Добірка наукової літератури з теми "Hyperacetylation"
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Статті в журналах з теми "Hyperacetylation"
Sudo, Haruka, and Akira Kubo. "The Aneugenicity of Ketone Bodies in Colon Epithelial Cells Is Mediated by Microtubule Hyperacetylation and Is Blocked by Resveratrol." International Journal of Molecular Sciences 22, no. 17 (August 30, 2021): 9397. http://dx.doi.org/10.3390/ijms22179397.
Повний текст джерелаRao, Rekha, Warren Fiskus, Yonghua Yang, Pearl Lee, Rajeshree Joshi, Pravina Fernandez, Aditya Mandawat, Peter Atadja, James E. Bradner, and Kapil Bhalla. "HDAC6 inhibition enhances 17-AAG–mediated abrogation of hsp90 chaperone function in human leukemia cells." Blood 112, no. 5 (September 1, 2008): 1886–93. http://dx.doi.org/10.1182/blood-2008-03-143644.
Повний текст джерелаCalestagne-Morelli, Alison, and Juan Ausió. "Long-range histone acetylation: biological significance, structural implications, and mechanismsThis paper is one of a selection of papers published in this Special Issue, entitled 27th International West Coast Chromatin and Chromosome Conference, and has undergone the Journal's usual peer review process." Biochemistry and Cell Biology 84, no. 4 (August 2006): 518–27. http://dx.doi.org/10.1139/o06-067.
Повний текст джерелаKajino, Hidetoshi, Tomomi Nagatani, Miku Oi, Tomoya Kujirai, Hitoshi Kurumizaka, Atsuya Nishiyama, Makoto Nakanishi, Kenzo Yamatsugu, Shigehiro A. Kawashima, and Motomu Kanai. "Synthetic hyperacetylation of nucleosomal histones." RSC Chemical Biology 1, no. 2 (2020): 56–59. http://dx.doi.org/10.1039/d0cb00029a.
Повний текст джерелаLutter, L. C., L. Judis, and R. F. Paretti. "Effects of histone acetylation on chromatin topology in vivo." Molecular and Cellular Biology 12, no. 11 (November 1992): 5004–14. http://dx.doi.org/10.1128/mcb.12.11.5004-5014.1992.
Повний текст джерелаLutter, L. C., L. Judis, and R. F. Paretti. "Effects of histone acetylation on chromatin topology in vivo." Molecular and Cellular Biology 12, no. 11 (November 1992): 5004–14. http://dx.doi.org/10.1128/mcb.12.11.5004.
Повний текст джерелаNa, Ann-Yae, Sanjita Paudel, Soyoung Choi, Jun Hyung Lee, Min-Sik Kim, Jong-Sup Bae, and Sangkyu Lee. "Global Lysine Acetylome Analysis of LPS-Stimulated HepG2 Cells Identified Hyperacetylation of PKM2 as a Metabolic Regulator in Sepsis." International Journal of Molecular Sciences 22, no. 16 (August 8, 2021): 8529. http://dx.doi.org/10.3390/ijms22168529.
Повний текст джерелаSudo, Haruka. "Microtubule Hyperacetylation Enhances KL1-Dependent Micronucleation under a Tau Deficiency in Mammary Epithelial Cells." International Journal of Molecular Sciences 19, no. 9 (August 23, 2018): 2488. http://dx.doi.org/10.3390/ijms19092488.
Повний текст джерелаWu, James T., Sonia Y. Archer, Brian Hinnebusch, Shufen Meng, and Richard A. Hodin. "Transient vs. prolonged histone hyperacetylation: effects on colon cancer cell growth, differentiation, and apoptosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 3 (March 1, 2001): G482—G490. http://dx.doi.org/10.1152/ajpgi.2001.280.3.g482.
Повний текст джерелаGlon, Damien, Géraldine Vilmen, Daniel Perdiz, Eva Hernandez, Guillaume Beauclair, Frédérique Quignon, Clarisse Berlioz-Torrent, et al. "Essential role of hyperacetylated microtubules in innate immunity escape orchestrated by the EBV-encoded BHRF1 protein." PLOS Pathogens 18, no. 3 (March 11, 2022): e1010371. http://dx.doi.org/10.1371/journal.ppat.1010371.
Повний текст джерелаДисертації з теми "Hyperacetylation"
Thompson, John William. "DNA Fragmentation and Histone Hyperacetylation in the Hypoxic-Acidotic Cardiomyocyte." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/169.
Повний текст джерелаOliveira, Clara Slade. "Efeitos da hiperaceleração de histonas na diferenciação in vitro de células tronco embrionárias murinas /." Jaboticabal : [s.n.], 2009. http://hdl.handle.net/11449/98206.
Повний текст джерелаBanca: Lígia Veiga Pereira
Banca: Irina Kerkis
Resumo: O estudo dos processos de diferenciação em células tronco embrionárias (CTE) representa uma importante ferramenta para o entendimento das vias moleculares que os regem, apresentando grande aplicação tanto na ciência básica quanto na engenharia de tecidos e medicina regenerativa. Pouco é conhecido sobre as marcas epigenéticas existentes na cromatina destas células, e de que forma a regulação da expressão gênica ocorre no momento da diferenciação. O presente trabalho teve como objetivo o estudo dos efeitos da hiperacetilação das histonas causada pela droga tricostatina A (TSA), uma inibidora das enzimas histona desacetilases, sobre a diferenciação destas células em estádios iniciais e avançados. Para tanto, a hiperacetilação induzida pela droga foi estimada por reações de imunocitoquímica para AcLys9H3. Os efeitos anti-proliferativos da TSA foram mensurados pelo teste de TUNEL e contagem de células. Ainda, foram conduzidos experimentos de diferenciação in vitro de CTE e análise da expressão de proteínas características de linhagens celulares diferenciadas por reações de imunocitoquímica (Oct3/4, nestina, âIII tubulina, desmina e troponina I), em cultivos tratados com TSA em diferentes concentrações e em diferentes momentos. Desta forma, foi estimada a população de tipos celulares oriundos dos folhetos embrionários ectodérmico e mesodérmico, como neurônios, e células musculares, quando foi promovida a hiperacetilação das histonas nas CTE, em diferentes momentos da diferenciação celular in vitro. A TSA induziu apoptose em níveis superiores aos do grupo controle, e retardou/inibiu a divisão celular. Promoveu hiperacetilação dose-dependente nos períodos estudados, e estimulou a diferenciação de precursores mesodérmicos (50nM d5) e ectodérmicos (15nMd0-5 e 50nMd5), cardiomiócitos (50nMd5 e 100nMd13) e neurônios (15nMd0-5, 50nMd5, 100nMd5, 100nMd13).
Abstract: Studies on embryonic stem cells (ESC) differentiation represents an important tool leading to understanding of its molecular pathways, with many applications both on basic research and tissue engineering / regenerative medicine. Little is known about epigenetic marks on ESC chromatin, and how gene expression occurs at differentiation time. The aim of this work was to study effects of histone hiperacetylation, induced by cell treatment with trichostatin A (TSA), an histone deacetylase inhibitor, on both initial and late differentiation. For that, drug-induced hyperacetylation was studied by AcLys9H3 immunocitochemistry. TSA anti-proliferative effects were analysed by TUNEL test and cell counts. Experiments on ESC in vitro differentiation and immunocitochemistry for specific cell types proteins (Oct3/4, nestin, âIII tubulin, desmin and troponin I) were performed, in treated and control groups, at different moments. This analysis showed specific cell types populations derived from embryonic ectodermal and mesodermal, such as neurons and cardiomyocytes, when histone hyperacetylation were induced, on both initial and late diferentiation. Our results showed that TSA induces apoptosis and inhibits cellular proliferation. Also, TSA promoted dose-dependent histone hyperacetylation at studied moments, and stimulated mesodermal (50nM d5) and ectodermal (15nMd0-5 e 50nMd5) precursors, cardiomyocytes (50nMd5 e 100nMd13) and neurons (15nMd0-5, 50nMd5, 100nMd5, 100nMd13) differentiation.
Mestre
Oliveira, Clara Slade [UNESP]. "Efeitos da hiperaceleração de histonas na diferenciação in vitro de células tronco embrionárias murinas." Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/98206.
Повний текст джерелаFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O estudo dos processos de diferenciação em células tronco embrionárias (CTE) representa uma importante ferramenta para o entendimento das vias moleculares que os regem, apresentando grande aplicação tanto na ciência básica quanto na engenharia de tecidos e medicina regenerativa. Pouco é conhecido sobre as marcas epigenéticas existentes na cromatina destas células, e de que forma a regulação da expressão gênica ocorre no momento da diferenciação. O presente trabalho teve como objetivo o estudo dos efeitos da hiperacetilação das histonas causada pela droga tricostatina A (TSA), uma inibidora das enzimas histona desacetilases, sobre a diferenciação destas células em estádios iniciais e avançados. Para tanto, a hiperacetilação induzida pela droga foi estimada por reações de imunocitoquímica para AcLys9H3. Os efeitos anti-proliferativos da TSA foram mensurados pelo teste de TUNEL e contagem de células. Ainda, foram conduzidos experimentos de diferenciação in vitro de CTE e análise da expressão de proteínas características de linhagens celulares diferenciadas por reações de imunocitoquímica (Oct3/4, nestina, âIII tubulina, desmina e troponina I), em cultivos tratados com TSA em diferentes concentrações e em diferentes momentos. Desta forma, foi estimada a população de tipos celulares oriundos dos folhetos embrionários ectodérmico e mesodérmico, como neurônios, e células musculares, quando foi promovida a hiperacetilação das histonas nas CTE, em diferentes momentos da diferenciação celular in vitro. A TSA induziu apoptose em níveis superiores aos do grupo controle, e retardou/inibiu a divisão celular. Promoveu hiperacetilação dose-dependente nos períodos estudados, e estimulou a diferenciação de precursores mesodérmicos (50nM d5) e ectodérmicos (15nMd0-5 e 50nMd5), cardiomiócitos (50nMd5 e 100nMd13) e neurônios (15nMd0-5, 50nMd5, 100nMd5, 100nMd13).
Studies on embryonic stem cells (ESC) differentiation represents an important tool leading to understanding of its molecular pathways, with many applications both on basic research and tissue engineering / regenerative medicine. Little is known about epigenetic marks on ESC chromatin, and how gene expression occurs at differentiation time. The aim of this work was to study effects of histone hiperacetylation, induced by cell treatment with trichostatin A (TSA), an histone deacetylase inhibitor, on both initial and late differentiation. For that, drug-induced hyperacetylation was studied by AcLys9H3 immunocitochemistry. TSA anti-proliferative effects were analysed by TUNEL test and cell counts. Experiments on ESC in vitro differentiation and immunocitochemistry for specific cell types proteins (Oct3/4, nestin, âIII tubulin, desmin and troponin I) were performed, in treated and control groups, at different moments. This analysis showed specific cell types populations derived from embryonic ectodermal and mesodermal, such as neurons and cardiomyocytes, when histone hyperacetylation were induced, on both initial and late diferentiation. Our results showed that TSA induces apoptosis and inhibits cellular proliferation. Also, TSA promoted dose-dependent histone hyperacetylation at studied moments, and stimulated mesodermal (50nM d5) and ectodermal (15nMd0-5 e 50nMd5) precursors, cardiomyocytes (50nMd5 e 100nMd13) and neurons (15nMd0-5, 50nMd5, 100nMd5, 100nMd13) differentiation.
Lin, Kuen-Tyng, and 林坤廷. "The epigenetic effects of trichostatin A-induced chromatin histone hyperacetylation on hepatocellular carcinoma cell migration." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/99561964352796142349.
Повний текст джерела國防醫學院
生命科學研究所
93
Trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, has been known to block cellular growth, induce apoptosis and inhibit cell migration in human cancer cell lines. In human hepatocellular carcinoma (HCC) cell lines, the effects of TSA treatment on cell migration are still unknown. In order to investigate the roles of epigenetic modulations, especially histone acetylation, on cancer genes participated in HCC metastasis, HCC cell lines were treated with different concentrations of TSA and in vitro migration activity was measured by using the transwell migration assay. The results indicated that the cell migration activity can be substantially enhanced by TSA treatment in a dose-dependent manner for HCC cell lines Huh7, PLC5 and Hep3B. By RT-PCR and Western blot analysis, the TSA induction on two migration-related gene families, matrix metalloproteinases (MMPs) and integrins, was first examined for revealing the molecular pathways in the enhancement of Hep3B cell migration. The results indicated that the enhancement of Hep3B cell migration was associated with up-regulation of several MMPs and integrin subunits including MMP-1, -2, -9, -10, -13 and integrin subunits of a4, b2, b6 in both mRNA and protein levels. Addition of specific inhibitors or neutralizing antibodies to those MMPs or integrins blocked the TSA-induced cell migration activity in the Hep3B cells. Up-regulated MMP-1, -2 and -9 were also clinicopathologically associated with HCC tumorigenesis (P<0.05) by quantitative RT-PCR analysis. In conclusion, the results suggest that TSA has a novel effect on enhancing migration activities and that histone acetylation plays an important role in HCC cell migration. With further evidence of epigenetic modulation in HCC tissues, TSA treatment or its revealed target pathways will add to the understanding of molecular mechanisms of HCC metastasis and treatment.
Sarikhani, Mohsen. "Understanding the Role of SIRT2 in Cardiac Hypertrophy, Cell Death and Glucose Homeostasis." Thesis, 2018. https://etd.iisc.ac.in/handle/2005/5424.
Повний текст джерелаТези доповідей конференцій з теми "Hyperacetylation"
Reske, Jake J., Mike R. Wilson, and Ronald L. Chandler. "Abstract PO008: ARID1A prevents H3K27-hyperacetylation at active super-enhancers." In Abstracts: AACR Virtual Special Conference: Endometrial Cancer: New Biology Driving Research and Treatment; November 9-10, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1557-3265.endomet20-po008.
Повний текст джерелаMethot, Joey L., Melissa Chenard, Close Joshua, Cruz Jonathan, William Dahlberg, Judith Fleming, Chris Hamblett, et al. "Abstract 5433: Prolonged histone hyperacetylation with a novel class of HDAC1/2 selective inhibitors." 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.am10-5433.
Повний текст джерелаOrdentlich, Peter. "Abstract PR-6: Pharmacodynamic analysis of ENCORE 301, a placebo-controlled, randomized phase 2 study of exemestane with and without entinostat in postmenopausal ER+ breast cancer patients demonstrates an association of lysine hyperacetylation with clinical outcome." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-pr-6.
Повний текст джерелаHa, Kyungsoo, Warren Fiskus, Ramesh Balusu, Rekha Rao, Sreedhar Venkannagari, and Kapil N. Bhalla. "Abstract 4698: Inhibition of histone deacetylase (HDAC) 3 induces hyperacetylation and inhibition of nuclear heat shock protein (hsp) 90 leading to depletion of ATR and CHK1 with sensitization to DNA damage in breast and cervical cancer cells." In 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.am2012-4698.
Повний текст джерела