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51دورية أكاديمية
المصدر: Proceedings of the National Academy of Sciences of the United States of America, 1981 Oct 01. 78(10), 6251-6255.
الوصول الحر: https://www.jstor.org/stable/11045Test
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52دورية أكاديمية
المؤلفون: Yang, Tracy C., Stampfer, Martha R., Smith, Helene S.
المصدر: Radiation Research, 1983 Dec 01. 96(3), 476-485.
الوصول الحر: https://www.jstor.org/stable/3576114Test
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53دورية أكاديمية
المساهمون: States, J.Christopher
المصدر: PLoS ONE ; volume 8, issue 1, page e54398 ; ISSN 1932-6203
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54دورية أكاديمية
المؤلفون: Overhoff, Marita G., Garbe, James C., Koh, James, Stampfer, Martha R., Beach, David H., Bishop, Cleo L.
المصدر: Nucleic Acids Research ; volume 42, issue 3, page 1606-1618 ; ISSN 1362-4962 0305-1048
مصطلحات موضوعية: Genetics
الإتاحة: https://doi.org/10.1093/nar/gkt1096Test
http://academic.oup.com/nar/article-pdf/42/3/1606/17065665/gkt1096.pdfTest -
55دورية أكاديمية
المؤلفون: Stovall, Daniel B., Wan, Meimei, Miller, Lance D., Cao, Paul, Maglic, Dejan, Zhang, Qiang, Stampfer, Martha R., Liu, Wennuan, Xu, Jianfeng, Sui, Guangchao
المصدر: The American Journal of Pathology ; volume 183, issue 5, page 1645-1653 ; ISSN 0002-9440
مصطلحات موضوعية: Pathology and Forensic Medicine
الإتاحة: https://doi.org/10.1016/j.ajpath.2013.07.025Test
https://api.elsevier.com/content/article/PII:S0002944013005464?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0002944013005464?httpAccept=text/plainTest -
56دورية أكاديمية
المؤلفون: Novak, Petr, Stampfer, Martha R., Munoz-Rodriguez, Jose L., Garbe, James C., Ehrich, Mathias, Futscher, Bernard W., Jensen, Taylor J.
المساهمون: Coleman, William B.
المصدر: PLoS ONE ; volume 7, issue 12, page e52299 ; ISSN 1932-6203
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57
المؤلفون: Lujan, Celia, Tyler, Eleanor J., Webster, Amy P., Stead, Eleanor R., Miguel, Victoria E. Martinez, Ecker, Simone, Milligan, Deborah, Garbe, James C., Stampfer, Martha R., Beck, Stephan, Lowe, Robert, Bishop, Cleo L., Bjedov, Ivana
الوصف: We aim to improve anti-ageing drug discovery, currently achieved through laborious and lengthy longevity analysis. Recent studies demonstrated that the most accurate molecular method to measure human age is based on CpG methylation profiles, as exemplified by several epigenetics clocks that can accurately predict an individual’s age. Here, we developed CellAge, a new epigenetic clock that measures subtle ageing changes in primary human cells in vitro . As such, it provides a unique tool to measure the effects of relatively short pharmacological treatments on ageing. We validated our CellAge clock against known longevity drugs such as rapamycin and trametinib. Moreover, we uncovered novel anti-ageing drugs, torin2 and Dactolisib (BEZ-235), demonstrating the value of our approach as a screening and discovery platform for anti-ageing strategies. CellAge outperforms other epigenetic clocks in measuring subtle ageing changes in primary human cells in culture. The tested drug treatments reduced senescence and other ageing markers, further consolidating our approach as a screening platform. Finally, we showed that the novel anti-ageing drugs we uncovered in vitro , indeed increased longevity in vivo . Our method expands the scope of CpG methylation profiling from measuring human chronological and biological age from human samples in years, to accurately and rapidly detecting anti-ageing potential of drugs using human cells in vitro , providing a novel accelerated discovery platform to test sought after geroprotectors.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=sharebioRxiv::d7941dd970668fd3377b37abbc292e99Test
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58دورية أكاديمية
مصطلحات موضوعية: RESEARCH
الوصف: Epigenetic mechanisms are important regulators of cell type–specific genes, including miRNAs. In order to identify cell type–specific miRNAs regulated by epigenetic mechanisms, we undertook a global analysis of miRNA expression and epigenetic states in three isogenic pairs of human mammary epithelial cells (HMEC) and human mammary fibroblasts (HMF), which represent two differentiated cell types typically present within a given organ, each with a distinct phenotype and a distinct epigenotype. While miRNA expression and epigenetic states showed strong interindividual concordance within a given cell type, almost 10% of the expressed miRNA showed a cell type–specific pattern of expression that was linked to the epigenetic state of their promoter. The tissue-specific miRNA genes were epigenetically repressed in nonexpressing cells by DNA methylation (38%) and H3K27me3 (58%), with only a small set of miRNAs (21%) showing a dual epigenetic repression where both DNA methylation and H3K27me3 were present at their promoters, such as MIR10A and MIR10B . Individual miRNA clusters of closely related miRNA gene families can each display cell type–specific repression by the same or complementary epigenetic mechanisms, such as the MIR200 family, and MIR205 , where fibroblasts repress MIR200C/141 by DNA methylation, MIR200A/200B/429 by H3K27me3, and MIR205 by both DNA methylation and H3K27me3. Since deregulation of many of the epigenetically regulated miRNAs that we identified have been linked to disease processes such as cancer, it is predicted that compromise of the epigenetic control mechanisms is important for this process. Overall, these results highlight the importance of epigenetic regulation in the control of normal cell type–specific miRNA expression.
وصف الملف: text/html
العلاقة: http://genome.cshlp.org/cgi/content/short/21/12/2026Test; http://dx.doi.org/10.1101/gr.123935.111Test
الإتاحة: https://doi.org/10.1101/gr.123935.111Test
http://genome.cshlp.org/cgi/content/short/21/12/2026Test -
59دورية أكاديمية
المؤلفون: Vrba, Lukas, Jensen, Taylor J., Garbe, James C., Heimark, Ronald L., Cress, Anne E., Dickinson, Sally, Stampfer, Martha R., Futscher, Bernard W.
المساهمون: Suter, Catherine M.
المصدر: PLoS ONE ; volume 5, issue 1, page e8697 ; ISSN 1932-6203
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60دورية أكاديمية
المؤلفون: Bishop, Cleo L., Bergin, Ann-Marie H., Fessart, Delphine, Borgdorff, Viola, Hatzimasoura, Elizabeth, Garbe, James C., Stampfer, Martha R., Koh, Jim, Beach, David H.
المساهمون: Wellcome Trust, National Institutes of Health, Cancer Research UK, Medical Research Council, U.S. Department of Energy
المصدر: Molecular Cell ; volume 40, issue 4, page 533-547 ; ISSN 1097-2765
مصطلحات موضوعية: Cell Biology, Molecular Biology
الإتاحة: https://doi.org/10.1016/j.molcel.2010.10.027Test
https://api.elsevier.com/content/article/PII:S1097276510008324?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1097276510008324?httpAccept=text/plainTest