Добірка наукової літератури з теми "SGTA; androgen receptor; ovary"
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Статті в журналах з теми "SGTA; androgen receptor; ovary"
Trotta, Andrew P., Eleanor F. Need, Lisa M. Butler, Luke A. Selth, Melissa A. O'Loughlin, Gerhard A. Coetzee, Wayne D. Tilley, and Grant Buchanan. "Subdomain structure of the co-chaperone SGTA and activity of its androgen receptor client." Journal of Molecular Endocrinology 49, no. 2 (June 12, 2012): 57–68. http://dx.doi.org/10.1530/jme-11-0152.
Повний текст джерелаTetsuka, M., P. F. Whitelaw, W. J. Bremner, M. R. Millar, C. D. Smyth, and S. G. Hillier. "Developmental regulation of androgen receptor in rat ovary." Journal of Endocrinology 145, no. 3 (June 1995): 535–43. http://dx.doi.org/10.1677/joe.0.1450535.
Повний текст джерелаLin, Lawrence H., Maria C. P. Baracat, Gustavo A. R. Maciel, José M. Soares, and Edmund C. Baracat. "Androgen receptor gene polymorphism and polycystic ovary syndrome." International Journal of Gynecology & Obstetrics 120, no. 2 (November 24, 2012): 115–18. http://dx.doi.org/10.1016/j.ijgo.2012.08.016.
Повний текст джерелаHampton, J. H., M. Manikkam, D. B. Lubahn, M. F. Smith, and H. A. Garverick. "Androgen receptor mRNA expression in the bovine ovary." Domestic Animal Endocrinology 27, no. 1 (July 2004): 81–88. http://dx.doi.org/10.1016/j.domaniend.2004.01.005.
Повний текст джерелаSalinas, Irving, Niharika Sinha, and Aritro Sen. "Androgen-induced epigenetic modulations in the ovary." Journal of Endocrinology 249, no. 3 (June 2021): R53—R64. http://dx.doi.org/10.1530/joe-20-0578.
Повний текст джерелаAbbott, David H. "Neuronal androgen receptor: Molecular gateway to polycystic ovary syndrome?" Proceedings of the National Academy of Sciences 114, no. 16 (April 4, 2017): 4045–47. http://dx.doi.org/10.1073/pnas.1703436114.
Повний текст джерелаWalters, Kirsty A. "Polycystic ovary syndrome: Is it androgen or estrogen receptor?" Current Opinion in Endocrine and Metabolic Research 12 (June 2020): 1–7. http://dx.doi.org/10.1016/j.coemr.2020.01.003.
Повний текст джерелаDuffy, Diane M., Salah E. Abdelgadir, Kenneth R. Stott, John A. Resko, Richard L. Stouffer, and Mary B. Zelinski-Wooten. "Androgen Receptor mRNA Expression in the Rhesus Monkey Ovary." Endocrine 11, no. 1 (1999): 23–30. http://dx.doi.org/10.1385/endo:11:1:23.
Повний текст джерелаHirai, Mitsuo, Shuji Hirata, Takaaki Osada, Kazuki Hagihara, and Junzo Kato. "Androgen receptor mRNA in the rat ovary and uterus." Journal of Steroid Biochemistry and Molecular Biology 49, no. 1 (May 1994): 1–7. http://dx.doi.org/10.1016/0960-0760(94)90294-1.
Повний текст джерелаWang, Fangfang, Jiexue Pan, Ye Liu, Qing Meng, Pingping Lv, Fan Qu, Guo-Lian Ding, et al. "Alternative splicing of the androgen receptor in polycystic ovary syndrome." Proceedings of the National Academy of Sciences 112, no. 15 (March 30, 2015): 4743–48. http://dx.doi.org/10.1073/pnas.1418216112.
Повний текст джерелаДисертації з теми "SGTA; androgen receptor; ovary"
Martínez, Pinto Jonathan Eloy. "Neonatal exposure to estradiol reprograms the expression of androgen receptor and anti-müllerian hormone [recurso electrónico]: short and long term effects and their relation to the polycystic ovary phenotype." Tesis, Universidad de Chile, 2014. http://www.repositorio.uchile.cl/handle/2250/116937.
Повний текст джерелаReproduction is regulated through the integration of information that comes from the hypothalamus, hypophysis, and the ovary. There are critical hormone sensitive periods during development during which they are especially vulnerable to exposure to abnormal hormonal levels resulting from metabolic problems or environmental sources. These exposures may permanently alter the differentiation and function of reproductive organs. Several studies performed in humans and animal models have suggested that polycystic ovary syndrome (PCOS) originates during early development due to exposure to abnormal steroidal hormone levels. Supporting this, our group recently reported that the administration of a single dose of estradiol valerate (EV) to newborn rats can irreversibly program the polycystic ovary condition during adulthood. However, there is no information about how this neonatal exposure to a single dose of EV can determine the functional and structural changes seen in the adult ovary. The aim of this research was to determine if there are genes—primarily those most reported to be related to PCOS in humans—with permanently altered expression and if these expression patterns are due to modifications in the methylation pattern in their DNA sequence. A single dose (10 mg/kg) of EV was administered to neonatal rats, and PCR array and real-time PCR analyses were conducted to examine the subsequent gene expression patterns of growth factors, nuclear receptors, and coregulators. Twenty-four hours after the exposure, the EV-exposed rat ovaries expressed more androgen receptor (Ar) than did the control ovaries; in the 60-day old rats, the Ar mRNA levels decreased 6.4-fold relative to the controls. The interstitial tissue and antral follicles from the adult EV-treated rats expressed more Ar than did the control preantral follicles, suggesting a failure of the control mechanism for Ar expression in antral follicles. Using the mass-array technique, the methylation patterns of different transcription factor binding sites were found to be associated with the Ar gene. NBRE, the response element of nerve growth factor-induced B (Ngfi-b), was hypomethylated in the Ar gene from the EV-treated ovaries. There was also an increase in anti-Müllerian hormone (AMH) expression in adult ovaries (mRNA and protein) that was induced by the neonatal exposure to estradiol. The EV-treated rat ovaries had a higher level of AMH immunoreactivity in the antral follicles than did the controls; however, no significant differences were seen between the preantral follicles of the treated and control groups. The methylation pattern of the Amh gene from the ovaries of EV-treated adult rats showed differential methylation in the CpGs related to the estradiol response element (ERE) in the Amh gene. The neonatal ovary samples had hypermethylated CpGs in comparison to the 30- and 60-day old rats; the samples (granulosa cells) from the 60-day old rats had more methylation of the CpGs than did those from the 30-day old rats; thus, the methylation pattern depended on the stage of development. When we compared the EV-exposed and control rats, we found more methylation of the CpGs in the samples from the 60-day old EV-exposed rats than in those from the controls; there were no differences between the groups for the 2- and 30-day old rats. This work demonstrated that the neonatal exposure to estradiol induces an overexpression of AMH and AR in the rat ovary. The mechanism by which these changes are induced may involve an increase in the methylation of the ERE associated with the Amh gene, suggesting that the change in methylation allows ESR1 to induce Amh expression. The hypomethylation of NBRE associated with the AR gene suggests that AR expression may be induced in response to nerve growth factor or luteinizing hormone. These epigenetic modifications found in the current rat model provide a new framework for understanding the genesis of the polycystic ovary and its maintenance in humans, allowing more focus on the effects due to estrogen exposure
Die Fortpflanzung in Säugetieren wird durch Signale aus dem Hypothalamus, der Hypophyse und der Gebärmutter gesteuert. Während der Anlage der Gebärmutter in der Embryonalentwicklung gibt es ein kritisches Zeitfenster bei dem die Entwicklung durch veränderte Hormonspiegel oder andere äußere Einflüsse gestört werden kann. Dabei kann es zur permanenten Schädigung der reproduktiven Organe kommen. Studien am Menschen und in Tiermodellen legen nahe, dass das sogenannte Polyzystische Ovarialsyndrom durch erhöhte Steroidhormonspiegel verursacht wird. So konnte unsere Arbeitsgruppe kürzlich zeigen, dass bei neugeborenen Ratten die Gabe einer einzigen Dosis Estradiolvalerat (EV) ausreicht um ein Polyzystisches Ovarialsyndrom in den erwachsenen Tieren zu erzeugen. Die zugrundeliegenden Mechanismen sind allerdings bis heute nicht bekannt. Ziel dieser Arbeit war es zu untersuchen, ob die Expression bestimmter Gene in erwachsenen Ratten durch die Estradiolvaleratgabe im neonatalen Stadium permanent verändert wird und ob die veränderte Genexpression mit epigenetischen Veränderungen auf der Ebene der DNA Methylierung einhergeht. Hierzu wurden neugeborene Ratten mit einer einzigen Dosis EV (10 mg/Kg) behandelt um anschließend die Genexpression von Wachstumsfaktoren, nukleären Hormonrezeptoren und ihre Kofaktoren mittels PCR Arrays und quantitativer RT-PCR zu untersuchen. Wir konnten zeigen, dass die Ovarien von EV-behandelten Ratten das Androgenrezeptorgen (Ar) nach 24h stärker exprimierten als die Kontrollen. Nach 60 Tagen ging die ovariale Ar Expression allerdings um das 4-6-fache gegenüber unbehandelten Tieren zurück. Histologisch war die Ar Expression in antralen Follikeln und im Interstitium vom EV-behandelten adulten Tieren stärker als in preantralen Follikeln, was auf eine Störung von Regulationsmechanismen in antralen Follikeln hindeutet. Mittels MassArray-Technologie konnte außerdem gezeigt werden, dass die veränderte Ar Expression in EV-behandelten Tieren mit der verringerten DNA Methylierung einer potentiellen Transkriptionsfaktorbindestelle (NBRE: nerve growth factor-induced B response element) korreliert. Daneben war die Expression des Anti-Müller-Hormons (AMH) in Ovarien von EV-behandelten adulten Tieren sowohl auf mRNA als auch auf Proteinebene erhöht. Immunhistologisch zeigten insbesondere die antralen Follikeln von EV-behandelten adulten Tieren (nicht aber Interstitium und preantrale Follikeln) eine stärkere Färbung für AMH. Auch im Amh Gen konnten entwicklungs- und behandlungsabhängige Veränderungen der DNA Methylierung gemessen werden. Eine Bindungsstelle für den Estrogenrezeptor (ERE: estradiol response element) im Amh Gen zeigte Methylierungsunterschiede in Ovarien von adulten EV-behandelten Ratten. In normalen Tieren war der Methylierungsstatus dieser Region abhängig vom Entwicklungsstadium: im Vergleich zu 30 und 60 Tage alten Ratten war das Element in neugeborenen Ratten hypermethyliert und in Granulosazellpräperaten von 30 Tage alten Ratten weniger methyliert als in Präparaten von 60 Tage alten Tieren. Im Vergleich mit EV-behandelten Tieren zeigten Proben von 60 Tage alten Tieren eine signifikant erhöhte DNA Methylierung, während EV-behandelte neugeborene und 30 Tage alte Tiere sich nicht signifikant von den Kontrollen unterschieden. In dieser Arbeit konnte also gezeigt werden, dass bei Ratten die Gabe von Estradiol im neonatalen Stadium zu einer ovarialen Überproduktion von AMH und AR führt. Die Mechanismen die zu diesen Veränderungen führen könnten mit dem Verlust der DNA Methylierung im ERE des Amh Gens zusammenhängen, was vermutlich zu einer erhöhten ESR1-Bindung und AMH Expression führt. Die Hypomethylierung des NBRE im Ar Gen deutet darauf hin, dass hier NGF (nerve growth factor) oder LH (luteinisierende Hormon) an der veränderten Regulation beteiligt sind. Die im Rattenmodel gefundenen epigenetischen Veränderungen bieten neue Anhaltspunkte um die Entstehung und die Persistenz des Polyzystische Ovarialsyndroms im Menschen besser zu verstehen und zukünftige Forschung wird sich noch gründlicher mit den Effekten der Estrogenexposition auseinandersetzen müssen
Conicyt Mecesup Fondecyt
Braun, Alyssa Maria. "The effects of androgens on steroidogenesis in the ovary of Atlantic croaker (Micropogonias undulatus) mechanism of action, the biochemical characterization of a membrane androgen receptor, and the chronic effects of exposure to an environmental antiandrogen /." Access restricted to users with UT Austin EID Full text (PDF) from UMI/Dissertation Abstracts International, 2002. http://wwwlib.umi.com/cr/utexas/fullcit?p3077433.
Повний текст джерелаBraun, Alyssa Maria. "The effects of androgens on steroidogensis in the ovary of Atlantic croaker (Micropogonias undulatus) : mechanism of action, the biochemical characterization of a membrane androgen receptor, and the chronic effects of exposure to an environmental antiandrogen /." Full text (PDF) from UMI/Dissertation Abstracts International, 2002. http://wwwlib.umi.com/cr/utexas/fullcit?p3077433.
Повний текст джерелаMartínez, Pinto Jonathan Eloy [Verfasser], Hernan [Akademischer Betreuer] Lara, and Michael [Akademischer Betreuer] Rehli. "“Neonatal exposure to estradiol reprograms the expression of androgen receptor and anti-Müllerian hormone: short and long term effects and their relation to the polycystic ovary phenotype” / Jonathan Eloy Martínez Pinto. Betreuer: Hernan Lara ; Michael Rehli." Regensburg : Universitätsbibliothek Regensburg, 2016. http://d-nb.info/1083250930/34.
Повний текст джерелаButler, Miriam Simone. "The role of small glutamine-rich tetratricopeptide repeat containing protein alpha in female reproductive tissues." Thesis, 2012. http://hdl.handle.net/2440/80189.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Medicine, 2012
Hickey, Theresa E. "Androgen receptor mediated activity in the ovary : implications for Polycystic Ovary Syndrome." 2006. http://hdl.handle.net/2440/37839.
Повний текст джерелаThesis (Ph.D.)--School of Paediatrics and Reproductive Health, 2006.
Hickey, Theresa E. "Androgen receptor mediated activity in the ovary : implications for Polycystic Ovary Syndrome." Thesis, 2006. http://hdl.handle.net/2440/37839.
Повний текст джерелаThesis (Ph.D.)--School of Paediatrics and Reproductive Health, 2006.
Zhang, Chenan. "Testosterone acts at the cell surface to induce granulosa/theca cell death via an apoptotic pathway in Atlantic croaker (Micropogonias undulatus)." Thesis, 2011. http://hdl.handle.net/2152/23902.
Повний текст джерелаtext
Braun, Alyssa Maria 1974. "The effects of androgens on steroidogenesis in the ovary of Atlantic croaker (Micropogonias undulatus) : mechanism of action, the biochemical characterization of a membrane androgen receptor, and the chronic effects of exposure to an environmental antiandrogen." 2002. http://hdl.handle.net/2152/10926.
Повний текст джерелаЧастини книг з теми "SGTA; androgen receptor; ovary"
L. Yanes Cardozo, Licy, Alexandra M. Huffman, Jacob E. Pruett, and Damian G. Romero. "Androgens and Cardiovascular Risk Factors in Polycystic Ovary Syndrome." In Reproductive Hormones. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96005.
Повний текст джерелаSacerdote, Alan. "Rare and Underappreciated Causes of Polycystic Ovarian Syndrome." In Polycystic Ovary Syndrome [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101946.
Повний текст джерелаButler, Gary, and Jeremy Kirk. "Differences of sex development (DSD)." In Paediatric Endocrinology and Diabetes, 335–50. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198786337.003.0011.
Повний текст джерелаТези доповідей конференцій з теми "SGTA; androgen receptor; ovary"
Trotta, Andrew P., Eleanor F. Need, Melissa O'Loughlin, Grant Buchanan, and Wayne D. Tilley. "Abstract 1704: The co-chaperone, SGTA, acts as a regulator of androgen receptor activity in prostate cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1704.
Повний текст джерела