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  • 1
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    Copy Number Profiling of Brazilian Astrocytomas (2016)
    Genetics Society of America (GSA)
    Details
    Publication Date: 2016-07-08
    Description: Copy number alterations (CNA) are one of the driving mechanisms of glioma tumorigenesis, and are currently used as important biomarkers in the routine setting. Therefore, we performed CNA profiling of 65 astrocytomas of distinct malignant grades (WHO grade I–IV) of Brazilian origin, using array-CGH and microsatellite instability analysis (MSI), and investigated their correlation with TERT and IDH1 mutational status and clinico-pathological features. Furthermore, in silico analysis using the Oncomine database was performed to validate our findings and extend the findings to gene expression level. We found that the number of genomic alterations increases in accordance with glioma grade. In glioblastomas (GBM), the most common alterations were gene amplifications ( PDGFRA , KIT , KDR , EGFR , and MET) and deletions ( CDKN2A and PTEN) . Log-rank analysis correlated EGFR amplification and/or chr7 gain with better survival of the patients. MSI was observed in 11% of GBMs. A total of 69% of GBMs presented TERT mutation, whereas IDH1 mutation was most frequent in diffuse (85.7%) and anaplastic (100%) astrocytomas. The combination of 1p19q deletion and TERT and IDH1 mutational status separated tumor groups that showed distinct age of diagnosis and outcome. In silico validation pointed to less explored genes that may be worthy of future investigation, such as CDK2 , DMRTA1 , and MTAP . Herein, using an extensive integrated analysis, we indicated potentially important genes, not extensively studied in gliomas, that could be further explored to assess their biological and clinical impact in astrocytomas.
    Electronic ISSN: 2160-1836
    Topics: Biology
    Published by Genetics Society of America (GSA)
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  • 2
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    Inhalation of the prodrug PI3K inhibitor CL27c improves lung function in asthma and fibrosis (2018)
    Springer Nature
    Details
    Publication Date: 2018
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 3
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    Induction of eosinophil apoptosis by hydrogen peroxide promotes the resolution of allergic inflammation (2015)
    Springer Nature
    Details
    Publication Date: 2015-02-13
    Description: Induction of eosinophil apoptosis by hydrogen peroxide promotes the resolution of allergic inflammation Cell Death and Disease 6, e1632 (February 2015). doi:10.1038/cddis.2014.580 Authors: A C Reis, A L Alessandri, R M Athayde, D A Perez, J P Vago, T V Ávila, T P T Ferreira, A CS de Arantes, D de Sá Coutinho, M A Rachid, L P Sousa, M A Martins, G B Menezes, A G Rossi, M M Teixeira & V Pinho
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 4
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    The Aspergillus nidulans ATM Kinase Regulates Mitochondrial Function, Glucose Uptake and the Carbon Starvation Response (2014)
    Genetics Society of America (GSA)
    Details
    Publication Date: 2014-01-11
    Description: Mitochondria supply cellular energy and also perform a role in the adaptation to metabolic stress. In mammals, the ataxia-telangiectasia mutated (ATM) kinase acts as a redox sensor controlling mitochondrial function. Subsequently, transcriptomic and genetic studies were utilized to elucidate the role played by a fungal ATM homolog during carbon starvation. In Aspergillus nidulans , AtmA was shown to control mitochondrial function and glucose uptake. Carbon starvation responses that are regulated by target of rapamycin (TOR) were shown to be AtmA-dependent, including autophagy and hydrolytic enzyme secretion. AtmA also regulated a p53-like transcription factor, XprG, inhibiting starvation-induced XprG-dependent protease secretion and cell death. Thus, AtmA possibly represents a direct or indirect link between mitochondrial stress, metabolism, and growth through the influence of TOR and XprG function. The coordination of cell growth and division with nutrient availability is crucial for all microorganisms to successfully proliferate in a heterogeneous environment. Mitochondria supply cellular energy but also perform a role in the adaptation to metabolic stress and the cross-talk between prosurvival and prodeath pathways. The present study of Aspergillus nidulans demonstrated that AtmA also controlled mitochondrial mass, function, and oxidative phosphorylation, which directly or indirectly influenced glucose uptake. Carbon starvation responses, including autophagy, shifting metabolism to the glyoxylate cycle, and the secretion of carbon scavenging enzymes were AtmA-dependent. Transcriptomic profiling of the carbon starvation response demonstrated how TOR signaling and the retrograde response, which signals mitochondrial dysfunction, were directly or indirectly influenced by AtmA. The AtmA kinase was also shown to influence a p53-like transcription factor, inhibiting starvation-induced XprG-dependent protease secretion and cell death. Therefore, in response to metabolic stress, AtmA appears to perform a role in the regulation of TOR signaling, involving the retrograde and SnfA pathways. Thus, AtmA may represent a link between mitochondrial function and cell cycle or growth, possibly through the influence of the TOR and XprG function.
    Electronic ISSN: 2160-1836
    Topics: Biology
    Published by Genetics Society of America (GSA)
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  • 5
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    14-3-3{sigma} links cytoskeletal dynamics with invasion [Medical Sciences] (2013)
    National Academy of Sciences
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    Publication Date: 2013-10-09
    Description: The protein 14-3-3σ (stratifin) is frequently described as a tumor suppressor silenced in about 80% of breast tumors. Intriguingly, we show that 14-3-3σ expression, which in normal breast is localized to the myoepithelial cells, tracks with malignant phenotype in two models of basal-like breast cancer progression, and in patients, it...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    Identification of a dendritic cell receptor that couples sensing of necrosis to immunity (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-02-17
    Description: Injury or impaired clearance of apoptotic cells leads to the pathological accumulation of necrotic corpses, which induce an inflammatory response that initiates tissue repair. In addition, antigens present in necrotic cells can sometimes provoke a specific immune response and it has been argued that necrosis could explain adaptive immunity in seemingly infection-free situations, such as after allograft transplantation or in spontaneous and therapy-induced tumour rejection. In the mouse, the CD8alpha+ subset of dendritic cells phagocytoses dead cell remnants and cross-primes CD8+ T cells against cell-associated antigens. Here we show that CD8alpha+ dendritic cells use CLEC9A (also known as DNGR-1), a recently-characterized C-type lectin, to recognize a preformed signal that is exposed on necrotic cells. Loss or blockade of CLEC9A does not impair the uptake of necrotic cell material by CD8+ dendritic cells, but specifically reduces cross-presentation of dead-cell-associated antigens in vitro and decreases the immunogenicity of necrotic cells in vivo. The function of CLEC9A requires a key tyrosine residue in its intracellular tail that allows the recruitment and activation of the tyrosine kinase SYK, which is also essential for cross-presentation of dead-cell-associated antigens. Thus, CLEC9A functions as a SYK-coupled C-type lectin receptor to mediate sensing of necrosis by the principal dendritic-cell subset involved in regulating cross-priming to cell-associated antigens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671489/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671489/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sancho, David -- Joffre, Olivier P -- Keller, Anna M -- Rogers, Neil C -- Martinez, Dolores -- Hernanz-Falcon, Patricia -- Rosewell, Ian -- Reis e Sousa, Caetano -- A3598/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2009 Apr 16;458(7240):899-903. doi: 10.1038/nature07750.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19219027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD8/metabolism ; CD8-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Cross-Priming/immunology ; Dendritic Cells/*immunology/*metabolism ; Humans ; Lectins, C-Type/deficiency/genetics/*metabolism ; Ligands ; Mice ; Necrosis/*immunology/*metabolism ; Phagocytosis ; Receptors, Immunologic/deficiency/genetics/*metabolism ; Receptors, Mitogen/genetics/*metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Broad line emission from iron K- and L-shell transitions in the active galaxy 1H 0707-495 (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-05-30
    Description: Since the 1995 discovery of the broad iron K-line emission from the Seyfert galaxy MCG-6-30-15 (ref. 1), broad iron K lines have been found in emission from several other Seyfert galaxies, from accreting stellar-mass black holes and even from accreting neutron stars. The iron K line is prominent in the reflection spectrum created by the hard-X-ray continuum irradiating dense accreting matter. Relativistic distortion of the line makes it sensitive to the strong gravity and spin of the black hole. The accompanying iron L-line emission should be detectable when the iron abundance is high. Here we report the presence of both iron K and iron L emission in the spectrum of the narrow-line Seyfert 1 galaxy 1H 0707-495. The bright iron L emission has enabled us to detect a reverberation lag of about 30 s between the direct X-ray continuum and its reflection from matter falling into the black hole. The observed reverberation timescale is comparable to the light-crossing time of the innermost radii around a supermassive black hole. The combination of spectral and timing data on 1H 0707-495 provides strong evidence that we are witnessing emission from matter within a gravitational radius, or a fraction of a light minute, from the event horizon of a rapidly spinning, massive black hole.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fabian, A C -- Zoghbi, A -- Ross, R R -- Uttley, P -- Gallo, L C -- Brandt, W N -- Blustin, A J -- Boller, T -- Caballero-Garcia, M D -- Larsson, J -- Miller, J M -- Miniutti, G -- Ponti, G -- Reis, R C -- Reynolds, C S -- Tanaka, Y -- Young, A J -- England -- Nature. 2009 May 28;459(7246):540-2. doi: 10.1038/nature08007.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Astronomy, Madingley Road, Cambridge CB3 0HA, UK. acf@ast.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478778" target="_blank"〉PubMed〈/a〉
    Keywords: Extraterrestrial Environment/*chemistry ; Iron/*analysis/chemistry
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 8
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    Telomeres avoid end detection by severing the checkpoint signal transduction pathway (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-09-11
    Description: Telomeres protect the normal ends of chromosomes from being recognized as deleterious DNA double-strand breaks. Recent studies have uncovered an apparent paradox: although DNA repair is prevented, several proteins involved in DNA damage processing and checkpoint responses are recruited to telomeres in every cell cycle and are required for end protection. It is currently not understood how telomeres prevent DNA damage responses from causing permanent cell cycle arrest. Here we show that fission yeast (Schizosaccharomyces pombe) cells lacking Taz1, an orthologue of human TRF1 and TRF2 (ref. 2), recruit DNA repair proteins (Rad22(RAD52) and Rhp51(RAD51), where the superscript indicates the human orthologue) and checkpoint sensors (RPA, Rad9, Rad26(ATRIP) and Cut5/Rad4(TOPBP1)) to telomeres. Despite this, telomeres fail to accumulate the checkpoint mediator Crb2(53BP1) and, consequently, do not activate Chk1-dependent cell cycle arrest. Artificially recruiting Crb2(53BP1) to taz1Delta telomeres results in a full checkpoint response and cell cycle arrest. Stable association of Crb2(53BP1) to DNA double-strand breaks requires two independent histone modifications: H4 dimethylation at lysine 20 (H4K20me2) and H2A carboxy-terminal phosphorylation (gammaH2A). Whereas gammaH2A can be readily detected, telomeres lack H4K20me2, in contrast to internal chromosome locations. Blocking checkpoint signal transduction at telomeres requires Pot1 and Ccq1, and loss of either Pot1 or Ccq1 from telomeres leads to Crb2(53BP1) foci formation, Chk1 activation and cell cycle arrest. Thus, telomeres constitute a chromatin-privileged region of the chromosomes that lack essential epigenetic markers for DNA damage response amplification and cell cycle arrest. Because the protein kinases ATM and ATR must associate with telomeres in each S phase to recruit telomerase, exclusion of Crb2(53BP1) has a critical role in preventing telomeres from triggering cell cycle arrest.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3196630/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3196630/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carneiro, Tiago -- Khair, Lyne -- Reis, Clara C -- Borges, Vanessa -- Moser, Bettina A -- Nakamura, Toru M -- Ferreira, Miguel Godinho -- 06-0396/Worldwide Cancer Research/United Kingdom -- GM078253/GM/NIGMS NIH HHS/ -- R01 GM078253/GM/NIGMS NIH HHS/ -- R01 GM078253-04/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Sep 9;467(7312):228-32. doi: 10.1038/nature09353.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto Gulbenkian de Ciencia, Oeiras 2781-901, Portugal.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829797" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; DNA Damage ; *DNA Repair ; Schizosaccharomyces/cytology/*genetics/*metabolism ; Schizosaccharomyces pombe Proteins/metabolism ; *Signal Transduction ; Telomere/*metabolism ; Telomere-Binding Proteins/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    Immunology. Eating in to avoid infection (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1376-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK. caetano@cancer.org.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17347432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cytokines/metabolism ; Dendritic Cells/*immunology/physiology/*virology ; Endosomes/immunology/virology ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Membrane Glycoproteins/immunology/physiology ; Mice ; Mice, Transgenic ; RNA, Viral/*immunology/metabolism ; Rhabdoviridae Infections/*immunology ; Signal Transduction ; Toll-Like Receptor 7/immunology/physiology ; Toll-Like Receptor 9/immunology/physiology ; Toll-Like Receptors/immunology/*physiology ; Vesicular stomatitis Indiana virus/*immunology/physiology ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    A 200-second quasi-periodicity after the tidal disruption of a star by a dormant black hole (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-04
    Description: Supermassive black holes (SMBHs; mass is greater than or approximately 10(5) times that of the Sun) are known to exist at the center of most galaxies with sufficient stellar mass. In the local universe, it is possible to infer their properties from the surrounding stars or gas. However, at high redshifts we require active, continuous accretion to infer the presence of the SMBHs, which often comes in the form of long-term accretion in active galactic nuclei. SMBHs can also capture and tidally disrupt stars orbiting nearby, resulting in bright flares from otherwise quiescent black holes. Here, we report on a ~200-second x-ray quasi-periodicity around a previously dormant SMBH located in the center of a galaxy at redshift z = 0.3534. This result may open the possibility of probing general relativity beyond our local universe.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reis, R C -- Miller, J M -- Reynolds, M T -- Gultekin, K -- Maitra, D -- King, A L -- Strohmayer, T E -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):949-51. doi: 10.1126/science.1223940. Epub 2012 Aug 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Astronomy, University of Michigan, Ann Arbor, MI 48109, USA. rdosreis@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859817" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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