olivier. "Le rôle de l'Epoxyde hydrolase soluble (sEH) dans la physiopathologie des calcifications vasculaires". Thesis, Amiens, 2018. http://www.theses.fr/2018AMIE0046/document.
Pełny tekst źródłaExpressed in the vasculature, soluble epoxide hydrolase (sEH) exhibits a COOH-terminal hydrolase domain metabolizing endothelial vasodilator and anti-inflammatory factors like epoxyeicosatrienoic acids (EETs) and, a NH2-terminal phosphatase domain whose biological role remains unclear. To assess the role of sEH phosphatase and hydrolase domains in vascular calcification, rat aortic rings and hVSMCs were exposed to procalcifying culture media for 7 and 14 days, respectively. N-acetyl-S-farnesyl-L-cysteine (AFC), an inhibitor of the phosphatase domain, and trans-4-(4-(3-adamantan-1-yl-ureido)-cyclohexyloxy)-benzoic acid (t-AUCB), a hydrolase domain inhibitor, were used at concentrations ranging from 0.1 to 10 μM. Under procalcifying culture condition, AFC significantly and dose-dependently reduces aortic calcification. Conversely, addition of t-AUCB results in a significant and dose-dependent increase in aortic calcification in rats, without modification of tissue viability. A concomitant increase in TNAP activity was observed in supernatants of aortic rings cultured in the presence of t-AUCB. On de-endothelialized aortic rings or hVSMCs cultures, both inhibitors had no significant effect on the calcification process, pointing out the crucial role played by endothelial factors metabolized by sEH in the control of this biomineralization process. Together, our data demonstrates that pharmacological inhibition of sEH hydrolase increases vascular calcification in vitro by majoring the bioavailability of endothelium- derived EETs. Contrarily, the inhibition of sEH phosphatase is protective against vascular calcification through an endothelium-dependent mechanism
Newman, John William. "Novel tools for the investigation of the endogenous role of soluble epoxide hydrolase /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.
Pełny tekst źródłaCodony, Gisbert Sandra. "From the design to the in vivo evaluation of novel soluble epoxide hydrolase inhibitors". Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/671480.
Pełny tekst źródłaLos ácidos epoxieicosatrienoicos (EETs) son mediadores químicos endógenos derivados del ácido araquidónico que presentan efectos antiinflamatorios, antihipertensivos y analgésicos entre otros, pero son metabolizados rápidamente por la epóxido hidrolasa soluble (sEH), disminuyendo o alterando sus efectos beneficiosos. Así pues, se ha demostrado que la inhibición de la sEH estabiliza los niveles de EETs in vivo y puede tener efectos terapéuticos en diversas enfermedades que cursan con inflamación y dolor. Recientemente se han desarrollado varios inhibidores de la sEH (sEHIs) muy potentes, y muchos de ellos presentan un adamantano en su estructura, hecho que puede explicar su baja solubilidad y su inadecuado perfil farmacocinético. Por este motivo, la presente tesis doctoral se ha centrado en el diseño y síntesis de nuevos sEHIs, reemplazando el anillo de adamantano por policiclos relacionados, para mejorar las propiedades farmacocinéticas de los compuestos existentes. Primero, la introducción de un oxígeno en el núcleo de adamantano dio lugar a una nueva familia de inhibidores que presentaban mejor solubilidad y permeabilidad manteniendo la potencia inhibidora. Se llevó a cabo una cascada de cribaje para seleccionar un candidato para los estudios in vivo, en los que se demostró que reducía los marcadores de inflamación y de estrés del retículo endoplásmico y disminuía el daño pancreático en un modelo murino de pancreatitis aguda (AP). En segundo lugar, la exploración del tamaño de la unidad lipofílica de los sEHIs mostró que el centro activo del enzima es flexible y puede acomodar policiclos más grandes y más pequeños que el adamantano, siendo los más grandes los que mostraban más potencia. Finalmente, se desarrolló una nueva familia de sEHIs con el núcleo de benzohomoadamantano, dando lugar a compuestos extremadamente potentes, mejorando la solubilidad y la estabilidad microsomal de los sEHIs conocidos. Estudios adicionales nos permitieron seleccionar dos candidatos para los estudios in vivo: el primero para el tratamiento de la AP que produjo una reducción del daño pancreático y mejoró del estado de salud de los animales tratados, mientras que el segundo eliminó por completo la alodinia en un modelo predictivo de dolor neuropático. Así pues, en la presente tesis doctoral se han desarrollado diferentes familias de sEHIs muy potentes con propiedades de DMPK mejoradas y se ha demostrado su eficacia en diferentes estudios in vivo.
Duflot, Thomas. "Rôle de l'époxyde hydrolase soluble dans les maladies cardiovasculaires". Thesis, Normandie, 2018. http://www.theses.fr/2018NORMR037.
Pełny tekst źródłaSoluble epoxide hydrolase (sEH) is an ubiquitous bifunctional enzyme that is encoded by the EPHX2 gene. The hydrolase activity (sEH-H) is responsible for the conversion of the endothelial vasodilator epoxyeicosatrienoic acids whereas the phosphatase activity (sEH-P) is involved in the metabolism of lysophosphatidic acids (LPAs).The aim of this work was to develop chromatographic methods and molecular biology techniques to evaluate sEH activities in cardiovascular diseases.We developed a LC-MS/MS method to quantify EETs and their metabolites, the dihydroxyeicosatrienoic acids (DHETs). Using this method, we showed that the endothelial dysfunction of hypertensive and type 2 diabetic patients is associated with a decrease in the local production of EETs during flow increase notably due to increased sEH-H activity. In a murine model of insulin resistance, pharmacological inhibition of sEH-H improved renal function by decreasing inflammation, oxidative stress and glomerular lesions. Moreover, genetic investigations of EPHX2 revealed that sEH-H may play a substantial role in the control of renal and vascular function in kidney recipients. Finally, experimental results obtained in knock-in sEH-P deficient rats and genetics findings in patients with heart failure strongly suggest that sEH-P is involved in lipid metabolism and cardiovascular homeostasis.Taken together, these results strengthen the interest of developing pharmacological inhibitors of sEH-H to be tested in patients with cardiovascular, renal or metabolic diseases and suggest that the modulation of sEH-P represents a new therapeutic target to treat these pathologies
Leuillier, Matthieu. "Rôle de l'activité phosphatase de l'époxyde hydrolase soluble dans la régulation de l'homéostasie métabolique et cardiovasculaire. In vivo inactivation of the phosphatase activity of soluble epoxide hydrolase potentiates brown adispose thermogenesis and protects against cardiovascular damage and remodeling Discovery of the first in vivo active inhibitors of the soluble epoxide hydrolase phosphatase domain Altered bioavailability of epoxyeicosatrienoic acids is associated with conduit artery endothelial dysfunction in type 2 diabetic patients". Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR150.
Pełny tekst źródłaNearly 40 years after its initial discovery in 1972, soluble epoxide hydrolase (sEH), encoded by the EPHX2 gene, was shown in 2003 to be a bifunctional protein that exhibits not only an epoxide hydrolase activity on its C-terminal domain but also a lipid phosphatase activity on its N-terminal domain. Indeed, the hydrolase activity metabolizes epoxides of polyunsaturated fatty acids. In particular, sEH converts the vasodilator and anti-inflammatory epoxyeicosatrienoic acids converts, generated by cytochromes P450, into dihydroxyeicosatrienoic acids, which are less biologically active. This activity is now the target of a new class of pharmacologicla inhibitors. Unlike the biological function of the hydrolase activity, the biological function of sEH phosphatase activity remains, this time, unknown. Although shown originally to contribute to the stabilization of hydrolase activity or dimerization of the protein, some recent data indicate that the sEH phosphatase metabolizes also important lipid mediators, such as intracellular lysophosphatidic acids, involved in a wide range of biological functions such as vascular tone and inflammation, into monoacylglycerols. In addition, in vitro studies also suggested that the two activities of sEH have a complementary role in cholesterol regulation and vascular homeostasis. Although recombinant mice that do not express the EPHX2 gene have been around for some time, they do not allow to specifically study the phosphatase activity because both activities are eliminated. However, studies examining the differences between the effects of the genetic deletion of sEH and those of the pharmacological inhibition of its hydrolase activity indicate that the phosphatase activity of sEH probably has also a distinct physiological role. In our study, to assess the role of sEH phosphatase activity in absence of an inhibitor of this activity usable in vivo, original transgenic rats expressing sEH without phosphatase activity were generated using the CRISPR/Cas9 method. A thorough metabolic and cardiovascular phenotyping was performed on these animals. The results of this study showed that Knock-In (KI) rats for the sEH phosphatase have a decrease in body weight and fat mass compared to wild type rats of the same age. In addition, their sensitivity to insulin is increased. This beneficial metabolic profile is explained on one hand by a decrease in food consumption and, on the other hand, by an increase in fat oxidation, potentiating thermogenesis in brown adipose tissue enhancing energy expenditure. In addition, when KI rats were fed a high fat diet, weight gain remains lower than that of the wild type rats. In addition, they do not develop insulin resistance or hepatic steatosis. Finally, at the cardiac level, KI rats have higher basal mitochondrial activity associated with increased left ventricular contractility. In addition, KI animals are protected against cardiac ischemia-reperfusion lesions and the development of pulmonary arterial hypertension. Our study thus reveals that the phosphatase activity of sEH is a key player in lipid and energy metabolism, thus contributing, like the sEH hydrolase activity, to the regulation of cardiometabolic homeostasis
Kamynina, Alisa. "Furthering the understanding of the redox control of soluble epoxide hydrolase and protein kinase G in the cardiovascular system". Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/furthering-the-understanding-of-the-redox-control-of-soluble-epoxide-hydrolase-and-protein-kinase-g-in-the-cardiovascular-system(f6909a1e-6b09-4c3b-8d36-b7e417f45a1d).html.
Pełny tekst źródłaMavrommatis, Ioannis. "The effects of dietary long chain n-3 polyunsaturated fatty acids on soluble epoxide hydrolase and related markers of cardiovascular health". Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=56261.
Pełny tekst źródłaKsiążki na temat "Soluble epoxide hydrolase subdomains"
Imig, John D., i Christophe Morisseau, red. Clinical Paths for Soluble Epoxide Hydrolase Inhibitors. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-161-9.
Pełny tekst źródłaCzęści książek na temat "Soluble epoxide hydrolase subdomains"
Singh, Nalin, i Bruce D. Hammock. "Soluble Epoxide Hydrolase". W Encyclopedia of Molecular Pharmacology, 1–7. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_10020-1.
Pełny tekst źródłaSingh, Nalin, i Bruce D. Hammock. "Soluble Epoxide Hydrolase". W Encyclopedia of Molecular Pharmacology, 1450–56. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_10020.
Pełny tekst źródłaNelson, Jonathan W., i Nabil J. Alkayed. "Soluble Epoxide Hydrolase as a Stroke Target". W Translational Stroke Research, 277–94. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-9530-8_13.
Pełny tekst źródła"Soluble epoxide hydrolase". W Class 3 Hydrolases, 228–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-85703-7_37.
Pełny tekst źródłaNayeem, Mohammed A., Werner J. Geldenhuys i Ahmad Hanif. "Role of cytochrome P450-epoxygenase and soluble epoxide hydrolase in the regulation of vascular response". W Advances in Pharmacology. Elsevier, 2023. http://dx.doi.org/10.1016/bs.apha.2022.12.003.
Pełny tekst źródłaKandasamy, Ram, i Stevan Pecic. "Treatment of pain with dual fatty acid amide hydrolase (FAAH) enzyme and human soluble epoxide hydrolase (sEH) enzyme inhibitors: Interlinking the endocannabinoid system". W Neurobiology and Physiology of the Endocannabinoid System, 175–87. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-323-90877-1.00039-5.
Pełny tekst źródłaHung, Shao-Wen, Chia-Chi Chen, Hsiao-Yun Chen, Ying-Ching Hung, Ping-Min Huang i Chia-Yu Lin. "The Role of Microglia in Neuroinflammation". W Epilepsy - Seizures Without Triggers [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105865.
Pełny tekst źródłaStreszczenia konferencji na temat "Soluble epoxide hydrolase subdomains"
Lazaar, Aili, Lucy Yang, Jon Robertson, Navin Goyal, Rebecca Boardley, Ruth Tal-Singer, Joseph Cheriyan, David Newby, Ian Wilkinson i Ruth Mayer. "Safety and pharmacology of a soluble epoxide hydrolase inhibitor". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2120.
Pełny tekst źródłaYang, Jun, Jennifer Bratt, Lisa Franzi, Junyan Liu, Guodong Zhang, Hua Dong, Keisha Williams i in. "Soluble Epoxide Hydrolase Inhibitor Attenuates The Ovalbumin-Induced Murine Asthmatic Symptoms". W 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.a1425.
Pełny tekst źródłaAchanta, S., A. Marcus, A. Caceres i S. E. Jordt. "Soluble Epoxide Hydrolase Inhibitors and ACE Inhibitors Ameliorate Phosgene Inhalation Injuries". W American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1171.
Pełny tekst źródłaDavis, Benjamin B., Jun-Yan Liu, Daniel J. Tancredi, Scott I. Simon, Bruce D. Hammock i Kent E. Pinkerton. "Anti-inflammatory Effects Of Soluble Epoxide Hydrolase Inhibition Are Independent Of Leukocyte Recruitment". W 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.a5751.
Pełny tekst źródłaLiao, Jie, Stephanie D. Norwood, Yeon Tae Chung, Haonan Li, Bruce D. Hammock i Guang-Yu Yang. "Abstract 5702: Soluble epoxide hydrolase: unique biomarker and chemopreventive target of chronic colitis-induced carcinogenesis". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5702.
Pełny tekst źródłaYang, Jun, Lisa Franzi, Hua Dong, Amir A. Zeki, Junyan Liu, Nicholas J. Kenyon i Bruce Hammock. "Soluble Epoxide Hydrolase Is A Novel Therapeutic Target In Asthma By Modulating The Inflammatory Response". W 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.a4241.
Pełny tekst źródłaYuan, Cassandra, Ashley Murray, Christopher Chin, Alyssa Fernandez, Stephanie Sanchez, Stevan Pecic i Ram Kandasamy. "Effects of Simultaneous Inhibition of Fatty Acid Amide Hydrolase and Soluble Epoxide Hydrolase on Acute and Persistent Pain in Male Rats". W ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.186070.
Pełny tekst źródłaZhang, Wanying, Jie Liao, Haonan Li, Hua Dong, Han Bai, Allison Liao Yang, Bruce D. Hammack i Guang-Yu Yang. "Abstract 1006: Soluble epoxide hydrolase gene deficiency attenuates colitis-induced carcinogenesis in IL-10 knockout mice". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1006.
Pełny tekst źródłaRehman, S. F., K. F. Budden, A. Quaranta, D. Fuchs, S. D. Shukla, A. Brown, C. Alemao i in. "Soluble epoxide hydrolase inhibition alleviates inflammation in cigarette smoke-induced experimental COPD irrespective of dietary fat content". W ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3378.
Pełny tekst źródłaCarlson, A., E. Nixon, K. Messenger, P. Johnson i K. Keegan. "Anti-nociceptive Efficacy of the Soluble Epoxide Hydrolase Inhibitor t-TUCB in Horses with Mechanically Induced Lameness". W Abstracts of the 6th World Veterinary Orthopedic Congress. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1758247.
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