Relevant bibliographies by topics / PTGFRN

Academic literature on the topic 'PTGFRN'

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Published: 6 September 2023

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Journal articles on the topic "PTGFRN"

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Marquez, Jorge, Jianping Dong, Chun Dong, Changsheng Tian, and 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 (January 27, 2021): e0246197. http://dx.doi.org/10.1371/journal.pone.0246197.

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Antibody-drug conjugates (ADC) are effective antibody-based therapeutics for hematopoietic and lymphoid tumors. However, there is need to identify new targets for ADCs, particularly for solid tumors and cancers with unmet needs. From a hybridoma library developed against cancer cells, we selected the mouse monoclonal antibody 33B7, which was able to bind to, and internalize, cancer cell lines. This antibody was used for identification of the target by immunoprecipitation and mass spectrometric analysis, followed by target validation. After target validation, 33B7 binding and target positivity were tested by flow cytometry and western blot analysis in several cancer cell lines. The ability of 33B7 conjugated to saporin to inhibit in vitro proliferation of PTFRN positive cell lines was investigated, as well as the 33B7 ADC in vivo effect on tumor growth in athymic mice. All flow cytometry and in vitro internalization assays were analyzed for statistical significance using a Welsh’s T-test. Animal studies were analyzed using Two-Way Analysis of Variance (ANOVA) utilizing post-hoc Bonferroni analysis, and/or Mixed Effects analysis. The 33B7 cell surface target was identified as Prostaglandin F2 Receptor Negative Regulator (PTGFRN), a transmembrane protein in the Tetraspanin family. This target was confirmed by showing that PTGFRN-expressing cells bound and internalized 33B7, compared to PTGFRN negative cells. Cells able to bind 33B7 were PTGFRN-positive by Western blot analysis. In vitro treatment PTGFRN-positive cancer cell lines with the 33B7-saporin ADC inhibited their proliferation in a dose-dependent fashion. 33B7 conjugated to saporin was also able to block tumor growth in vivo in mouse xenografts when compared to a control ADC. These findings show that screening antibody libraries for internalizing antibodies in cancer cell lines is a good approach to identify new cancer targets for ADC development. These results suggest PTGFRN is a possible therapeutic target via antibody-based approach for certain cancers.
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Muraoka, Satoshi, Mark P. Jedrychowski, Kiran Yanamandra, Seiko Ikezu, Steven P. Gygi, and Tsuneya Ikezu. "Proteomic Profiling of Extracellular Vesicles Derived from Cerebrospinal Fluid of Alzheimer’s Disease Patients: A Pilot Study." Cells 9, no. 9 (August 25, 2020): 1959. http://dx.doi.org/10.3390/cells9091959.

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Pathological hallmarks of Alzheimer’s disease (AD) are deposits of amyloid beta (Aβ) and hyper-phosphorylated tau aggregates in brain plaques. Recent studies have highlighted the importance of Aβ and tau-containing extracellular vesicles (EVs) in AD. We therefore examined EVs separated from cerebrospinal fluid (CSF) of AD, mild cognitive impairment (MCI), and control (CTRL) patient samples to profile the protein composition of CSF EV. EV fractions were separated from AD (n = 13), MCI (n = 10), and CTRL (n = 10) CSF samples using MagCapture Exosome Isolation kit. The CSF-derived EV proteins were identified and quantified by label-free and tandem mass tag (TMT)-labeled mass spectrometry. Label-free proteomics analysis identified 2546 proteins that were significantly enriched for extracellular exosome ontology by Gene Ontology analysis. Canonical Pathway Analysis revealed glia-related signaling. Quantitative proteomics analysis, moreover, showed that EVs expressed 1284 unique proteins in AD, MCI and CTRL groups. Statistical analysis identified three proteins—HSPA1A, NPEPPS, and PTGFRN—involved in AD progression. In addition, the PTGFRN showed a moderate correlation with amyloid plaque (rho = 0.404, p = 0.027) and tangle scores (rho = 0.500, p = 0.005) in AD, MCI and CTRL. Based on the CSF EV proteomics, these data indicate that three proteins, HSPA1A, NPEPPS and PTGFRN, may be used to monitor the progression of MCI to AD.
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Chandras, C., T. E. Harris, A. López Bernal, D. R. E. Abayasekara, and 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 (September 2007): 595–602. http://dx.doi.org/10.1677/joe-07-0128.

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In luteinizing granulosa cells, prostaglandin E2 (PGE2) can exert luteotrophic actions, apparently via the cAMP signalling pathway. In addition to stimulating progesterone synthesis, PGE2 can also stimulate oxidation of the physiological glucocorticoid, cortisol, to its inactive metabolite, cortisone, by the type 1 11β-hydroxysteroid dehydrogenase (11βHSD1) enzyme in human granulosa–lutein cells. Having previously shown these human ovarian cells to express functional G-protein coupled, E-series prostaglandin (PTGER)1, PTGER2 and PTGER4 receptors, the aim of this study was to delineate the roles of PTGER1 and PTGER2 receptors in mediating the effects of PGE2 on steroidogenesis and cortisol metabolism in human granulosa–lutein cells. PGE2-stimulated concentration-dependent increases in both progesterone production and cAMP accumulation (by 1.9 ± 0.1- and 18.7 ± 6.8-fold respectively at 3000 nM PGE2). While a selective PTGER1 antagonist, SC19220, could partially inhibit the steroidogenic response to PGE2 (by 55.9 ± 4.1% at 1000 nM PGE2), co-treatment with AH6809, a mixed PTGER1/PTGER2 receptor antagonist, completely abolished the stimulation of progesterone synthesis at all tested concentrations of PGE2 and suppressed the stimulation of cAMP accumulation. Both PGE2 and butaprost (a preferential PTGER2 receptor agonist) stimulated concentration-dependent increases in cortisol oxidation by 11βHSD1 (by 42.5 ± 3.1 and 40.0 ± 3.0% respectively, at PGE2 and butaprost concentrations of 1000 nM). Co-treatment with SC19220 enhanced the ability of both PGE2 and butaprost to stimulate 11βHSD1 activity (by 30.2 ± 0.2 and 30.5 ± 0.6% respectively), whereas co-treatment with AH6809 completely abolished the 11βHSD1 responses to PGE2 and butaprost. These findings implicate the PTGER2 receptor–cAMP signalling pathway in the stimulation of progesterone production and 11βHSD1 activity by PGE2 in human granulosa–lutein cells.
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Kowalewski, Mariusz Pawel, Hakki Bülent Beceriklisoy, Christiane Pfarrer, Selim Aslan, Hans Kindahl, Ibrahim Kücükaslan, and Bernd Hoffmann. "Canine placenta: a source of prepartal prostaglandins during normal and antiprogestin-induced parturition." REPRODUCTION 139, no. 3 (March 2010): 655–64. http://dx.doi.org/10.1530/rep-09-0140.

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Expression of cyclooxygenase 2 (COX2, now known as PTGS2), prostaglandin E2 synthase (PTGES, PGES), and prostaglandin F2α synthase (PGFS), of the respective receptors PTGFR (FP), PTGER2 (EP2), and PTGER4 (EP4) and of the progesterone receptor (PGR, PR) was assessed by real-time PCR, immunohistochemistry (IHC), or in situ hybridization (ISH) in utero/placental tissue samples collected from three to five bitches on days 8–12 (pre-implantation), 18–25 (post-implantation), and 35–40 (mid-gestation) of pregnancy and during the prepartal luteolysis. Additionally, ten mid-pregnant bitches were treated with the antiprogestin aglepristone (10 mg/kg bw (2×/24 h)); ovariohysterectomy was 24 and 72 h after the second treatment. Plasma progesterone and 15-ketodihydro-PGF2α (PGFM) concentrations were determined by RIA. Expression of the PGR was highest before implantation and primarily located to the endometrium; expression in the placenta was restricted to the decidual cells. PTGS2 was constantly low expressed until mid-gestation; a strong upregulation occurred at prepartal luteolysis concomitant with an increase in PGFM. PGFS was upregulated after implantation and significantly elevated through early and mid-gestation. PTGES showed a gradual increase and a strong prepartal upregulation. PTGFR, PTGER2, and PTGER4 were downregulated after implantation; a gradual upregulation of PTGFR and PTGER2 occurred towards parturition. ISH and IHC co-localized PGFS, PTGFR, PTGES, and PTGS2 in the trophoblast and endometrium. The changes following application of aglepristone were in the same direction as those observed from mid-gestation to prepartal luteolysis. These data suggest that the prepartal increase of PGF2α results from a strong upregulation of PTGS2 in the fetal trophoblast with the withdrawal of progesterone having a signalling function and the decidual cells playing a key role in the underlying cell-to-cell crosstalk.
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Aguila, Brittany, Adina Brett Morris, Raffaella Spina, Eli Bar, Julie Schraner, Robert Vinkler, Jason W. Sohn, and Scott M. Welford. "The Ig superfamily protein PTGFRN coordinates survival signaling in glioblastoma multiforme." Cancer Letters 462 (October 2019): 33–42. http://dx.doi.org/10.1016/j.canlet.2019.07.018.

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Kim, Soon Ok, Nune Markosyan, Gerald J. Pepe, and Diane M. Duffy. "Estrogen promotes luteolysis by redistributing prostaglandin F2α receptors within primate luteal cells." REPRODUCTION 149, no. 5 (May 2015): 453–64. http://dx.doi.org/10.1530/rep-14-0412.

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Prostaglandin F2α (PGF2α) has been proposed as a functional luteolysin in primates. However, administration of PGF2α or prostaglandin synthesis inhibitors in vivo both initiate luteolysis. These contradictory findings may reflect changes in PGF2α receptors (PTGFRs) or responsiveness to PGF2α at a critical point during the life span of the corpus luteum. The current study addressed this question using ovarian cells and tissues from female cynomolgus monkeys and luteinizing granulosa cells from healthy women undergoing follicle aspiration. PTGFRs were present in the cytoplasm of monkey granulosa cells, while PTGFRs were localized in the perinuclear region of large, granulosa-derived monkey luteal cells by mid-late luteal phase. A PTGFR agonist decreased progesterone production in luteal cells obtained at mid-late and late luteal phases, but did not decrease progesterone production by granulosa cells or luteal cells from younger corpora lutea. These findings are consistent with a role for perinuclear PTGFRs in functional luteolysis. This concept was explored using human luteinizing granulosa cells maintained in vitro as a model for luteal cell differentiation. In these cells, PTGFRs relocated from the cytoplasm to the perinuclear area in an estrogen- and estrogen receptor-dependent manner. Similar to our findings with monkey luteal cells, human luteinizing granulosa cells with perinuclear PTGFRs responded to a PTGFR agonist with decreased progesterone production. These data support the concept that PTGFR stimulation promotes functional luteolysis only when PTGFRs are located in the perinuclear region. Estrogen receptor-mediated relocation of PTGFRs within luteal cells may be a necessary step in the initiation of luteolysis in primates.
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Zschockelt, Lina, Olga Amelkina, Marta J. Siemieniuch, Mariusz P. Kowalewski, Martin Dehnhard, Katarina Jewgenow, and Beate C. Braun. "Synthesis and reception of prostaglandins in corpora lutea of domestic cat and lynx." Reproduction 152, no. 2 (August 2016): 111–26. http://dx.doi.org/10.1530/rep-16-0180.

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Felids show different reproductive strategies related to the luteal phase. Domestic cats exhibit a seasonal polyoestrus and ovulation is followed by formation ofcorpora lutea(CL). Pregnant and non-pregnant cycles are reflected by diverging plasma progesterone (P4) profiles. Eurasian and Iberian lynxes show a seasonal monooestrus, in which physiologically persistent CL (perCL) support constantly elevated plasma P4 levels. Prostaglandins (PGs) represent key regulators of reproduction, and we aimed to characterise PG synthesis in feline CL to identify their contribution to the luteal lifespan. We assessed mRNA and protein expression of PG synthases (PTGS2/COX2, PTGES, PGFS/AKR1C3) and PG receptors (PTGER2, PTGER4, PTGFR), and intra-luteal levels of PGE2and PGF2α. Therefore, CL of pregnant (pre-implantation, post-implantation, regression stages) and non-pregnant (formation, development/maintenance, early regression, late regression stages) domestic cats, and prooestrous Eurasian (perCL, pre-mating) and metoestrous Iberian (perCL, freshCL, post-mating) lynxes were investigated. Expression ofPTGS2/COX2, PTGES and PTGER4 was independent of the luteal stage in the investigated species. High levels of luteotrophic PGE2in perCL might be associated with persistence of luteal function in lynxes. Signals for PGFS/AKR1C3 expression were weak in mid and late luteal stages of cats but were absent in lynxes, concomitant with low PGF2αlevels in these species. Thus, regulation of CL regression by luteal PGF2αseems negligible. In contrast, expression of PTGFR was evident in nearly all investigated CL of cat and lynxes, implying that luteal regression, e.g. at the end of pregnancy, is triggered by extra-luteal PGF2α.
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Waclawik, Agnieszka, Piotr Kaczynski, and 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 (October 1, 2013): 3864–76. http://dx.doi.org/10.1210/en.2012-2271.

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The conceptus and endometrium secrete large amounts of prostaglandin E2 (PGE2) into the porcine uterine lumen during the periimplantation period. We hypothesized that PGE2 acts on conceptus/trophoblast cells through auto- and paracrine mechanisms. Real-time RT-PCR analysis revealed that PGE2 receptor (PTGER)2 mRNA was 14-fold greater in conceptuses/trophoblasts on days 14–25 (implantation and early placentation period) vs preimplantation day 10–13 conceptuses (P < .05). Similarly, expression of PTGER2 protein increased during implantation. Conceptus expression of PTGER4 mRNA and protein did not differ on days 10–19. PGE2 stimulated PTGER2 mRNA expression in day 15 trophoblast cells through PTGER2 receptor signaling. PGE2 elevated aromatase expression and estradiol-17β secretion by trophoblast cells. Moreover, PGE2 and the PTGER2 agonist, butaprost, increased the adhesive capacity of both human HTR-8/SVneo trophoblast and primary porcine trophoblast cells to extracellular matrix. This PGE2-induced alteration in trophoblast cell adhesion to extracellular matrix was abolished by incubation of these cells with AH6809 (PTGER2 antagonist), ITGAVB3-directed tetrapeptide arg-gly-asp-ser or integrin ITGAVB3 antibody. PGE2 stimulated adhesion of porcine trophoblast cells via the estrogen receptor and MEK/MAPK signaling pathway. PGE2 induced phosphorylation of MAPK1/MAPK3 through PTGER2 and up-regulated expression of cell adhesion proteins such as focal adhesion kinase and intercellular adhesion molecule-1. Our study indicates that elevated PGE2 in the periimplantation uterine lumen stimulates conceptus PTGER2 expression, which in turn promotes trophoblast adhesion via integrins, and synthesis and secretion of the porcine embryonic signal estradiol-17β. Moreover, the mechanism through which PGE2 increases trophoblast adhesion is not species specific because it is PTGER2- and integrin-dependent in both porcine and human trophoblast cells.
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Kauke, 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 (November 2020): A745. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0703.

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BackgroundExosomes are natural, abundant extracellular vesicles capable of transferring complex molecules between neighboring and distant cell types. Translational research efforts have focused on co-opting this communication mechanism to deliver exogenous payloads to treat a variety of diseases. Important strategies to maximize the therapeutic potential of exosomes therefore include payload loading, functionalization of the exosome surface with pharmacologically active proteins, and delivery to target cells of interest.MethodsThrough comparative proteomic analysis of purified exosomes, we identified several highly enriched and exosome-specific proteins, including a transmembrane glycoprotein (PTGFRN) belonging to the immunoglobulin superfamily. Leveraging PTGFRN as a scaffold for exosome surface display, we developed our engExTM platform to generate engineered exosomes functionalized with a variety of structurally and biologically diverse proteins.Systemically administered exosomes are primarily taken up by macrophages in the liver and spleen. To redirect exosome uptake to other cell types, we employed our engineering platform to display functional targeting ligands, including single domain antibodies, single chain variable fragments, single chain Fabs (scFabs), and receptor ligands, on the exosome surface at high density. To demonstrate that exosome surface modifications can alter cellular tropism, we generated exosomes displaying anti-Clec9A scFabs to target conventional type 1 dendritic cells (cDC1s), anti-CD3 scFabs to target T cells, and CD40 ligand to target B cells. The engineered exosomes exhibited functional antigen binding that led to greater association with the cell types expressing the cognate receptor both in vitro and in vivo.ResultsIn mice, systemic administration of exosomes engineered to display scFabs targeting Clec9A resulted in a 4-fold increase in the percentage of cDC1 cells in the blood that had taken up exosomes over controls, and a 6-fold increase in the number of exosomes taken up per cell. We further showed that compared to untargeted exosomes, those with altered tropism achieved increased functional payload delivery to the target cell of interest. In primary mouse dendritic cells, anti-Clec9A exosomes loaded with a cyclic dinucleotide STING agonist achieved greater pathway induction, 2.3-fold greater as measured by IFNβ production, 2-fold by IFNα, and 15-fold by IL-12, when compared to an untargeted control. Preliminary in vivo data show that intra-tumorally administered anti-Clec9A exosomes reduce the required STING agonist dose 10-fold to achieve single-agent tumor control and induce immune responses against tumor-associated antigen, compared to controls.ConclusionsThese results demonstrate the potential of our engExTM platform to generate targeted exosome therapeutics capable of immune cell stimulation and tumor growth inhibition in vivo.Ethics ApprovalAll experimental animal studies were performed according to Codiak BioSciences IACUC approved AUP CB2020-001.
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Przygrodzka, E., M. M. Kaczmarek, P. Kaczynski, and A. J. Ziecik. "Steroid hormones, prostanoids, and angiogenic systems during rescue of the corpus luteum in pigs." REPRODUCTION 151, no. 2 (February 2016): 135–47. http://dx.doi.org/10.1530/rep-15-0332.

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In order to characterize the transition of the corpora lutea (CL) from acquisition of luteolytic sensitivity to rescue of luteal function: i) the expression of 38 factors associated with steroids, prostanoids, and angiogenic systems and ii) concentrations of the main hormones responsible for maintenance of CL function in cyclic and pregnant pigs were examined. Additionally, the effect of prostaglandin (PG) E2 and F2α on luteal function during the estrous cycle and pregnancy was evaluated in vitro. Significantly up-regulated gene expression was revealed in CL collected on day 14 of the estrous cycle (CYP19A1, ESR2, PTGS2, HIF1A, and EDN1) and on days 12–14 of pregnancy (SCARB1, PGRMC1, STAR, HSD3B1, NR5A1, PTGFR, PTGER4, and VEGFA). Elevated concentrations of estradiol-17β and PGE2 occurred in CL on days 12 and 14 of pregnancy respectively, while an increased intraluteal PGF2α content was noted on day 14 of the estrous cycle. Both PGs increased the synthesis of progesterone by cultured luteal slices obtained on day 14 of pregnancy, in contrast to the action of PGF2α on the corresponding day of the estrous cycle. PGE2 stimulated cAMP production via PTGER2 and PTGER4, while PGF2α elevated the content of CREB in cultured luteal slices from CL of pregnant pigs. In silico analysis showed that infiltration of lymphocytes and apoptosis of microvascular endothelium were activated in CL on day 12 of the estrous cycle vs pregnancy. Summarizing, an abundance of E2 and PGE2 during pregnancy regulates specific pathways responsible for steroidogenesis, the prostanoid signaling system and angiogenesis during rescue from luteolysis in porcine CL.
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Dissertations / Theses on the topic "PTGFRN"

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Heumann, Tina [Verfasser], and 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.

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Mesa, 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.

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Pasciuto, Giulia [Verfasser], and 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.

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WU, PEI-JU, and 吳佩儒. "PTGFRN Expression Correlate with WHO Grades in Gliomas." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/f88244.

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碩士
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.
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Chen, Ni-Yun, and 陳倪芸. "A Strategic Analysis of the Electronic Health Record." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/ptg99n.

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碩士
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.
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Guo, Chien-Jung, and 郭千榕. "The role of Glucocorticoid receptor(GR) in PTGR2 regulation." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/u2p5xy.

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碩士
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.
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Chen, Kuan-Ju, and 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.

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碩士
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.
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Hsieh, Meng-Lun, and 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.

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碩士
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.
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9

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.

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La Prostaglandina E2 (PGE2) è coinvolta in diversi processi fisiopatologici. PGE2 è una molecola chiave nel processo di cancerogenesi, essendo coinvolta nella proliferazione cellulare, nell'angiogenesi, nella sorveglianza immunitaria e nell’apoptosi. La sintesi di PGE2 richiede tre enzimi che agiscono in sequenza: la Fosfolipasi A2, la cicloossigenasi e la sintetasi della prostaglandina E. La Fosfolipasi A2 (PLA2) permette il rilascio di acido arachidonico (AA) dai fosfolipidi di membrana, la cicloossigenasi (COX) converte l’AA a PGH2, che viene isomerizzato a PGE2 dalla sintasi della prostaglandina E (PGES). PGE2 viene rilasciato dalle cellule e interagisce con quattro distinti recettori, EP1, EP2, EP3 e EP4. Una sovra-espressione della forma inducibile di COX (Cox-2) e di PGES microsomiale-1 (mPGES-1), con conseguente eccessiva produzione di PGE2, è stata osservata in vari tessuti tumorali, tra cui alcuni tumori cutanei. Una sovra-espressione di EP1 è stata osservata in tumori cutanei indotti da UVB. Varianti genetiche, situate nella regione del promotore dei geni codificanti per la prostaglandina sintasi-2 (PTGS2/COX2), PGES microsomiale-1 (mPGES-1), o per il recettore EP1 (PTGER1), potrebbero determinare alterazioni nella espressione genica, con una conseguente aumentata sintesi di PGE2 o alterata risposta a PGE2. Tali varianti potrebbero pertanto rappresentare fattori di rischio per lo sviluppo di tumore cutaneo non melanoma (non melanoma skin cancer NMSC) in individui riceventi trapianto d’organo (OTRs). Per determinare se polimorfismi in questi geni potessero costituire utili marcatori genetici di suscettibilità, contribuendo alla individuazione precoce di individui a maggiore rischio di NMSC, è stato eseguito uno studio caso-controllo. Due polimorfismi nel gene PTGS2, tre nel gene mPGES-1 e tre nel gene PTGER1 sono stati genotipizzati in 286 OTRs, 144 casi NMSC e 142 controlli. L’allele –765G del gene PTGS2 è significativamente più frequente nei casi rispetto ai controlli [p=0.015; OR=9.59 (1.36-192.66)], suggerendo che questa variante possa rappresentare un fattore di rischio per lo sviluppo di tumori basocellulari (BCC) nei soggetti sottoposti a trapianto prima dei 50 anni. L’analisi dei polimorfismi –1760C>A (rs3810254), -1728G>A (rs3810255) e –1113C>T (rs2241359) della regione 5' prossimale del gene PTGER1 ha dimostrato che gli alleli minori per queste varianti erano più rappresentati in individui con tumore squamocellulare (SCC), rispetto ai corrispondenti controlli sottoposti a trapianto prima dei 50 anni, ma la differenza non è risultata statisticamente significativa. Per verificare se una regione di 1452 pb del 5' fiancheggiante il gene, e contenente i tre polimorfismi, esercitasse un'attività di promotore, è stata eseguita l’analisi funzionale in colture cellulari HeLa e HaCat (cheratinociti umani). Nonostante una debole attività di promotore sia stata osservata in cellule HeLa, non siamo stati in grado di dimostrare attività di promotore nelle cellule HaCat, anche dopo stimolazione con LPS. La regione del 5' fiancheggiante il gene mPGES-1 è stata analizzata mediante l’analisi degli eteroduplici per identificare nuove varianti. Tre polimorfismi, situati all'interno di regioni conservate del gene e riportati nel database NCBI come –664T>A (rs7873087), –663A>T (rs7859349) e –439T>C (rs7872802), sono stati identificati. Le distribuzioni genotipiche osservate hanno indicato completo linkage disequilibrium per i tre polimorfismi, e nessuna associazione con NMSC. In conclusione, l’allele -765C nel gene PTGS2 sembra rappresentare un fattore protettivo verso lo sviluppo di BCC negli individui sottoposti a trapianto prima dei 50 anni. L’analisi dei polimorfismi nella regione 5’ fiancheggiante i geni mPGES-1 e PTGER1 tende ad escludere l’ipotesi che varianti in queste regioni possano rappresentare fattori di rischio per la predisposizione a NMSC.
Prostaglandin 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.
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Book chapters on the topic "PTGFRN"

1

"PTGER2." In Encyclopedia of Signaling Molecules, 4286. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_103155.

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2

"PTGF-b." In Encyclopedia of Cancer, 3848. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_101922.

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3

"PTGF-β." In Encyclopedia of Cancer, 3121. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4859.

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4

"Post-Transcriptional Gene Regulation (PTGR)." In Encyclopedia of Systems Biology, 1728. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_101172.

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Conference papers on the topic "PTGFRN"

1

Marquez, Jorge, Jianping Dong, Chun Dong, and Ginette Serrero. "Abstract LB116: Prostaglandin F2 Receptor Negative Regulator (PTGFRN) is a novel target to inhibit tumor growth via antibody drug conjugate." In 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.

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Bayraktar, Emine, Cristian Rodriguez-Aguayo, Junhua Mai, Cristina Ivan, Cristina Ivan, Arturo Chavez-Reyes, Anil K. Sood, Mauro Ferrari, Haifa Shen, and Gabriel Lopez-Berestein. "Abstract 4668: Silencing PTGER3 enhances chemotherapeutic responses." In 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.

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Gui, 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." 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.a3044.

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4

Qin, Haonan, Weiying Xie, Yunsong Li, Kai Jiang, Jie Lei, and Qian Du. "PTGAN: A Proposal-Weighted Two-Stage GAN with Attention for Hyperspectral Target Detection." In IGARSS 2021 - 2021 IEEE International Geoscience and Remote Sensing Symposium. IEEE, 2021. http://dx.doi.org/10.1109/igarss47720.2021.9553721.

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5

Hess, 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." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604759.

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Bayraktar, Emine, Cristian Rodriguez-Aguayo, Zahid Siddik, and Gabriel Lopez-Berestein. "Abstract 2066: Delivery of 2`F-PS2 PTGER3 siRNA-DOPC enhances anti-tumoral activity in cisplatin resistant ovarian cancer model." In 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.

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7

Gou, Xiaochuan, Chih-Chieh Hung, Guanyao Li, and Wen-Chih Peng. "PTGF: Public Transport General Framework for Identifying Transport Modes Based on Cellular Data." In 2019 20th IEEE International Conference on Mobile Data Management (MDM). IEEE, 2019. http://dx.doi.org/10.1109/mdm.2019.00120.

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Schlegel, Anne, Oliver Hasinger, Selina Esche, Melanie Martini, Thomas König, and 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." In 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.

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9

Wagner, Michael J., Sanford A. Klein, and Douglas T. Reindl. "Simulation of Utility-Scale Central Receiver System Power Plants." In 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.

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The operation of solar energy systems is necessarily transient. Over the lifetime of a concentrating solar power plant, the system operates at design conditions only occasionally, with the bulk of operation occurring under part-load conditions depending on solar resource availability. Credible economic analyses of solar-electric systems requires versatile models capable of predicting system performance at both design and off-design conditions. This paper introduces new and adapted simulation tools for power tower systems including models for the heliostat field, central receiver, and the power cycle. The design process for solar power tower systems differs from that for other concentrating solar power (CSP) technologies such as the parabolic trough or parabolic dish systems that are nearly modular in their design. The design of an optimum power tower system requires a determination of the heliostat field layout and receiver geometry that results in the greatest long-term energy collection per unit cost. Research presented in this paper makes use of the DELSOL3 code (Kistler, 1986) which provides this capability. An interface program called PTGEN was developed to simplify the combined use of DELSOL3 and TRNSYS. The final product integrates the optimization tool with the detailed component models to provide a comprehensive modeling tool set for the power tower technology.
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