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Artykuły w czasopismach na temat "G-Protein Coupled Estrogen Receptor (GPER)"
Arterburn, Jeffrey B., i Eric R. Prossnitz. "G Protein–Coupled Estrogen Receptor GPER: Molecular Pharmacology and Therapeutic Applications". Annual Review of Pharmacology and Toxicology 63, nr 1 (20.01.2023): 295–320. http://dx.doi.org/10.1146/annurev-pharmtox-031122-121944.
Pełny tekst źródłaMeyer, Matthias R., Natalie C. Fredette, Matthias Barton i Eric R. Prossnitz. "G protein-coupled estrogen receptor inhibits vascular prostanoid production and activity". Journal of Endocrinology 227, nr 1 (24.08.2015): 61–69. http://dx.doi.org/10.1530/joe-15-0257.
Pełny tekst źródłaQian, Hongyan, Jingxiu Xuan, Yuan Liu i Guixiu Shi. "Function of G-Protein-Coupled Estrogen Receptor-1 in Reproductive System Tumors". Journal of Immunology Research 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/7128702.
Pełny tekst źródłaFilardo, Edward J., i Peter Thomas. "Minireview: G Protein-Coupled Estrogen Receptor-1, GPER-1: Its Mechanism of Action and Role in Female Reproductive Cancer, Renal and Vascular Physiology". Endocrinology 153, nr 7 (11.04.2012): 2953–62. http://dx.doi.org/10.1210/en.2012-1061.
Pełny tekst źródłaPetrie, Whitney K., Megan K. Dennis, Chelin Hu, Donghai Dai, Jeffrey B. Arterburn, Harriet O. Smith, Helen J. Hathaway i Eric R. Prossnitz. "G Protein-Coupled Estrogen Receptor-Selective Ligands Modulate Endometrial Tumor Growth". Obstetrics and Gynecology International 2013 (2013): 1–17. http://dx.doi.org/10.1155/2013/472720.
Pełny tekst źródłaHsu, Li-Han, Nei-Min Chu, Yung-Feng Lin i Shu-Huei Kao. "G-Protein Coupled Estrogen Receptor in Breast Cancer". International Journal of Molecular Sciences 20, nr 2 (14.01.2019): 306. http://dx.doi.org/10.3390/ijms20020306.
Pełny tekst źródłaMolina, Luis, Felipe A. Bustamante, Kanti D. Bhoola, Carlos D. Figueroa i Pamela Ehrenfeld. "Possible role of phytoestrogens in breast cancer via GPER-1/GPR30 signaling". Clinical Science 132, nr 24 (13.12.2018): 2583–98. http://dx.doi.org/10.1042/cs20180885.
Pełny tekst źródłaLu, Dingqiang, Xinqian Wang, Chunlei Feng, Danyang Liu, Yixuan Liu, Yujiao Liu, Jie Li i in. "Study of the Sensing Kinetics of G Protein-Coupled Estrogen Receptor Sensors for Common Estrogens and Estrogen Analogs". Molecules 28, nr 8 (7.04.2023): 3286. http://dx.doi.org/10.3390/molecules28083286.
Pełny tekst źródłaYu, Xuan, Handong Ma, Scott A. Barman, Alexander T. Liu, Minga Sellers, John N. Stallone, Eric R. Prossnitz, Richard E. White i Guichun Han. "Activation of G protein-coupled estrogen receptor induces endothelium-independent relaxation of coronary artery smooth muscle". American Journal of Physiology-Endocrinology and Metabolism 301, nr 5 (listopad 2011): E882—E888. http://dx.doi.org/10.1152/ajpendo.00037.2011.
Pełny tekst źródłaChuang, Shu-Chun, Chung-Hwan Chen, Ya-Shuan Chou, Mei-Ling Ho i Je-Ken Chang. "G Protein-Coupled Estrogen Receptor Mediates Cell Proliferation through the cAMP/PKA/CREB Pathway in Murine Bone Marrow Mesenchymal Stem Cells". International Journal of Molecular Sciences 21, nr 18 (5.09.2020): 6490. http://dx.doi.org/10.3390/ijms21186490.
Pełny tekst źródłaRozprawy doktorskie na temat "G-Protein Coupled Estrogen Receptor (GPER)"
Attarhaie, Tehrani Mahtab. "Anatomical Expression and Functional Role of the G-Protein Coupled Estrogen Receptor 1 in the Song System of Zebra Finches (Taeniopygia guttata)". Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent152416406994131.
Pełny tekst źródłaAcharya, Kalpana D. Ms. "ROLE OF MEMBRANE BOUND G-PROTEIN COUPLED ESTROGEN RECEPTOR GPR30 AND Z-LINKED RIBOSOMAL GENE S6 (RPS6) IN SEXUALLY DIMORPHIC DEVELOPMENT OF THE ZEBRA FINCH BRAIN". Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1341338394.
Pełny tekst źródłaWaghulde, Harshal B. "Mapping and CRISPR/Cas9 Gene Editing for Identifying Novel Genomic Factors Influencing Blood Pressure". University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1470402637.
Pełny tekst źródła"GPER-1 mediates the inhibitory actions of estrogen on adipogenesis in 3T3-L1 cells through perturbation of mitotic clonal expansion". 2012. http://library.cuhk.edu.hk/record=b5549500.
Pełny tekst źródła脂肪發育調控乃一複雜且精妙之排程，而雌激素已被證明能抑制脂肪形成，是故雌激素替代療法可舒減絶經後婦女之脂肪代謝問題。此項研究發現GPER於小鼠腹部脂肪組織及小鼠前脂肪細胞系3T3-L1中均有表達，且其信使RNA量於受誘導之3T3-L1成脂作用中錄得上調。
3T3-L1細胞分化作用會被名為G1之特異性GPER激動劑阻撓於克隆擴增階段（MCE），此即表明GPER有參與成脂調控之可能。通過油紅O染色發現，受G1處理之3T3-L1細胞於分化後所產生之油滴量實比其對照組為低，但此一效果能被特異性GPER小干擾RNA預處理抹除。另外，本研究以流式細胞儀及西方墨點法對細胞週期及細胞週期因子進行分析後，認為激活GPER能觸發對G1期細胞週期停滯之抑制。另一方面，受G1處理並分化中之3T3-L1細胞出現蛋白激酶B磷酸化效應，意味雌激素與GPER結合對成脂作用有雙向調節之可能性。
總而言之，本研究結果斷定GPER能介導雌激素對脂肪組織發育之影響，並為成脂作用之負調節因子，故此，一系列成果將有助肥胖症藥物之研發。
A novel transmembrane estrogen receptor, G-protein coupled estrogen receptor (GPER, also known as GPR30), is recently identified in various animals including mouse, rat, human and zebrafish. GPER is expressed in many organs including fatty tissues, and has been demonstrated to mediate various rapid responses and transcriptional events upon estrogen binding. The study on the role of GPER in adipogenesis would lead to a more comprehensive understanding of estrogenic actions, with the view of identifying novel therapeutic targets for the treatment of obesity.
Regulation of adipose development is a complex and subtly orchestrated process. Estrogen has been shown to inhibit adipogenesis. Estrogen replacement therapy therefore affects fat metabolism in post-menopausal women. In this study, GPER is identified in mouse abdominal fatty tissues; and there is an up-regulation of GPER in the mouse preadipocyte cell line 3T3-L1 during induced adipogenesis.
Differentiation of 3T3-L1 cells is perturbed by the selective GPER agonist G1 at mitotic clonal expansion (MCE), indicating a possible involvement of GPER in the regulation of adipogenesis. By means of Oil-Red-O staining, the production of oil droplets in the G1-treated, differentiated 3T3-L1 cells is shown to be lower than the untreated control; and such effect is reversed by a specific siRNA knockdown of GPER. FACS analysis and Western blot analysis of cell cycle factors during MCE suggest that GPER activation triggers an inhibition of cell cycle arrest at the G1 stage. On the other hand, phosphorylation of Akt in G1-treated differentiating cells implies a possibility of bi-directional estrogenic regulation of adipogenesis via GPER.
To conclude, it is postulated that GPER mediates estrogenic actions in adipose tissues as a negative regulator of adipogenesis. These results provide insights into the development of therapeutic agents for the treatment of human obesity.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Yuen, Man Leuk.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2012.
Includes bibliographical references (leaves 144-166).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
Abstract (English version) --- p.I
Abstract (Chinese version) --- p.III
Acknowledgement --- p.V
Table of Contents --- p.VII
List of Abbreviations --- p.XI
List of Tables --- p.XII
List of Figures --- p.XIII
Chapter Chapter 1: --- Introduction --- p.1
Chapter 1.1. --- Obesity and adipose tissue --- p.1
Chapter 1.1.1. --- Obesity --- p.1
Chapter 1.1.2. --- Fat deposition --- p.3
Chapter 1.1.3. --- Origin and development of white adipose tissue --- p.5
Chapter 1.2. --- Adipogenesis --- p.7
Chapter 1.2.1. --- Origins of white adipocytes --- p.7
Chapter 1.2.2. --- Signals for adipogenesis --- p.10
Chapter 1.2.3. --- Regulation of gene expression during adipogenesis --- p.12
Chapter 1.2.4. --- Common adipose cell lines --- p.16
Chapter 1.2.5. --- Mechanism of in vitro adipogenesis --- p.21
Chapter 1.2.5.1. --- Growth arrest --- p.23
Chapter 1.2.5.2. --- Mitotic clonal expansion --- p.23
Chapter 1.2.5.3. --- Early and terminal differentiation --- p.24
Chapter 1.3. --- Estrogen and adipogenesis --- p.28
Chapter 1.4. --- G-protein coupled estrogen receptor-1 --- p.33
Chapter 1.4.1. --- General introduction of GPER --- p.33
Chapter 1.4.2. --- Ligands of GPER --- p.36
Chapter 1.4.3. --- Cellular signaling of GPER --- p.38
Chapter 1.4.4. --- Metabolic actions of GPER: A brief introduction --- p.43
Chapter 1.4.5. --- Metabolic actions of GPER on obesity and glucose metabolism --- p.48
Chapter 1.4.6. --- Study objectives --- p.53
Chapter Chapter 2: --- Expression profiles and cellular localization of Gper/GPER in mouse adipose, 3T3-L1 preadipocytes and 3T3-L1 mature adipocytes --- p.54
Chapter 2.1. --- Introduction --- p.54
Chapter 2.1.1. --- Expression and functional roles of GPER in adipose. --- p.55
Chapter 2.1.2. --- Swiss mouse preadipocytes 3T3-L1 --- p.57
Chapter 2.1.3. --- Study objectives --- p.57
Chapter 2.2. --- Materials and Methods --- p.59
Chapter 2.2.1. --- Reagents --- p.59
Chapter 2.2.2. --- Animal tissues --- p.59
Chapter 2.2.3. --- Cell culture --- p.60
Chapter 2.2.4. --- Reverse transcription polymerase chain reaction (RT-PCR) --- p.62
Chapter 2.2.5. --- Quantitative real-time RT-PCR (qRT-PCR) --- p.66
Chapter 2.2.6. --- SDS-PAGE and Western blot analysis --- p.68
Chapter 2.2.7. --- Immunofluorescence assay --- p.69
Chapter 2.2.8. --- Statistical analysis --- p.70
Chapter 2.3. --- Results --- p.71
Chapter 2.3.1. --- Expression of Gper/GPER in mouse visceral adipose tissues --- p.72
Chapter 2.3.2. --- Expression profiles of Gper/GPER in undifferentiated 3T3-L1 preadipocytes and differentiated 3T3-L1 adipocytes --- p.73
Chapter 2.3.3. --- Cellular localization of GPER in undifferentiated 3T3-L1 preadipocytes and differentiated 3T3-L1 adipocytes --- p.75
Chapter 2.4. --- Discussion --- p.76
Chapter Chapter 3: --- Rapid cellular responses induced by GPER activation in 3T3-L1 preadipocytes --- p.78
Chapter 3.1. --- Introduction --- p.78
Chapter 3.1.1. --- Rapid cellular response of estrogen via GPER --- p.79
Chapter 3.1.2. --- Study objectives --- p.81
Chapter 3.2. --- Materials and Methods --- p.82
Chapter 3.2.1. --- Reagents --- p.82
Chapter 3.2.2. --- Cell culture --- p.82
Chapter 3.2.3. --- SDS-PAGE and Western blot analysis --- p.83
Chapter 3.2.4. --- Statistical analysis --- p.84
Chapter 3.3. --- Results --- p.86
Chapter 3.3.1. --- Phosphorylation of p44/42 MAPK after time-dependent activation of GPER by ICI182,780 and G1 --- p.87
Chapter 3.3.2. --- Phosphorylation of p44/42 MAPK after dose-dependent activation of GPER by a combination of chemical agents --- p.88
Chapter 3.4. --- Discussion --- p.89
Chapter Chapter 4: --- GPER activation on cell viability of 3T3-L1 preadipocytes --- p.90
Chapter 4.1. --- Introduction --- p.90
Chapter 4.1.1. --- Cell proliferation mediated by GPER --- p.90
Chapter 4.1.2. --- Study objectives --- p.92
Chapter 4.2. --- Materials and Methods --- p.93
Chapter 4.2.1. --- Reagents --- p.93
Chapter 4.2.2. --- Cell culture --- p.93
Chapter 4.2.3. --- MTT assay for cell viability --- p.94
Chapter 4.2.4. --- Statistical analysis --- p.95
Chapter 4.3. --- Results --- p.96
Chapter 4.3.1. --- Cell viability of 3T3-L1 after dose-dependent activation of GPER by 17β-estradiol, ICI182,780 and G1 --- p.97
Chapter 4.4. --- Discussion --- p.99
Chapter Chapter 5: --- GPER-mediated estrogenic action on lipid accumulation in the mature 3T3-L1 adipocytes --- p.101
Chapter 5.1. --- Introduction --- p.101
Chapter 5.1.1. --- Induction of differentiation in Swiss mouse preadipocyte 3T3-L1 --- p.101
Chapter 5.1.2. --- Study objectives --- p.102
Chapter 5.2. --- Materials and Methods --- p.103
Chapter 5.2.1. --- Reagents --- p.103
Chapter 5.2.2. --- Cell culture --- p.103
Chapter 5.2.3. --- Oil-Red-O staining and measurement of absorbance --- p.105
Chapter 5.2.4. --- Knockdown of Gper/GPER by siRNA --- p.107
Chapter 5.2.5. --- Reverse transcription polymerase chain reaction (RT-PCR) --- p.110
Chapter 5.2.6. --- SDS-PAGE and Western blot analysis --- p.110
Chapter 5.2.7. --- Statistical analysis --- p.110
Chapter 5.3. --- Results --- p.112
Chapter 5.3.1. --- GPER activation on 3T3-L1 differentiation --- p.114
Chapter 5.3.2. --- Knockdown of Gper/GPER in Swiss mouse preadipocyte 3T3-L1 --- p.114
Chapter 5.3.3. --- Phosphorylation of p44/42 MAPK in Gper/GPER-knockdown 3T3-L1 after time-dependent activation of GPER by G1 --- p.117
Chapter 5.3.4. --- Action of drugs on differentiation of Gper/GPER-knockdown 3T3-L1 --- p.117
Chapter 5.4. --- Discussion --- p.118
Chapter Chapter 6: --- Role of GPER in regulating cell cycle progression during mitotic clonal expansion (MCE) stage in adipogenesis of 3T3-L1 --- p.120
Chapter 6.1. --- Introduction --- p.120
Chapter 6.1.1. --- Differentiation stages of Swiss mouse preadipocyte 3T3-L1 --- p.121
Chapter 6.1.2. --- Apoptosis and cell cycle progression --- p.122
Chapter 6.1.3. --- Study objectives --- p.126
Chapter 6.2. --- Materials and Methods --- p.127
Chapter 6.2.1. --- Reagents --- p.127
Chapter 6.2.2. --- Cell culture --- p.127
Chapter 6.2.3. --- Oil-Red-O staining and measurement of absorbance --- p.129
Chapter 6.2.4. --- Trypan blue exclusion assay for cell viability determination --- p.129
Chapter 6.2.5. --- SDS-PAGE and Western blot analysis --- p.131
Chapter 6.2.6. --- Flow cytometry for analysis of cell cycle progression --- p.132
Chapter 6.2.7. --- Statistical analysis --- p.133
Chapter 6.3. --- Results --- p.134
Chapter 6.3.1. --- Temporal effect of GPER activation on differentiation progress of Swiss mouse preadipocyte 3T3-L1 --- p.137
Chapter 6.3.2. --- Effect of GPER activation on cell viability during adipogenesis --- p.139
Chapter 6.3.3. --- Effect of GPER activation on apoptosis during adipogenesis --- p.139
Chapter 6.3.4. --- Effect of GPER activation on cell cycle distribution during induced adipogenesis --- p.140
Chapter 6.3.5. --- Effect of GPER activation on expression of cell cycle markers during induced adipogenesis --- p.142
Chapter 6.3.6. --- Activation of PI3K/Akt pathway by GPER stimulation during induced adipogenesis --- p.143
Chapter 6.4. --- Discussion --- p.144
Chapter Chapter 7: --- Conclusions and Future Perspectives --- p.148
References --- p.155
Peyton, Candace Ann. "Involvement of epidermal growth factor receptor (EGFR) signaling in estrogen inhibition of oocyte maturation mediated through G protein-coupled estrogen receptor 1 (GPER) in zebrafish (Danio rerio)". Thesis, 2010. http://hdl.handle.net/2152/ETD-UT-2010-05-1083.
Pełny tekst źródłatext
"Expression of G protein-coupled estrogen receptor (GPER) and its effects on P2Y receptor-mediated Ca²⁺ signalling and cytokine secretion in human bronchial epithelia". 2014. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1290692.
Pełny tekst źródłaEstrogen (or E₂) is an important hormone in human physiology. In addition to the classical nuclear hormone receptors ERα and ERβ, a novel estrogen receptor, G protein-coupled estrogen receptor (GPER), was recently identified and found to be involved in both rapid signalling and transcriptional regulations. The action of GPER is unclear, but it has been implicated in mediating anti-inflammatory responses.
In our experiments, both human bronchial epithelial cell line, 16HBE14o-, and primary normal human bronchial epithelial cells expressed GPER at mRNA and protein levels, as demonstrated by RT-PCR and western blotting, respectively. ERα and ERβ expression were also detected at mRNA and protein level. Expression of GPER receptors was localized in the human bronchial epithelial cells by immunofluorescence staining and western blotting of fractionated cell lysates.
[Ca²⁺]ᵢ induced by nucleotides were monitored by calcium imaging technique using MetaFluor fluorescence ratio imaging system. Stimulation of epithelial cells with E₂ or with the specific agonist of GPER, G1, rapidly attenuated a UDP-, UTP- or ATPyS- evoked increase in [Ca²⁺]ᵢ in both 16HBE14o- cell line and primary cells. This inhibitory effect of E₂ and G1 were concentration dependent, while this effect was reversed by GPER specific antagonist, G15. To examine the effect of E₂ and G1 on UDP-activated intracellular Ca²⁺ release and influx, the epithelia were exposed to nominally Ca²⁺ -free solution in the presence or absence of G1 or E₂, and then stimulated with UDP. Subsequently, Ca²⁺ was added to the perfusate. Both E₂ and G1 could inhibit UDP-induced Ca²⁺ release. However, only E₂ but not G1 could inhibit UDP-induced Ca²⁺ influx.
E₂ or G1 inhibited the secretion of two pro-inflammatory cytokines, interleukin (IL)-6 or IL-8, in cells stimulated by different nucleotides or the cationic protein, poly-L-arginie, as quantified by ELISA. CFP-Epac-YPF, an Epac-based polypeptide FRET reporter was used to monitor the real-time cAMP changes in 16HBE14o- cells. Both G1 and E₂ induced an increase in cAMP production. The transepithelial chloride (Cl⁻) secretion was measured using short circuit current technique in cells grown on permeable support. Cl⁻ secretion induced by apical UDP was partially inhibited by G1 in a concentration dependent manner.
Our results provide the first evidence that human bronchial epithelia express GPER, which interact with the P2Y receptor-mediated calcium signalling pathway and cytokine secretion. Moreover, the anti-inflammatory role of GPER may be due to its opposing effect on the pro-inflammatory pathway activated by the P2Y receptors in inflamed airway epithelia.
气道上皮具有调节运输以及参与免疫反应等功能，在呼吸生理学研究中有着十分关键的意义。我们曾经的研究发现P2Y受体在气道上皮中表达并调节上皮细胞离子运输过程。P2Y受体属于嘌呤受体，可被三磷酸尿苷（UTP），二磷酸尿苷（UDP）等核苷酸激活。同时，P2Y受体也是一类G蛋白偶联受体，可通过活化G[subscript q]蛋白调控细胞内钙离子浓度而激活钙依赖性离子通道及其他下游信号通路。此外P2Y受体还参与哮喘炎症的调控。
雌激素（或雌二醇，E₂）是人体一类十分重要的激素。除传统的核受体ERα与ERβ外，一类新型雌激素受体GPER已被发现和鉴定。GPER属于G蛋白偶联受体，可同时参与转录调控和非基因依赖的快速信号调节。尽管具体机理尚不明确，但研究发现GPER可介导抗炎症反应。
实验结果显示，在支气管上皮细胞株16HBE14o-和原代人支气管上皮细胞中GPER都被检测到基因和蛋白水平的表达。GPER在人支气管上皮细胞中的定位也通过免疫荧光染色（immunofluorescence）和亚细胞组分蛋白质印迹（western blot of fractionated cells）得到鉴定。
本研究中，荧光显微技术（fluorescence microscopy）被用于测定核苷酸介导的细胞内钙离子浓度（[Ca²⁺]ᵢ）。在16HBE14o- 和原代培养人支气管上皮细胞中，E₂和GPER特异性激动剂G1都可抑制核苷酸介导的 [Ca²⁺]ᵢ增加，且这种抑制作用呈浓度依赖。GPER特异性拮抗剂G15可抵消G1的抑制作用。进一步研究表明，E₂和G1都可抑制UTP诱导的胞内钙库释放，然而只有E₂抑制UTP诱导的胞外钙离子内流。
除钙离子调节外，E₂和G1还可抑制支气管上皮细胞中核苷酸或聚精氨酸（poly-L-arginine）刺激介导的两种促炎症细胞因子，白介素6（IL-6）和白介素8（IL-8）的分泌。酶联免疫法（ELISA）被用于细胞因子的定量。同时，CFP-Epac-YPF作为一类多肽荧光共振能量转移（FRET）探针被转染入16HBE14o- ，探测细胞内腺苷-3',5'-环化一磷酸（cAMP）的实时变化。结果显示在人支气管上皮细胞中E₂和G1都可引导cAMP生成。此外，我们使用短路电流（short-circuit current, Isc）技术测定单层上皮细胞的氯离子（Cl⁻）分泌，并发现人支气管上皮顶膜面UDP诱导的Cl⁻ 分泌可被G1部分抑制，且抑制效果呈浓度依赖。
本研究首次证明GPER表达于人支气管上皮, 且激活GPER对P2Y受体介导的钙离子信号通路以及细胞因子生成起到抑制作用。这些结果表明在气道炎症反应中，GPER可通过反向调节P2Y受体激活的促炎症作用，达到抗炎症的效果。
Hao, Yuan.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2014.
Includes bibliographical references (leaves 187-211).
Abstracts also in Chinese.
Title from PDF title page (viewed on 03, November, 2016).
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Rago, Vittoria, Diego Sisci i Amalia Carpino. "Identificazione del recettore strogenico GPER (G-protein-couple estrogen receptor) nella ghiandola prostatica umana: valutazione del GPER nei tessuti prostateci benigni e neoplastici". Thesis, 2015. http://hdl.handle.net/10955/1549.
Pełny tekst źródłaGli estrogeni sono coinvolti nella crescita, differenziazione e patogenesi della prostata umana attraverso la mediazione dei classici recettori estrogenici (ER e ER). D'altro canto, il meccanismo non genomico degli estrogeni sembra esercitare un ruolo importante su segnalazioni di percorsi che dirigono o indirettamente modulano l'espressione genica. In questo scenario, il G protein-coupled receptor, GPER (precedentemente chiamato GPR30), è stato implicato nella mediazione rapida degli eventi trascrizionali in risposta agli estrogeni. Alcuni studi supportano l'ipotesi che GPER rappresenta un recettore estrogeno-sensibile e la sua iper-espressione sembra essere fondamentale i diverse patologie neoplasiche. L’espressione di GPER è stata recentemente evidenziata in alcuni tessuti riproduttivi umani, ma la sua espressione a livello prostatico è ancora sconosciuta. In questo studio, abbiamo valutato, l’espressione di GPER in 5 pazienti affetti da patologie prostatiche non neoplastiche, e in 50 pazienti affetti da adenocarcinoma, mediante analisi immunoistochimica e Western blot.. Le aree normali della prostata benigna hanno mostrato una forte immunoreattività del GPER nel citoplasma delle cellule epiteliali basali insieme ad una debole colorazione nel citoplasma delle cellule stromali. Nessuna immunocolorazione è stata invece osservata nelle cellule epiteliali luminali secretorie. L’analisi immunoistochimica ha evidenziato l’espressione cellulare di GPER in tutti i campioni di adenocarcinoma esaminati ma con una variabilità correlata alle diverse architetture delle cellule tumorali (Gleason patterns). Le regioni che presentavano lesioni pre-neoplastiche HGPIN (high-grade prostatic intraepithelial neoplasia) hanno evidenziato una intensa immunoreattività per il recettore, mentre nelle aree tumorali la positività al GPER è stata correlata ai “Gleason patterns” e valutata con il metodo di Allred. Una intensa immunoposititvità al GPER è stata evidenziata nelle aree tumorali Gleason pattern 2 e pattern Gleason 3 (leggermente ridotta in queste ultime), mentre debolmente colorate apparivano le aree con Gleason pattern 4. L’analisi Western blot degli estratti proteici benigni e tumorali ha confermato questo risultato. È stato inoltre osservato un aumento delle forme fosforilate dei livelli di Akt e di CREB nei campioni di pazienti affetti da adenocarcinoma scarsamente differenziato rispetto alle altre categorie. In conclusione, nel presente lavoro, per la prima volta, abbiamo identificato GPER nelle cellule basali epiteliali della prostata umana non neoplastica, con una diversa localizzazione rispetto ai classici recettori estrogenici. Abbiamo inoltre evidenziato l'espressione di GPER nelle cellule di adenocarcinoma prostatico ma con una modulazione della sua intensità dipendente dall’organizzazione delle cellule neoplastiche. La immunoreattività al GPER appare quindi inversamente correlata al grado di differenziazione tumoral
Università della Calabria
Thangavel, Hariprasad, Bartolo Gabriele, Giovanni Sindona i Anna Napoli. "Advanced mass spectrometry-based strategies for the isolation and characterization of G protein-coupled estrogen receptor 1(GPR)". Thesis, 2014. http://hdl.handle.net/10955/1269.
Pełny tekst źródłaEstrogen signaling plays a vital role in breast, ovarian and endometrial cancers. The actions of estrogen are mainly mediated by classical estrogen receptors, ERα and ERβ that belongs to the nuclear receptor superfamily. In recent years, a class of membrane-associated estrogen receptors are found to mimic the functions of classical ERs, including genomic as well as non-genomic signaling. These non-genomic signaling events include pathways that are usually thought of as arising from transmembrane growth factor receptors and G protein-coupled receptors (GPCRs). GPCRs belong to a superfamily of cell surface signaling proteins. GPCRs represent the most significant family of validated pharmacological targets in medical biology. A member of the GPCR family, named GPER, mediates rapid biological responses to estrogen in diverse normal and cancer cells, as well as transformed cell types. The identification and characterization of GPER will lead to understand the mechanisms underlying complex biological pathways and identify potentially new drug targets. Here, we proposed a novel gel-free method to isolate and enrich GPER from crude lysate using home-made hydroxyapatite column (HTP). The HTP eluate was subjected to cellulose acetate (CA) filteration, followed by on-membrane protein digestion with different proteases and analyzed by MALDI MS. GPER was identified by peptide mass fingerprinting (PMF) after intensive data analysis. Sequence analysis reports 3 potential N-glycosylation in GPER. We manually validated 2 out of 3 glycosylation sites in GPER from the obtained MS/MS data and also validated the glycan moieties predicted by Glycomod. This approach is the first of its kind to identify GPER and characterize post-translational modifications (PTMs) by MS-based proteomic analysis. The proposed method is simple, robust and unique with great reproducibility. Finally, we designed and synthesized polymer nanoparticles (NPs) in an effort to capture GPER with high affinity and selectivity from crude lysate. PNIPAm-based NPs were synthesized by a free radical precipitation polymerization method with no control over the functional monomer sequence. The NP binding affinity was evaluated against both truncated-GPER (short peptide epitopes) and GPER (whole protein). As the NPs were designed with complementary functionality against the peptides/protein, the NPspeptide/ protein binding will be through multipoint interactions. The initial qualitative results obtained by immunoblotting analysis revealed interesting hints on GPER’s competitive affinity towards NPs when probed against multiple antibodies. We anticipate to use this strategy as a sample purification step prior to MS-based proteomic analysis
Università della Calabria
Bernardino, Ana Carolina de Matos. "Evaluation of the antioxidant action of the G protein-coupled estrogen receptor". Master's thesis, 2020. http://hdl.handle.net/10400.6/10803.
Pełny tekst źródłaO cérebro caracteriza-se por apresentar um elevado metabolismo, e contém várias substâncias facilmente oxidáveis, tais como aminas e lípidos, o que resulta numa exposição a elevados níveis de stress oxidativo. Foi demonstrado que na doença de Parkinson (DP), o stress oxidativo está correlacionado com a peroxidação lipídica, inflamação, disfunção mitocondrial e agregação da a-synucleína (a-syn). Isto demonstra que o stress oxidativo pode ser um dos desencadeadores da doença de Parkinson, por ser capaz de induzir uma série de mecanismos patogénicos característicos da doença, contribuindo de forma crucial para a sua progressão. Neste sentido, a identificação de mecanismos que ajudem a reduzir o stress oxidativo podem ser estratégias interessantes para o controlo da progressão da doença. Uma vez que o 17ß-estradiol foi classificado como neuroprotetor e já demonstrou efeitos benéficos em diversos mecanismos como neuroinflamação, excitotoxicidade, entre outros, fomos avaliar se a ativação seletiva do recetor de estrogénios acoplado à proteína G (GPER), caracterizado por estar envolvido em ações não genómicas rápidas do 17ßestradiol, pode exercer um efeito neuroprotetor associado à modulação do stress oxidativo na DP. Com este objetivo, desenvolvemos um estudo in vivo com murganhos injetados com 6-OHDA, que foram, posteriormente, submetidos a tratamento subcutâneo ou intranasal com um agonista do recetor, o G1. Assim, avaliámos de que forma a ativação seletiva do recetor pode contribuir para a reversão do stress oxidativo. Para isso, foram efetuados vários testes comportamentais para avaliar a função motora, como o Grip Test, o Rotarod e o Open Field Test, e foram medidos os níveis de mRNA de enzimas antioxidantes, por PCR em tempo real (RT-PCR). A partir dos testes comportamentais, foi possível concluir que a injeção da toxina não afetou o comportamento motor uma vez que os resultados obtidos no Rotarod, e distância total percorrida obtida no Open Field Test não mostraram diferenças significativas. Por outro lado, foi possível observar que a injeção com 6-OHDA aumentou os parâmetros relacionados com o comportamento ansioso. Desta forma, é possível concluir que a toxina não exerceu efeito ao nível do comportamento motor, porém, induziu alterações a nível não-motor. Relativamente à expressão das enzimas antioxidantes, observou-se um aumento, ainda que sem significância estatística, dos níveis de mRNA da Gpx4 e do Nrf2 em animais injetados com 6-OHDA. Este aumento, pode querer evidenciar um mecanismo de proteção desencadeado por estas enzimas para lidar com o stress oxidativo. No entanto, mais estudos seriam necessários para conseguir comprovar esta hipótese. Os nossos resultados evidenciaram efeitos exercidos pelo G1, quando entregue pelos dois tipos de administração. No entanto, não foi possível concluir se os dois tipos de entrega do G1 têm um efeito antioxidante na presença de um insulto dopaminérgico. Neste sentido, mais estudos seriam necessários para perceber se a ativação do GPER é capaz de modular o stress oxidativo e, se este efeito está relacionado com os seus efeitos neuroprotetores atualmente reconhecidos.
Albanito, Lidia, Marcello Maggiolini i Benedictis Giovanna De. "The G protein-coupled receptor GPR30 mediates estrogen signaling in cancer cells". Thesis, 2013. http://hdl.handle.net/10955/349.
Pełny tekst źródłaCzęści książek na temat "G-Protein Coupled Estrogen Receptor (GPER)"
Sharma, Geetanjali, i Eric R. Prossnitz. "G-Protein-Coupled Estrogen Receptor (GPER) and Sex-Specific Metabolic Homeostasis". W Sex and Gender Factors Affecting Metabolic Homeostasis, Diabetes and Obesity, 427–53. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70178-3_20.
Pełny tekst źródłaThekkumkara, Thomas, Russell Snyder i Vardan T. Karamyan. "Competitive Binding Assay for the G-Protein-Coupled Receptor 30 (GPR30) or G-Protein-Coupled Estrogen Receptor (GPER)". W Methods in Molecular Biology, 11–17. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3127-9_2.
Pełny tekst źródłaArnatt, Christopher K., i Yan Zhang*. "Chapter 7. A Nuclear G Protein-coupled Estrogen Receptor, GPER. Homology Modeling Studies Toward Its Ligand-binding Mode Characterization". W Drug Discovery, 117–37. Cambridge: Royal Society of Chemistry, 2012. http://dx.doi.org/10.1039/9781849735353-00117.
Pełny tekst źródłaFilardo, Edward J., Jeffrey A. Quinn i C. Thomas Graeber. "Evidence Supporting a Role for Gpr30, an Orphan Member of the G-Protein-Coupled Receptor Superfamily, in Rapid Estrogen Signaling". W The Identities of Membrane Steroid Receptors, 139–46. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0339-2_17.
Pełny tekst źródłaZhang, Hong-Bing, Yao Wang i Bing Wang. "The Research Advances in G-Protein-Coupled Estrogen Receptor". W Estrogens - Recent Advances [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105822.
Pełny tekst źródłaTorres-Reveron, Annelyn, Wayne G. Brake i Teresa A. Milner. "Estrogen Receptor Distribution in the Hippocampus and Prefrontal Cortex". W Estrogens and Memory, 11–23. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190645908.003.0002.
Pełny tekst źródłaShi, Haifei, Shiva Priya Dharshan Senthil Kumar i Xian Liu. "G Protein-Coupled Estrogen Receptor in Energy Homeostasis and Obesity Pathogenesis". W Progress in Molecular Biology and Translational Science, 193–250. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-386933-3.00006-6.
Pełny tekst źródłaSrivastava, Deepak P., Katherine J. Sellers i Peter D. Evans. "Rapid Modulation of Spinogenesis by Estradiol in the Neocortex". W Estrogens and Memory, 48–68. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190645908.003.0005.
Pełny tekst źródłaLi, XY, Y. Lu, HY Sun, MY Liu, J. Yang i G. Ning. "G Protein Coupled Receptor 48 Up-Regulates Estrogen Receptor Alpha Expression Via cAMP/PKA Signaling in Male Reproductive Tract." W The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–321—P1–321. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p7.p1-321.
Pełny tekst źródłaStreszczenia konferencji na temat "G-Protein Coupled Estrogen Receptor (GPER)"
Jala, Venkatakrishna R., Haribabu Bodduluri, Brandie Radde i Carolyn M. Klinge. "Abstract 4548: The role of GPR30/G-protein coupled estrogen receptor (GPER) in lung cancer development". W 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.am2011-4548.
Pełny tekst źródłaCastillo, Maryann, Angelique M. Wimbley, Jacob J. Mayfield, Jenifer C. Lascano i Kevin D. Houston. "Abstract 1305: Activation of G-protein coupled estrogen receptor (GPER) inhibits ELT-3 uterine leiomyoma cell proliferation." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1305.
Pełny tekst źródłaLv, Xiangmin, Guohua Hua, Chunbo He, John S. Davis i Cheng Wang. "Abstract B82: G-protein coupled estrogen receptor (GPER) agonist G-1 inhibits growth of human granulosa cell tumor cells via blocking microtubule assembly". W Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research: From Concept to Clinic; September 18-21, 2013; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1078-0432.ovca13-b82.
Pełny tekst źródłaWang, Cheng, Chao Jiang, Xiangmin Lv, Lan Fu i John S. Davis. "Abstract 3920: Off-target effects of the putative G-protein coupled estrogen receptor 1 (GPER) agonist G1 in ovarian and breast cancer cells". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3920.
Pełny tekst źródłaNatale, Chris, Tina Garyantes i Todd Ridky. "Abstract 1225: LNS8801: A novel, enantiomerically pure, small molecule agonist of the G protein-coupled estrogen receptor (GPER) for the treatment of cancer". W 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.am2021-1225.
Pełny tekst źródłaMeng, Ran, Ying Xiong, Yuan Zhao, Yan Wang, Tao Tao, Qiqi Wang, Hua Liu i in. "Abstract 1149: Interaction with NHERF1 enhances protein stability of G protein-coupled estrogen receptor". W 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.am2016-1149.
Pełny tekst źródłaNatale, Christopher, Jinyang Li, Tzvete Dentchev, Brian Capell, John Seykora, Ben Stanger i Todd Ridky. "Abstract B21: Pharmacologic activation of G protein-coupled estrogen receptor inhibits pancreatic ductal adenocarcinoma". W Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-b21.
Pełny tekst źródłaGohar, Eman, Ravneet Singh, Rawan Almutlaq i Victoria Nasci. "G Protein-coupled Estrogen Receptor 1 and Pregnancy Confer Protection against Hypertension in Aged Female Mice". W ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.140420.
Pełny tekst źródłaDeming-Halverson, Sandra L., Carl Graeber, Jason Machan, Edmond Sabo, Wei Zheng i Edward J. Filardo. "Abstract 2272: Association of G-protein estrogen receptor (GPER) in primary breast cancer in Caucasian and Black women by tumor immunophenotype and menopausal status". W 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.am2016-2272.
Pełny tekst źródłaLeeb-Lundberg, FLM, M. Sjöström, S. Broselid, K. Jirström, M. Belting, B. Olde, K. Lövgren i in. "P4-09-02: G Protein-Coupled Estrogen Receptor 1 Positively Correlates with Estrogen Receptor a Expression and Increased Distant Disease-Free Survival of Breast Cancer Patients." W Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p4-09-02.
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