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  • 1
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    Uhrf1-dependent H3K23 ubiquitylation couples maintenance DNA methylation and replication (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-09-10
    Description: Faithful propagation of DNA methylation patterns during DNA replication is critical for maintaining cellular phenotypes of individual differentiated cells. Although it is well established that Uhrf1 (ubiquitin-like with PHD and ring finger domains 1; also known as Np95 and ICBP90) specifically binds to hemi-methylated DNA through its SRA (SET and RING finger associated) domain and has an essential role in maintenance of DNA methylation by recruiting Dnmt1 to hemi-methylated DNA sites, the mechanism by which Uhrf1 coordinates the maintenance of DNA methylation and DNA replication is largely unknown. Here we show that Uhrf1-dependent histone H3 ubiquitylation has a prerequisite role in the maintenance DNA methylation. Using Xenopus egg extracts, we successfully reproduce maintenance DNA methylation in vitro. Dnmt1 depletion results in a marked accumulation of Uhrf1-dependent ubiquitylation of histone H3 at lysine 23. Dnmt1 preferentially associates with ubiquitylated H3 in vitro though a region previously identified as a replication foci targeting sequence. The RING finger mutant of Uhrf1 fails to recruit Dnmt1 to DNA replication sites and maintain DNA methylation in mammalian cultured cells. Our findings represent the first evidence, to our knowledge, of the mechanistic link between DNA methylation and DNA replication through histone H3 ubiquitylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishiyama, Atsuya -- Yamaguchi, Luna -- Sharif, Jafar -- Johmura, Yoshikazu -- Kawamura, Takeshi -- Nakanishi, Keiko -- Shimamura, Shintaro -- Arita, Kyohei -- Kodama, Tatsuhiko -- Ishikawa, Fuyuki -- Koseki, Haruhiko -- Nakanishi, Makoto -- England -- Nature. 2013 Oct 10;502(7470):249-53. doi: 10.1038/nature12488. Epub 2013 Sep 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan. anishiya@med.nagoya-cu.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24013172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA Methylation/genetics/*physiology ; DNA Replication/genetics/*physiology ; HEK293 Cells ; HeLa Cells ; Histones/*metabolism ; Humans ; Mice ; Ovum/chemistry ; Protein Binding ; Ubiquitin-Protein Ligases/genetics/*metabolism ; Ubiquitination ; Xenopus Proteins/genetics/*metabolism ; Xenopus laevis/*genetics/*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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  • 2
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    Intracellular signaling by 14-hydroxy-4,14-retro-retinol (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-13
    Description: In mammals, retinol is the precursor for retinoids, which affect various aspects of morphogenesis and development. However, B lymphocytes, although retinol-dependent, do not use retinoic acid as mediator. Retinol is metabolized by B lymphocytes and other cell lines to optically active 14-hydroxy-4,14-retro-retinol; it is this compound that mediates the growth control. Thus another second messenger molecule, in addition to retinoic acid and retinal, is derived from retinol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buck, J -- Derguini, F -- Levi, E -- Nakanishi, K -- Hammerling, U -- AI38351/AI/NIAID NIH HHS/ -- CA49933/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 13;254(5038):1654-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1749937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/physiology ; Cell Line ; Growth Substances ; Humans ; Magnetic Resonance Spectroscopy ; Mice ; Retinoids/*chemistry ; Second Messenger Systems ; Signal Transduction ; Spectrophotometry, Ultraviolet ; Vitamin A/*analogs & derivatives/chemistry/physiology
    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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  • 3
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    Activation of interferon-gamma inducing factor mediated by interleukin-1beta converting enzyme (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: The interleukin-1beta (IL-1beta) converting enzyme (ICE) processes the inactive IL-1beta precursor to the proinflammatory cytokine. ICE was also shown to cleave the precursor of interferon-gamma inducing factor (IGIF) at the authentic processing site with high efficiency, thereby activating IGIF and facilitating its export. Lipopolysaccharide-activated ICE-deficient (ICE-/-) Kupffer cells synthesized the IGIF precursor but failed to process it into the active form. Interferon-gamma and IGIF were diminished in the sera of ICE-/- mice exposed to Propionibacterium acnes and lipopolysaccharide. The lack of multiple proinflammatory cytokines in ICE-/- mice may account for their protection from septic shock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Y -- Kuida, K -- Tsutsui, H -- Ku, G -- Hsiao, K -- Fleming, M A -- Hayashi, N -- Higashino, K -- Okamura, H -- Nakanishi, K -- Kurimoto, M -- Tanimoto, T -- Flavell, R A -- Sato, V -- Harding, M W -- Livingston, D J -- Su, M S -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):206-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vertex Pharmaceuticals, Inc., 130 Waverly Street, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Caspase 1 ; Caspase 3 ; *Caspases ; Caspases, Initiator ; Culture Media, Conditioned ; Cysteine Endopeptidases/*metabolism ; Cytokines/blood/*metabolism/pharmacology ; Humans ; Interferon-gamma/biosynthesis/blood ; Interleukin-18 ; Kupffer Cells/*metabolism ; Lipopolysaccharides/pharmacology ; Mice ; Protein Precursors/metabolism ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism/pharmacology ; Spleen/cytology/metabolism ; Transfection
    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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  • 4
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    Antisense transcription in the mammalian transcriptome (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-06
    Description: Antisense transcription (transcription from the opposite strand to a protein-coding or sense strand) has been ascribed roles in gene regulation involving degradation of the corresponding sense transcripts (RNA interference), as well as gene silencing at the chromatin level. Global transcriptome analysis provides evidence that a large proportion of the genome can produce transcripts from both strands, and that antisense transcripts commonly link neighboring "genes" in complex loci into chains of linked transcriptional units. Expression profiling reveals frequent concordant regulation of sense/antisense pairs. We present experimental evidence that perturbation of an antisense RNA can alter the expression of sense messenger RNAs, suggesting that antisense transcription contributes to control of transcriptional outputs in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katayama, S -- Tomaru, Y -- Kasukawa, T -- Waki, K -- Nakanishi, M -- Nakamura, M -- Nishida, H -- Yap, C C -- Suzuki, M -- Kawai, J -- Suzuki, H -- Carninci, P -- Hayashizaki, Y -- Wells, C -- Frith, M -- Ravasi, T -- Pang, K C -- Hallinan, J -- Mattick, J -- Hume, D A -- Lipovich, L -- Batalov, S -- Engstrom, P G -- Mizuno, Y -- Faghihi, M A -- Sandelin, A -- Chalk, A M -- Mottagui-Tabar, S -- Liang, Z -- Lenhard, B -- Wahlestedt, C -- RIKEN Genome Exploration Research Group -- Genome Science Group (Genome Network Project Core Group) -- FANTOM Consortium -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1564-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Genome Exploration Research Group, RIKEN Genomic Sciences Centre (GSC), RIKEN Yokohama Institute, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141073" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; *Genome ; Humans ; Mice/*genetics ; RNA Interference ; RNA, Antisense/*biosynthesis ; RNA, Messenger/biosynthesis ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    EGFR modulates microRNA maturation in response to hypoxia through phosphorylation of AGO2 (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-05-03
    Description: MicroRNAs (miRNAs) are generated by two-step processing to yield small RNAs that negatively regulate target gene expression at the post-transcriptional level. Deregulation of miRNAs has been linked to diverse pathological processes, including cancer. Recent studies have also implicated miRNAs in the regulation of cellular response to a spectrum of stresses, such as hypoxia, which is frequently encountered in the poorly angiogenic core of a solid tumour. However, the upstream regulators of miRNA biogenesis machineries remain obscure, raising the question of how tumour cells efficiently coordinate and impose specificity on miRNA expression and function in response to stresses. Here we show that epidermal growth factor receptor (EGFR), which is the product of a well-characterized oncogene in human cancers, suppresses the maturation of specific tumour-suppressor-like miRNAs in response to hypoxic stress through phosphorylation of argonaute 2 (AGO2) at Tyr 393. The association between EGFR and AGO2 is enhanced by hypoxia, leading to elevated AGO2-Y393 phosphorylation, which in turn reduces the binding of Dicer to AGO2 and inhibits miRNA processing from precursor miRNAs to mature miRNAs. We also identify a long-loop structure in precursor miRNAs as a critical regulatory element in phospho-Y393-AGO2-mediated miRNA maturation. Furthermore, AGO2-Y393 phosphorylation mediates EGFR-enhanced cell survival and invasiveness under hypoxia, and correlates with poorer overall survival in breast cancer patients. Our study reveals a previously unrecognized function of EGFR in miRNA maturation and demonstrates how EGFR is likely to function as a regulator of AGO2 through novel post-translational modification. These findings suggest that modulation of miRNA biogenesis is important for stress response in tumour cells and has potential clinical implications.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717558/" 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/PMC3717558/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Jia -- Xia, Weiya -- Khotskaya, Yekaterina B -- Huo, Longfei -- Nakanishi, Kotaro -- Lim, Seung-Oe -- Du, Yi -- Wang, Yan -- Chang, Wei-Chao -- Chen, Chung-Hsuan -- Hsu, Jennifer L -- Wu, Yun -- Lam, Yung Carmen -- James, Brian P -- Liu, Xiuping -- Liu, Chang-Gong -- Patel, Dinshaw J -- Hung, Mien-Chie -- CA099031/CA/NCI NIH HHS/ -- CA109311/CA/NCI NIH HHS/ -- CA16672/CA/NCI NIH HHS/ -- P01 CA099031/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- R01 CA109311/CA/NCI NIH HHS/ -- England -- Nature. 2013 May 16;497(7449):383-7. doi: 10.1038/nature12080. Epub 2013 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23636329" target="_blank"〉PubMed〈/a〉
    Keywords: Argonaute Proteins/*chemistry/*metabolism ; Breast Neoplasms/genetics/metabolism/mortality/pathology ; Cell Hypoxia/genetics/*physiology ; Cell Line, Tumor ; Cell Survival ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/biosynthesis/chemistry/genetics/*metabolism ; Neoplasm Invasiveness ; Nucleic Acid Conformation ; Phosphorylation ; Phosphotyrosine/metabolism ; Prognosis ; Protein Binding ; RNA Precursors/chemistry/genetics/metabolism ; Receptor, Epidermal Growth Factor/*metabolism ; Ribonuclease III/metabolism ; Survival Analysis
    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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  • 6
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    Molecular diversity of glutamate receptors and implications for brain function (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-23
    Description: The glutamate receptors mediate excitatory neurotransmission in the brain and are important in memory acquisition, learning, and some neurodegenerative disorders. This receptor family is classified in three groups: the N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-kainate, and metabotropic receptors. Recent molecular studies have shown that many receptor subtypes exist in all three groups of the receptors and exhibit heterogeneity in function and expression patterns. This article reviews the molecular and functional diversity of the glutamate receptors and discusses their implications for integrative brain function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakanishi, S -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):597-603.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Immunology, Kyoto University Faculty of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1329206" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Brain/*physiology ; Cloning, Molecular ; Humans ; Molecular Sequence Data ; Oxadiazoles ; Receptors, AMPA ; *Receptors, Glutamate/chemistry/physiology ; *Receptors, Metabotropic Glutamate ; *Receptors, N-Methyl-D-Aspartate/chemistry/physiology ; *Receptors, Neurotransmitter/chemistry/physiology
    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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