Littérature scientifique sur le sujet « PTGER1 »
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Articles de revues sur le sujet "PTGER1"
Chandras, C., T. E. Harris, A. López Bernal, D. R. E. Abayasekara et A. E. Michael. « PTGER1 and PTGER2 receptors mediate regulation of progesterone synthesis and type 1 11β-hydroxysteroid dehydrogenase activity by prostaglandin E2 in human granulosa–lutein cells ». Journal of Endocrinology 194, no 3 (septembre 2007) : 595–602. http://dx.doi.org/10.1677/joe-07-0128.
Texte intégralMiyoshi, Moe, Masayuki Sato, Kenji Saito, Lila Otani, Katsuhiko Shirahige, Fumihito Miura, Takashi Ito, Huijuan Jia et Hisanori Kato. « Maternal Protein Restriction Alters the Renal Ptger1 DNA Methylation State in SHRSP Offspring ». Nutrients 10, no 10 (5 octobre 2018) : 1436. http://dx.doi.org/10.3390/nu10101436.
Texte intégralGonzález, Luz María, Nicolás Roberto Robles, Sonia Mota-Zamorano, José Manuel Valdivielso, Juan López-Gómez et Guillermo Gervasini. « Genetic Variants in PGE2 Receptors Modulate the Risk of Nephrosclerosis and Clinical Outcomes in These Patients ». Journal of Personalized Medicine 11, no 8 (6 août 2021) : 772. http://dx.doi.org/10.3390/jpm11080772.
Texte intégralKowalewski, Mariusz Pawel, Hakki Bülent Beceriklisoy, Christiane Pfarrer, Selim Aslan, Hans Kindahl, Ibrahim Kücükaslan et Bernd Hoffmann. « Canine placenta : a source of prepartal prostaglandins during normal and antiprogestin-induced parturition ». REPRODUCTION 139, no 3 (mars 2010) : 655–64. http://dx.doi.org/10.1530/rep-09-0140.
Texte intégralZschockelt, Lina, Olga Amelkina, Marta J. Siemieniuch, Mariusz P. Kowalewski, Martin Dehnhard, Katarina Jewgenow et Beate C. Braun. « Synthesis and reception of prostaglandins in corpora lutea of domestic cat and lynx ». Reproduction 152, no 2 (août 2016) : 111–26. http://dx.doi.org/10.1530/rep-16-0180.
Texte intégralThibodeau, Jean-François, Rania Nasrallah, Anthony Carter, Ying He, Rhian Touyz, Richard L. Hébert et Christopher R. J. Kennedy. « PTGER1 Deletion Attenuates Renal Injury in Diabetic Mouse Models ». American Journal of Pathology 183, no 6 (décembre 2013) : 1789–802. http://dx.doi.org/10.1016/j.ajpath.2013.08.022.
Texte intégralNuttinck, Fabienne, Brigitte Marquant-Le Guienne, Laetitia Clément, Pierrette Reinaud, Gilles Charpigny et Bénédicte Grimard. « Expression of genes involved in prostaglandin E2 and progesterone production in bovine cumulus–oocyte complexes during in vitro maturation and fertilization ». REPRODUCTION 135, no 5 (mai 2008) : 593–603. http://dx.doi.org/10.1530/rep-07-0453.
Texte intégralWaclawik, Agnieszka, Piotr Kaczynski et Henry N. Jabbour. « Autocrine and Paracrine Mechanisms of Prostaglandin E2 Action on Trophoblast/Conceptus Cells through the Prostaglandin E2 Receptor (PTGER2) during Implantation ». Endocrinology 154, no 10 (1 octobre 2013) : 3864–76. http://dx.doi.org/10.1210/en.2012-2271.
Texte intégralJamshed, Laiba, Genevieve A. Perono, Shanza Jamshed, Kim Ann Cheung, Philippe J. Thomas et Alison Holloway. « The Effects of Naphthenic Acids on Tryptophan Metabolism and Peripheral Serotonin Signalling ». Journal of the Endocrine Society 5, Supplement_1 (1 mai 2021) : A493. http://dx.doi.org/10.1210/jendso/bvab048.1008.
Texte intégralZhao, Xin-mei, Yuan-Bin Li, Peng Sun, Ya-di Pu, Meng-jie shan et Yuan-meng Zhang. « Bioinformatics analysis of key biomarkers for retinoblastoma ». Journal of International Medical Research 49, no 6 (juin 2021) : 030006052110222. http://dx.doi.org/10.1177/03000605211022210.
Texte intégralThèses sur le sujet "PTGER1"
Heumann, Tina [Verfasser], et Ursula [Akademischer Betreuer] Klingmüller. « Characterization of the novel pericyte receptors S1PR3 and PTGER2 / Tina Heumann ; Betreuer : Ursula Klingmüller ». Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1178010465/34.
Texte intégralMesa, Solís Julio. « Human prostaglandin reductase 1 (PTGR1) : Substrate specificity, site-directed mutagenesis and catalytic mechanism ». Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/394081.
Texte intégralEllo, Serge. « Préparation de catalyseurs bimétalliques PtGe/Al2O3 par voie organométallique pour une application en reformage ». Poitiers, 2005. http://www.theses.fr/2005POIT2303.
Texte intégralThe objective of this work was centered on the preparation of bimetallic catalysts Pt-Ge/Al2 O3 and the evaluation of their performances for a possible application in reforming. The catalysts were prepared by organometallic grafting. This technique of preparation made it possible to deposit very small quantity of germanium on the surface of the catalyst Pt/Al2O3. These catalysts then underwent various techniques of characterization: microscopy electronic by transmission (MET), chemisorption of hydrogen, carbon monoxide chemisorption and tests of characterization: the hydrogenation of benzene, the dehydrogenation of cyclohexene and the transformation of the ethylcyclopentane. We have obtained bimetallic catalysts of various structures according to the quantity of gemanium deposited. For the low contents we obtain a deposit (selective) germanium on the sites of high coordination (faces) then for the strong germanium contents, the deposit becomes nonselective. Beyond half monocouche of germanium, compounds definis are formed PtXGey. For the performance evaluation, the rearrangement of n-hexan, and n-heptan were selected for model reaction. In the case of n-hexane one obtained the results according to; For small germanium contents (P76Ge1/8, P60Ge1/8, P60Ge1/2), there is a high selectivity in isomerization, deshydrocyclisation (methyclopentane) and very little fragmentation and aromatization. For strong content (P76Ge2, P60Ge1, P60Ge2) we obtain also more aromatization than catalysts with weak addition, less isomers, and products cyclized and much of fragmentation. For catalysts with low content of germanium, there is a reduction in the selectivity of the products resulting from fragmentation, an increase in isomerization and a reduction in the deshydrocyclisation compared to the catalyst Pt/Al2O3. Catalysts with strong content prove more reactive for the reactions of deshydrocyclisation (aromatization), of fragmentation, but less active for isomerization
Berry-Mortada, Fadwa. « Stabilité des plasmides recombinés en cellules libres et immobilisées : développement d'un système à double réacteur en continu en vue d'une surproduction de catéchol 2,3-dioxygénase ». Compiègne, 1989. http://www.theses.fr/1989COMPD211.
Texte intégralPasciuto, Giulia [Verfasser], et Stephan [Akademischer Betreuer] Brand. « Neue Krankheitssuszeptibilitätsgene bei chronisch entzündlichen Darmerkrankungen und deren phänotypische Auswirkungen : der Einfluss von Polymorphismen im PTGER4-, PHOX2B-, NCF4- und FAM92B-Gen und in der chromosomalen Region 10q21.1 auf die Suszeptibilität und den Phänotyp von chronisch entzündlichen Darmerkrankungen / Giulia Pasciuto ; Betreuer : Stephan Brand ». München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1136270590/34.
Texte intégralWU, PEI-JU, et 吳佩儒. « PTGFRN Expression Correlate with WHO Grades in Gliomas ». Thesis, 2018. http://ndltd.ncl.edu.tw/handle/f88244.
Texte intégral國防醫學院
病理及寄生蟲學研究所
106
Recent studies have shown Prostaglandin F2 Receptor Inhibitor (PTGFRN) is related to angiogenesis and tumor overgrowth in human. De novo glioblastoma multiforme (GBM) is the most common and highly malignant form of brain tumor. It is aggressive and challenging to be treated. Due to their finger-like tentacles, they are difficult to be completely removed by surgery. Median survival time for patients receiving only surgical resection is 4 months. The median survival time is extended to 9 to 10 months with conventional radiation therapy. The current standard treatment for glioblastoma is concurrent chemo-radiation therapy (CCRT) with median survival time of 15 months. 5-year survival rate of GBM ≤ 5% which is less than ideal. The objective of this study is to explore human genes that is associated with GBM. We sincerely hope to achieve better outcomes via pharmacology target therapy in the future. U87MG, LN229 and GBM8401 cell lines were cultured to determine the mRNA and protein expression level of PTGFRN in gliomas. For the immunohistochemistry (IHC) stain, 85 glioma brain tissues and 5 non-neoplastic brain tissues were collected to make the tissue microarray. The expression level of PTGFRN was evaluated by real-time PCR, western blot and IHC. Our results showed mRNA and protein expression level of PTGFRN is up-regulated in glioma cells/tissues as compared to normal brain tissues. The expression level of PTGFRN is thus positively correlated to WHO tumor grades of gliomas. PTGFRN serve as a promising candidate for future research to place upon in observing its inhibition on the effects on cell cycle, growth rate, and invasion ability. This may serve to verify in determining whether PTGFRN can act as new therapeutic target for glioma patients.
Guo, Chien-Jung, et 郭千榕. « The role of Glucocorticoid receptor(GR) in PTGR2 regulation ». Thesis, 2017. http://ndltd.ncl.edu.tw/handle/u2p5xy.
Texte intégral國立臺灣大學
分子醫學研究所
105
Adipocyte differentiation is an elegant, complicated process involving sequentially activation of thousands of transcriptional factors. Our group previously discovered a novel enzyme, called prostaglandin reductase 2 (PTGR2) through mRNA differential display. PTGR2 is an oxidoreductase which catalyze 15-keto PGE2 to 13,14-dihydro-15-keto PGE2 as final product. In functional study, overexpression PTGR2 rather than its catalytic mutant inhibited adipocyte differentiation and relatively triacylglycerol content,which suggest a role of PTGR2 in adipogenesis. Additionally, PTGR2 is upregulated in omental fat in obese mouse model. However, the molecular mechanism of PTGR2 expression remains unknown. Results from promoter assay and inhibitors of different signaling pathways indicated that PTGR2 transcriptional regulation is possibly mediated via dexamethasone-GR pathway. Moreover, the predicted TF binding sites also indicated presence of GR binding sites on PTGR2 promoter. With site-direct mutagenesis, we confirmed the proximal GR binding site at -277/-283 is responsible for promoter activation by dexamethasone. We then performed chromatin immunoprecipitation (ChIP) and demonstrated a direct binding of GR on PTGR2 promoter site. To further investigate the regulation of PTGR2 in vivo, we discovered that dexamethasone pulse therapy significantly upregulate PTGR2 mRNA in in inguinal fat tissue. Our findings thus support the dexamethasone-GR pathway that leads to PTGR2 activation in both cell and animal models.
Chen, Kuan-Ju, et 陳冠如. « Triage of Endometrial Atypical Hyperplasia by DNA Methylation of SOX1, HS3ST2, AJAP1 and PTGDR ». Thesis, 2012. http://ndltd.ncl.edu.tw/handle/35059509426421457312.
Texte intégral國防醫學院
病理及寄生蟲學研究所
100
Endometrial carcinoma (EC) is the one of the most common cancers in female genital tract worldwide. It can be classified into two major subtypes with respect to histopathology, cell biology and clinical course. Epigenetic aberration is known to be important in human carcinogenesis. Promoter methylation status of SOX1, HS3ST2, AJAP1 and PTGDR, was evaluated in 20 endometrial carcinomas (EC) and normal endometrial tissue by methylation specific PCR. These 4 genes had higher methylation value in patients with EC than in normal controls of AJAP1, PTGDR, HS3ST2, and SOX1 (p < 0.0001, p = 0.0002, p = 0.0004, p = 0.0035, respectively). Atypical hyperplasia (AH) is a premalignant lesion of endometrial pathology. Women with this diagnosis based on endometrial sampling are frequently found to have EC at hysterectomy. The failure of accurately diagnose EC preoperatively in these women can lead to inadequate staging and potentially suboptimal treatment for some women. So, there is a need for other markers to identify women with AH in endometrial sampling harboring an underlying EC. Sixty-one endometrial sampling with pathological diagnosis of AH were analyzed. Fourteen of the sixty-one (23%) AH patients were confirmed to have EC at hysterectomy. Three of 4 genes had higher methylation value in patients with EC hidden in AH compared with AH of AJAP1, HS3ST2 and SOX1 (p = 0.0005, p = 0.014, p = 0.023, respectively). Best cutoff values of the methylation data for different genes were determined to test the sensitivity, specificity, positive predict value (PPV), negative predict value (NPV) and to generate receiver operating characteristic (ROC) curve. ROC curve analysis demonstrated that the sensitivity, specificity, accuracy, PPV and NPV for the best performance for separating EC from AH has a sensitivity of 0.86, 0.71 and 0.71, respectively, and a specificity of 0.72, 0.70 and 0.60, respectively and accuracy of 0.81, 0.72 and 0.70, respectively, and a PPV of 0.48, 0.42 and 0.35, respectively, and a NPV of 0.94, 0.89 and 0.88, respectively. In conclusion, promoter hypermethylation of AJAP1, HS3ST2, PTGDR and SOX1 is found in EC. In addition, we also show for the first time that AJAP1, HS3ST2 and SOX1 hypermethylation analysis may have potential as a EC biomarker for endometrial malignancy.
Ye, Yan-Ting, et 葉延廷. « Tailoring the Schottky-Barrier Height of a PtGex/Ge Contact by Combining the Experiments and First-principles Calculations ». Thesis, 2016. http://ndltd.ncl.edu.tw/handle/32041341404494249416.
Texte intégral國立交通大學
電子研究所
105
In this thesis, we combine the first-principles simulations and experiments to study the Pt-germanide/Ge Schottky junction. In experiments, we first investigate how various PDA treatments affect the SBHs of a Pt-germanide/Ge junction. The I-V measurements show that SBHs are slightly reduced and gradually saturated as the annealing temperature increases. As being inspected by GIXRD analysis, the Pt-germanide phase and crystalline plane is found to vary slightly and gradually saturated as the annealing temperature increases. In order to realize the Pt-germanide/Ge interface structure in atomic scale and also to reduce possible computational trials, we use the XPS analysis to eliminate the possibility that the materials surrounding the junctions diffuse in during annealing. Next, we figure out the Pt-germanide compositions and crystalline planes from the GIXRD analysis, and do an initial screening to keep only several crystalline planes of the stronger peak signals for simulation modeling. After further considering the lattice mismatches and their desire computational resources, we finally choose and construct the three interfaces: PtGe(121)/Ge, PtGe(800)/Ge, and PtGe(120)/Ge, corresponding to the junctions formation under different annealing temperatures. By the first-principles calculations, we first investigate how SBH changes with these three single-crystalline PtmGen/Ge interfaces. We find that their SBHs depend on different Pt-germanide phases in a way in agreement with the experiments. In addition, their values differ by less than 0.1eV, consistent with the experiments. This can result from the strong Fermi level pinning. Finally, we compare the SBH-lowering effects under segregation of various dopants. Calculations reveal that they tend to segregate to the interface, and the conventional N-type dopants P and As can both reduce SBH. In addition, we find that the Sc dopant can reduce SBH from 0.671 to 0.388eV. It is the most effective among these dopants, which can be testified in the further experiments. In summary, first-principles calculations can help us explore SBHs of different crystalline planes and dopants, and pursue its reduction for device purposes. We expect that such calculations can provide a better direction for realistic fabrication, and can further shorten process development cycles and lower the cost.
Hsieh, Meng-Lun, et 謝孟倫. « Identification of small-molecule human PTGR-2 inhibitor through high-throughput compound screening ». Thesis, 2017. http://ndltd.ncl.edu.tw/handle/11717556324919987625.
Texte intégral國立臺灣大學
基因體暨蛋白體醫學研究所
105
Peroxisome proliferator-activated receptor γ (PPARγ) is a master regulator of whole-body energy metabolism, glucose homeostasis, and insulin resistance mainly expressed in adipose tissue. PPARγ acts through transcriptional regulation of genes involved in glucose and energy homeostasis upon ligand binding. The widely used anti-diabetic agent thiazolidinediones (TZD) are potent synthetic PPARγ agonist. However, most PPARγ agonists are associated with significant side effects, such as water retention, increased adiposity, and osteoporosis. There is an urgent need to develop effective way to modulate PPARγ activity without unwanted side effects. Nowadays, the natural ligands for PPARγ are still not certain (mostly oxidized fatty acids). Our team previously found prostaglandin reductase-2 (PTGR2) can catalyze15-keto-PGE2 to 13,14-dihydro-15-keto-PGE2, and provided further evidence that15-keto-PGE2 is an endogenous PPARγ ligand. Our team further found that Ptgr2 knockout mice are leaner, more insulin sensitive, and more glucose tolerant than control in high-fat high-sucrose (HFHS) diet without fluid retention and osteoporosis, indicating PTGR2 inhibition is a novel therapeutic approach for treating type 2 diabetes and obesity. In this study, we sought to identify PTGR2 small-molecule inhibitor through rational drug design and high-throughput compound screening. We further validated the enzymatic inhibitory activities, the PPARγ transactivating activities, and the cytotoxicity of these hits. Based on this study, we identified potential PTGR2 inhibitors for further optimization and animal experiment.
Chapitres de livres sur le sujet "PTGER1"
« PTGER2 ». Dans Encyclopedia of Signaling Molecules, 4286. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_103155.
Texte intégral« Ptgs1 ». Dans Encyclopedia of Pain, 3319. Berlin, Heidelberg : Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_101923.
Texte intégralLea, Robert, Yashvant Jani, GianGuido Rizzotto, Hans Hellendoorn, Toshio Fukuda, Yasuhisa Hasegawa, Jyh-Shing Roger Jang et al. « Operations Research ». Dans Handbook of Fuzzy Computation. Taylor & ; Francis, 1998. http://dx.doi.org/10.1201/9781420050394.ptg1.
Texte intégralMakin-Iniesta, F. « Kinetic Study of pTG201 Plasmid Stability in Escherichia coli ». Dans 1988, 311–18. De Gruyter, 1988. http://dx.doi.org/10.1515/9783112581803-003.
Texte intégral« Post-Transcriptional Gene Regulation (PTGR) ». Dans Encyclopedia of Systems Biology, 1728. New York, NY : Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_101172.
Texte intégralActes de conférences sur le sujet "PTGER1"
Bayraktar, Emine, Cristian Rodriguez-Aguayo, Junhua Mai, Cristina Ivan, Cristina Ivan, Arturo Chavez-Reyes, Anil K. Sood, Mauro Ferrari, Haifa Shen et Gabriel Lopez-Berestein. « Abstract 4668 : Silencing PTGER3 enhances chemotherapeutic responses ». Dans Proceedings : AACR 107th Annual Meeting 2016 ; April 16-20, 2016 ; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4668.
Texte intégralDong, Sheng, et Xiaoli Hao. « Statistical Analysis of Ocean Environmental Conditions With PTGEVD ». Dans ASME 2004 23rd International Conference on Offshore Mechanics and Arctic Engineering. ASMEDC, 2004. http://dx.doi.org/10.1115/omae2004-51615.
Texte intégralGui, H., D. Hu, P. Sleiman, A. M. Levin, S. Xiao, M. Yang, J. J. Yang et al. « Genome-Wide Association Study of Asthma Exacerbation in African Americans Identify PTGER3 as New Susceptibility Gene ». Dans 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.a3044.
Texte intégralHess, T., L. Hamann, YK Vashist, K. Butterbach, T. Schmidt, I. Krasniuk, A. Höblinger et al. « Evidence for PTGER4, PSCA and MBOAT7 as risk genes for gastric cancer on the genome and transcriptome level ». Dans Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604759.
Texte intégralBayraktar, Emine, Cristian Rodriguez-Aguayo, Zahid Siddik et Gabriel Lopez-Berestein. « Abstract 2066 : Delivery of 2`F-PS2 PTGER3 siRNA-DOPC enhances anti-tumoral activity in cisplatin resistant ovarian cancer model ». Dans Proceedings : AACR Annual Meeting 2017 ; April 1-5, 2017 ; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2066.
Texte intégralSchlegel, Anne, Oliver Hasinger, Selina Esche, Melanie Martini, Thomas König et Gunter Weiss. « Abstract 2260 : Classification of patients with lung cancer and benign lung disease via assessment of DNA methylation of SHOX2 and PTGER4 in plasma ». Dans Proceedings : AACR 107th Annual Meeting 2016 ; April 16-20, 2016 ; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2260.
Texte intégralSilva, Gustavo Figueiredo da, Bruno Mattei Lopes, Vinicius Moser et Leslie Ecker Ferreira. « Impact of pharmacogenetics on aspirin resistance : a systematic review ». Dans XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.663.
Texte intégralHabermann, Nina, Martha L. Slattery, Elizabeth M. Poole, Liren Xiao, Rachel L. Galbraith, David Duggan, Richard J. Kulmacz et al. « Abstract 3757 : PTGS1 and PTGS2 polymorphisms, fatty acid intake, and risk of colon and rectal cancer ». Dans Proceedings : AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011 ; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3757.
Texte intégralMarquez, Jorge, Jianping Dong, Chun Dong et Ginette Serrero. « Abstract LB116 : Prostaglandin F2 Receptor Negative Regulator (PTGFRN) is a novel target to inhibit tumor growth via antibody drug conjugate ». Dans Proceedings : AACR Annual Meeting 2021 ; April 10-15, 2021 and May 17-21, 2021 ; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-lb116.
Texte intégralWagner, Michael J., Sanford A. Klein et Douglas T. Reindl. « Simulation of Utility-Scale Central Receiver System Power Plants ». Dans ASME 2009 3rd International Conference on Energy Sustainability collocated with the Heat Transfer and InterPACK09 Conferences. ASMEDC, 2009. http://dx.doi.org/10.1115/es2009-90132.
Texte intégral