Molecular endocrinology最新文献

Editorial: Reflections on the Impact of Molecular Endocrinology on a Scientific Career. 社论:反思分子内分泌学对科学事业的影响。

Molecular endocrinology Pub Date : 2016-10-03 DOI: 10.1210/me.2016-1127

D. DeFranco

引用次数: 0

Editorial: Final Musings on the Impact of Molecular Endocrinology. 社论:对分子内分泌学影响的最终思考。

Molecular endocrinology Pub Date : 2016-10-03 DOI: 10.1210/me.2016-1129

S. Hammes

引用次数: 0

Bidding a Fond Farwell to Molecular Endocrinology. 告别分子内分泌学。

Molecular endocrinology Pub Date : 2016-10-03 DOI: 10.1210/ME.2016-1130

J. Nilson

引用次数: 0

Reflections on the Merger of Molecular Endocrinology and Endocrinology. 关于分子内分泌学与内分泌学合并的思考。

Molecular endocrinology Pub Date : 2016-10-03 DOI: 10.1210/me.2016-1128

E. B. Thompson

引用次数: 0

Editorial Reflections on the Demise of Molecular Endocrinology and the Future of Molecular Hormone Action Research. 编辑反思分子内分泌学的消亡和分子激素作用研究的未来。

Molecular endocrinology Pub Date : 2016-10-03 DOI: 10.1210/ME.2016-1131

A. Means

引用次数: 0

Origins of the Field of Molecular Endocrinology: A Personal Perspective. 分子内分泌学领域的起源:个人视角。

Molecular endocrinology Pub Date : 2016-10-03 DOI: 10.1210/ME.2016-1132

B. O’Malley

引用次数: 7

ERα-XPO1 Cross Talk Controls Tamoxifen Sensitivity in Tumors by Altering ERK5 Cellular Localization. ERα-XPO1 交叉对话通过改变 ERK5 细胞定位控制肿瘤对他莫昔芬的敏感性

Molecular endocrinology Pub Date : 2016-10-01 Epub Date: 2016-08-17 DOI: 10.1210/me.2016-1101

Kinga Wrobel, Yiru Chen Zhao, Eylem Kulkoyluoglu, Karen Lee Ann Chen, Kadriye Hieronymi, Jamie Holloway, Sarah Li, Tania Ray, Partha Sarathi Ray, Yosef Landesman, Alexander Edward Lipka, Rebecca Lee Smith, Zeynep Madak-Erdogan

{"title":"ERα-XPO1 Cross Talk Controls Tamoxifen Sensitivity in Tumors by Altering ERK5 Cellular Localization.","authors":"Kinga Wrobel, Yiru Chen Zhao, Eylem Kulkoyluoglu, Karen Lee Ann Chen, Kadriye Hieronymi, Jamie Holloway, Sarah Li, Tania Ray, Partha Sarathi Ray, Yosef Landesman, Alexander Edward Lipka, Rebecca Lee Smith, Zeynep Madak-Erdogan","doi":"10.1210/me.2016-1101","DOIUrl":"10.1210/me.2016-1101","url":null,"abstract":"Most breast cancer deaths occur in women with recurrent, estrogen receptor (ER)-α(+), metastatic tumors. There is a critical need for therapeutic approaches that include novel, targetable mechanism-based strategies by which ERα (+) tumors can be resensitized to endocrine therapies. The objective of this study was to validate a group of nuclear transport genes as potential biomarkers to predict the risk of endocrine therapy failure and to evaluate the inhibition of XPO1, one of these genes as a novel means to enhance the effectiveness of endocrine therapies. Using advanced statistical methods, we found that expression levels of several of nuclear transport genes including XPO1 were associated with poor survival and predicted recurrence of tamoxifen-treated breast tumors in human breast cancer gene expression data sets. In mechanistic studies we showed that the expression of XPO1 determined the cellular localization of the key signaling proteins and the response to tamoxifen. We demonstrated that combined targeting of XPO1 and ERα in several tamoxifen-resistant cell lines and tumor xenografts with the XPO1 inhibitor, Selinexor, and tamoxifen restored tamoxifen sensitivity and prevented recurrence in vivo. The nuclear transport pathways have not previously been implicated in the development of endocrine resistance, and given the need for better strategies for selecting patients to receive endocrine modulatory reagents and improving therapy response of relapsed ERα(+) tumors, our findings show great promise for uncovering the role these pathways play in reducing cancer recurrences.","PeriodicalId":18812,"journal":{"name":"Molecular endocrinology","volume":"30 10","pages":"1029-1045"},"PeriodicalIF":0.0,"publicationDate":"2016-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1210/me.2016-1101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34314496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 14

The Estrogen Receptor α-Cistrome Beyond Breast Cancer. 乳腺癌外的雌激素受体α-胞质。

Molecular endocrinology Pub Date : 2016-10-01 Epub Date: 2016-08-04 DOI: 10.1210/me.2016-1062

Marjolein Droog, Mark Mensink, Wilbert Zwart

{"title":"The Estrogen Receptor α-Cistrome Beyond Breast Cancer.","authors":"Marjolein Droog, Mark Mensink, Wilbert Zwart","doi":"10.1210/me.2016-1062","DOIUrl":"https://doi.org/10.1210/me.2016-1062","url":null,"abstract":"Although many tissues express estrogen receptor (ER)α, most studies focus on breast cancer where ERα occupies just a small fraction of its total repertoire of potential DNA-binding sites, based on sequence. This raises the question: Can ERα occupy these other potential binding sites in a different context? Ligands, splice variants, posttranslational modifications, and acquired mutations of ERα affect its conformation, which may alter chromatin interactions. To date, literature describes the DNA-binding sites of ERα (the ERα cistrome) in breast, endometrium, liver, and bone, in which the receptor mainly binds to enhancers. Chromosomal boundaries provide distinct areas for dynamic gene regulation between tissues, where the usage of enhancers deviates. Interactions of ERα with enhancers and its transcriptional complex depend on the proteome, which differs per cell type. This review discusses the biological variables that influence ERα cistromics, using reports from human specimens, cell lines, and mouse tissues, to assess whether ERα genomics in breast cancer can be translated to other tissue types.","PeriodicalId":18812,"journal":{"name":"Molecular endocrinology","volume":"30 10","pages":"1046-1058"},"PeriodicalIF":0.0,"publicationDate":"2016-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1210/me.2016-1062","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34729760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 19

Phosphorylation of Farnesoid X Receptor at Serine 154 Links Ligand Activation With Degradation. 淀粉样蛋白X受体丝氨酸154位点的磷酸化与配体激活和降解相关。

Molecular endocrinology Pub Date : 2016-10-01 Epub Date: 2016-08-29 DOI: 10.1210/me.2016-1105

Takuyu Hashiguchi, Shingo Arakawa, Shogo Takahashi, Frank J Gonzalez, Tatsuya Sueyoshi, Masahiko Negishi

引用次数: 22

Elevated Basal Insulin Secretion in Type 2 Diabetes Caused by Reduced Plasma Membrane Cholesterol. 质膜胆固醇降低导致2型糖尿病基础胰岛素分泌升高。

Molecular endocrinology Pub Date : 2016-10-01 Epub Date: 2016-08-17 DOI: 10.1210/me.2016-1023

Vini Nagaraj, Abdulla S Kazim, Johan Helgeson, Clemens Lewold, Satadal Barik, Pawel Buda, Thomas M Reinbothe, Stefan Wennmalm, Enming Zhang, Erik Renström

{"title":"Elevated Basal Insulin Secretion in Type 2 Diabetes Caused by Reduced Plasma Membrane Cholesterol.","authors":"Vini Nagaraj, Abdulla S Kazim, Johan Helgeson, Clemens Lewold, Satadal Barik, Pawel Buda, Thomas M Reinbothe, Stefan Wennmalm, Enming Zhang, Erik Renström","doi":"10.1210/me.2016-1023","DOIUrl":"https://doi.org/10.1210/me.2016-1023","url":null,"abstract":"Elevated basal insulin secretion under fasting conditions together with insufficient stimulated insulin release is an important hallmark of type 2 diabetes, but the mechanisms controlling basal insulin secretion remain unclear. Membrane rafts exist in pancreatic islet cells and spatially organize membrane ion channels and proteins controlling exocytosis, which may contribute to the regulation of insulin secretion. Membrane rafts (cholesterol and sphingolipid containing microdomains) were dramatically reduced in human type 2 diabetic and diabetic Goto-Kakizaki (GK) rat islets when compared with healthy islets. Oxidation of membrane cholesterol markedly reduced microdomain staining intensity in healthy human islets, but was without effect in type 2 diabetic islets. Intriguingly, oxidation of cholesterol affected glucose-stimulated insulin secretion only modestly, whereas basal insulin release was elevated. This was accompanied by increased intracellular Ca2+ spike frequency and Ca2+ influx and explained by enhanced single Ca2+ channel activity. These results suggest that the reduced presence of membrane rafts could contribute to the elevated basal insulin secretion seen in type 2 diabetes.","PeriodicalId":18812,"journal":{"name":"Molecular endocrinology","volume":"30 10","pages":"1059-1069"},"PeriodicalIF":0.0,"publicationDate":"2016-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1210/me.2016-1023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34376519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 18