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  • 1
    Language: English
    In: Nature neuroscience, August 2018, Vol.21(8), pp.1139
    Description: In the version of this article initially published online, there were errors in URLs for www.southernbiotech.com, appearing in Methods sections "m6A dot-blot" and "Western blot analysis." The first two URLs should be https://www.southernbiotech.com/?catno=4030-05&type=Polyclonal#&panel1-1 and the third should be https://www.southernbiotech.com/?catno=6170-05&type=Polyclonal. In addition, some Methods URLs for bioz.com, www.abcam.com and www.sysy.com were printed correctly but not properly linked. The errors have been corrected in the PDF and HTML versions of this article.
    Keywords: Neural Stem Cells ; RNA Modification ; Ribonucleic Acid–RNA ; Stem Cells;
    ISSN: 10976256
    E-ISSN: 1546-1726
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  • 2
    Language: English
    In: Science (New York, N.Y.), 19 December 2014, Vol.346(6216), pp.1458-9
    Description: Diffuse intrinsic pontine glioma (DIPG) is an incurable pediatric brain tumor. About 80% of these tumors contain mutations in genes that encode histones (H3.3 or H3.1) ( 1 , 2 ), proteins that package DNA into chromatin. These mutations, which change lysine 27 to methionine (K27M), are believed to sequester Polycomb repressive complex 2 (PRC2), which normally represses gene expression through histone methylation (see the figure). In the absence of PRC2, genes that should be silent are expressed, which is thought to drive cell transformation ( 3 – 5 ). However, the precise role of histone mutations in tumorigenesis is unclear, and strategies to target the mutations remain elusive. As reported by Funato et al. on page 1529 of this issue ( 6 ), as well as by Hashizume et al. ( 7 ), models of K27M-mutant DIPG can be used to elucidate the mechanisms of transformation and to identify new approaches to therapy.
    Keywords: Models, Genetic ; Brain Stem Neoplasms -- Genetics ; Cell Transformation, Neoplastic -- Genetics ; Embryonic Stem Cells -- Metabolism ; Glioma -- Genetics ; Histones -- Genetics ; Neural Stem Cells -- Metabolism
    ISSN: 00368075
    E-ISSN: 1095-9203
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  • 3
    Language: English
    In: Cancer Research, 04/15/2011, Vol.71(8 Supplement), pp.3443-3443
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 4
    Language: English
    In: Cancer Research, 12/01/2015, Vol.75(23 Supplement), pp.A46-A46
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 5
    Language: English
    In: Cancer Research, 10/01/2014, Vol.74(19 Supplement), pp.LB-203-LB-203
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 6
    Language: English
    In: Nat Neurosci, 2018, Vol.21(2), pp.195-206
    Description: Internal N-methyladenosine (mA) modification is widespread in messenger RNAs (mRNAs) and is catalyzed by heterodimers of methyltransferase-like protein 3 (Mettl3) and Mettl14. To understand the role of mA in development, we deleted Mettl14 in embryonic neural stem cells (NSCs) in a mouse model. Phenotypically, NSCs lacking Mettl14 displayed markedly decreased proliferation and premature differentiation, suggesting that mA modification enhances NSC self-renewal. Decreases in the NSC pool led to a decreased number of late-born neurons during cortical neurogenesis. Mechanistically, we discovered a genome-wide increase in specific histone modifications in Mettl14 knockout versus control NSCs. These changes correlated with altered gene expression and observed cellular phenotypes, suggesting functional significance of altered histone modifications in knockout cells. Finally, we found that mA regulates histone modification in part by destabilizing transcripts that encode histone-modifying enzymes. Our results suggest an essential role for mA in development and reveal mA-regulated histone modifications as a previously unknown mechanism of gene regulation in mammalian cells.
    Keywords: Neural Stem Cells ; Embryo Cells ; Cortex ; Methyltransferase ; Gene Expression ; Neurogenesis ; Embryogenesis ; Gene Expression ; Genomes ; Mammalian Cells ; Stem Cell Transplantation ; Gene Regulation ; Stem Cells ; Stem Cells ; Gene Expression ; Ribonucleic Acids ; RNA Modification ; Chromatin;
    ISSN: 1097-6256
    E-ISSN: 15461726
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  • 7
    Language: English
    In: Developmental Biology, 01 August 2010, Vol.344(1), pp.443-443
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2010.05.125 Byline: Tian Yu (a), Yuichiro Yaguchi (b), Diego Echevarria (c), Salvador Martinez (c), Robert Wechsler-Reya (d), M. Albert Basson (a) Author Affiliation: (a) Department of Craniofacial Development, King's College London, UK (b) Department of Otorhinolaryngology, The Jikei University School of Medicine, Tokyo, Japan (c) Instituto de Neurociencias de Alicante, Campus de San Juan, Alicante, Spain (d) Duke University Medical Center, Durham NC , USA
    Keywords: Biology ; Zoology
    ISSN: 0012-1606
    E-ISSN: 1095-564X
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  • 8
    Language: English
    In: Trends in Neurosciences, 2001, Vol.24(12), pp.680-682
    Description: Cerebellar granule cells are the most abundant neurons in the brain and are crucial to the circuitry that controls motor coordination. The proliferation of granule cell precursors (GCPs) is controlled by the secreted signaling molecule Sonic hedgehog (Shh), but the factors that regulate GCP differentiation remain a mystery. A recent study suggests that the extracellular matrix protein vitronectin might tell GCPs when to stop dividing and begin differentiation. The extracellular matrix protein vitronectin might be involved in the signal that tells granule cell precursors to stop dividing and when to start differentiation.
    Keywords: Neuroscience ; Development ; Medicine ; Anatomy & Physiology
    ISSN: 0166-2236
    E-ISSN: 1878-108X
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  • 9
    In: Nature, 2017
    Description: Human cells have twenty-three pairs of chromosomes. In cancer, however, genes can be amplified in chromosomes or in circular extrachromosomal DNA (ecDNA), although the frequency and functional importance of ecDNA are not understood. We performed whole-genome sequencing, structural modelling and cytogenetic analyses of 17 different cancer types, including analysis of the structure and function of chromosomes during metaphase of 2,572 dividing cells, and developed a software package called ECdetect to conduct unbiased, integrated ecDNA detection and analysis. Here we show that ecDNA was found in nearly half of human cancers; its frequency varied by tumour type, but it was almost never found in normal cells. Driver oncogenes were amplified most commonly in ecDNA, thereby increasing transcript level. Mathematical modelling predicted that ecDNA amplification would increase oncogene copy number and intratumoural heterogeneity more effectively than chromosomal amplification. We validated these predictions by quantitative analyses of cancer samples. The results presented here suggest that ecDNA contributes to accelerated evolution in cancer.
    Keywords: Sciences (General) ; Physics;
    ISSN: 0028-0836
    E-ISSN: 1476-4687
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  • 10
    Language: English
    In: Cancer Cell, 17 January 2012, Vol.21(1), pp.1-3
    Description: The capacity for self-renewal is thought to be a critical property of tumor-initiating cells. This capacity is often associated with the ability to generate spheres in vitro. In this issue of , Barrett et al. show that cells lacking sphere-forming ability can still be very efficient at propagating tumors.
    Keywords: Medicine
    ISSN: 1535-6108
    E-ISSN: 1878-3686
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