Littérature scientifique sur le sujet « PTGFRN »
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Articles de revues sur le sujet "PTGFRN"
Marquez, Jorge, Jianping Dong, Chun Dong, Changsheng Tian et Ginette Serrero. « Identification of Prostaglandin F2 Receptor Negative Regulator (PTGFRN) as an internalizable target in cancer cells for antibody-drug conjugate development ». PLOS ONE 16, no 1 (27 janvier 2021) : e0246197. http://dx.doi.org/10.1371/journal.pone.0246197.
Texte intégralMuraoka, Satoshi, Mark P. Jedrychowski, Kiran Yanamandra, Seiko Ikezu, Steven P. Gygi et Tsuneya Ikezu. « Proteomic Profiling of Extracellular Vesicles Derived from Cerebrospinal Fluid of Alzheimer’s Disease Patients : A Pilot Study ». Cells 9, no 9 (25 août 2020) : 1959. http://dx.doi.org/10.3390/cells9091959.
Texte intégralChandras, 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 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 intégralAguila, Brittany, Adina Brett Morris, Raffaella Spina, Eli Bar, Julie Schraner, Robert Vinkler, Jason W. Sohn et Scott M. Welford. « The Ig superfamily protein PTGFRN coordinates survival signaling in glioblastoma multiforme ». Cancer Letters 462 (octobre 2019) : 33–42. http://dx.doi.org/10.1016/j.canlet.2019.07.018.
Texte intégralKim, Soon Ok, Nune Markosyan, Gerald J. Pepe et Diane M. Duffy. « Estrogen promotes luteolysis by redistributing prostaglandin F2α receptors within primate luteal cells ». REPRODUCTION 149, no 5 (mai 2015) : 453–64. http://dx.doi.org/10.1530/rep-14-0412.
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 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 intégralKauke, Monique, Nikki Ross, Dalia Burzyn, Shelly Martin, Ke Xu, Nuruddeen Lewis, Charan Leng et al. « 703 Engineered exosomes with altered cellular tropism achieve targeted STING agonist delivery and single-agent tumor control in vivo ». Journal for ImmunoTherapy of Cancer 8, Suppl 3 (novembre 2020) : A745. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0703.
Texte intégralPrzygrodzka, E., M. M. Kaczmarek, P. Kaczynski et A. J. Ziecik. « Steroid hormones, prostanoids, and angiogenic systems during rescue of the corpus luteum in pigs ». REPRODUCTION 151, no 2 (février 2016) : 135–47. http://dx.doi.org/10.1530/rep-15-0332.
Texte intégralThèses sur le sujet "PTGFRN"
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 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.
Chen, Ni-Yun, et 陳倪芸. « A Strategic Analysis of the Electronic Health Record ». Thesis, 2015. http://ndltd.ncl.edu.tw/handle/ptg99n.
Texte intégral國立交通大學
管理學院科技管理學程
103
This thesis reports on an analysis of operating strategy of the Electronic Health Record industry based on the model of innovation intensive services (IIS). Electronic health record ( EHR ) can be effective with good quality in medical care. It also provide people better medical care due to the business transfer process between medical organizations enhanced by electronic health record (EHR ). The model respectively dissects four influential factors of industrial environments and technological systems at the industry-level analysis to verify the requirements of industrial innovation system. IIS Matrix will help deduce critical elements of industrial environment and technological systems at the industry level by strategic positioning and KSFs in the firm level. The requirements of industrial environment and technological systems will be consolidated into the industrial innovation systems by using the IIS approach. Results showed that in the Electronic Health Record industry, the future trend needs to be moved to “Unique Service”, “Selective Service” with “Process Innovation” and “Unique Service” with “ Process Innovation” . The industry is still in its infancy stage; product innovation and the process innovation are the vendors’ first step to become a member of Electronic Health Record industry.
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.
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.
MAZZOLA, Silvia. « Mutation search and association study of candidate genes in non melanoma skin cancer after organ transplantation ». Doctoral thesis, 2011. http://hdl.handle.net/11562/349795.
Texte intégralProstaglandin E2 (PGE2) is a prostanoid with a variety of bioactivities, and has been implicated in various pathologies. PGE2 appears as a key molecule in tumour formation, involved in cell proliferation, angiogenesis, immune surveillance, and apoptosis. PGE2 is produced via three sequential enzymatic reactions: release of arachidonic acid (AA) from membrane glycerophospholipids by phospholipase A2 (PLA2), conversion of AA to the unstable intermediate prostanoid PGH2 by cyclooxygenase (COX), and isomerization of PGH2 to PGE2 by prostaglandin E synthase (PGES). PGE2 is released from cells and it interacts with four distinct receptors, EP1, EP2, EP3, and EP4. Over-expression of the inducible form of COX (Cox-2) and microsomal-prostaglandin E synthase-1 (mPGES-1), resulting in excessive prostaglandin E 2 (PGE2) production, has been observed in cancer of various tissues, including skin cancer. An over-expression of EP1 has been observed in skin cancer development induced by UVB. Alteration in gene expression, due to genetic variants located in the promoter region of the genes for prostaglandin synthase-2 (PTGS2/COX2), microsomal prostaglandin E synthase (mPGES-1), or prostaglandin E receptor 1 (PTGER1) may result in augmented PGE2 synthesis or in altered response to PGE2, and could represent risk factors for the development of non melanoma skin cancer (NMSC) in organ transplant recipients (OTRs). To determine if polymorphisms in these genes can be useful genetic markers of susceptibility that may contribute to early detection of individuals at greater risk of NMSC, a case-control study was performed. Two polymorphisms in the PTGS2 gene, three in the mPGES-1 gene, and three in the PTGER1 gene were genotyped in 286 OTRs, 144 NMSC cases and 142 controls. Allele –765G in the PTGS2 gene was more frequent in cases than in controls [p=0.015, OR=9.59 (1.36-192.66)], suggesting that this variant might represented a risk factor in the development of basal cell cancer (BCC) in individuals undergoing transplantation before 50 years of age. Analysis of polymorphisms –1760C>A (rs3810254), -1728G>A (rs3810255), and –1113C>T (rs2241359) in the 5’ proximal region of the PTGER1 gene showed that minor alleles of these variants were more represented in individuals with squamous cell cancer (SCC), when compared to matched controls who underwent transplantation before 50 years of age, but the difference did not reach significance. To verify if the 1452 bp fragment of the 5’ flanking region, which contains the three polymorphisms could exert promoter activity, we performed functional analysis in HeLa and HaCat cultured cells. Although a weak promoter activity was observed in HeLa cells, we were unable to demonstrate any promoter activity in HaCat cells, even after LPS stimulation. The 5’ flanking region of the mPGES-1 gene was screened by heteroduplex analysis to identify new variants. Three polymorphisms, located within conserved regions of the gene, and reported in NCBI databases as –664T>A (rs7873087), –663A>T (rs7859349) and –439T>C (rs7872802), were identified. The observed genotype distributions indicated complete linkage disequilibrium for the three polymorphisms, and no association with NMSC was observed. In conclusion, allele –765C in the PTGS2 gene seems to represent a protection factor against the development of BCC tumours in individuals undergoing transplantation before 50 years of age. Analysis of polymorphisms in the 5’ regions of the mPGES-1 and PTGER1 genes did not support the hypothesis that variants in these regions could play a major role in NMSC predisposition.
Chapitres de livres sur le sujet "PTGFRN"
« 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« PTGF-b ». Dans Encyclopedia of Cancer, 3848. Berlin, Heidelberg : Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_101922.
Texte intégral« PTGF-β ». Dans Encyclopedia of Cancer, 3121. Berlin, Heidelberg : Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4859.
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 "PTGFRN"
Marquez, 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 intégralBayraktar, 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 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 intégralQin, Haonan, Weiying Xie, Yunsong Li, Kai Jiang, Jie Lei et Qian Du. « PTGAN : A Proposal-Weighted Two-Stage GAN with Attention for Hyperspectral Target Detection ». Dans IGARSS 2021 - 2021 IEEE International Geoscience and Remote Sensing Symposium. IEEE, 2021. http://dx.doi.org/10.1109/igarss47720.2021.9553721.
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 intégralGou, Xiaochuan, Chih-Chieh Hung, Guanyao Li et Wen-Chih Peng. « PTGF : Public Transport General Framework for Identifying Transport Modes Based on Cellular Data ». Dans 2019 20th IEEE International Conference on Mobile Data Management (MDM). IEEE, 2019. http://dx.doi.org/10.1109/mdm.2019.00120.
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 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