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  • Lunar and Planetary Science and Exploration  (222)
  • Magnetism  (152)
  • Cell Line  (111)
  • ASTROPHYSICS
  • Life and Medical Sciences
  • MATERIALS, METALLIC
  • 2010-2014  (309)
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  • 2010-2014  (309)
  • 2005-2009  (176)
  • 1975-1979
  • 1970-1974
  • 1950-1954  (12)
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  • 1
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    TLR3 deficiency in patients with herpes simplex encephalitis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-18
    Description: Some Toll and Toll-like receptors (TLRs) provide immunity to experimental infections in animal models, but their contribution to host defense in natural ecosystems is unknown. We report a dominant-negative TLR3 allele in otherwise healthy children with herpes simplex virus 1 (HSV-1) encephalitis. TLR3 is expressed in the central nervous system (CNS), where it is required to control HSV-1, which spreads from the epithelium to the CNS via cranial nerves. TLR3 is also expressed in epithelial and dendritic cells, which apparently use TLR3-independent pathways to prevent further dissemination of HSV-1 and to provide resistance to other pathogens in TLR3-deficient patients. Human TLR3 appears to be redundant in host defense to most microbes but is vital for natural immunity to HSV-1 in the CNS, which suggests that neurotropic viruses have contributed to the evolutionary maintenance of TLR3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Shen-Ying -- Jouanguy, Emmanuelle -- Ugolini, Sophie -- Smahi, Asma -- Elain, Gaelle -- Romero, Pedro -- Segal, David -- Sancho-Shimizu, Vanessa -- Lorenzo, Lazaro -- Puel, Anne -- Picard, Capucine -- Chapgier, Ariane -- Plancoulaine, Sabine -- Titeux, Matthias -- Cognet, Celine -- von Bernuth, Horst -- Ku, Cheng-Lung -- Casrouge, Armanda -- Zhang, Xin-Xin -- Barreiro, Luis -- Leonard, Joshua -- Hamilton, Claire -- Lebon, Pierre -- Heron, Benedicte -- Vallee, Louis -- Quintana-Murci, Lluis -- Hovnanian, Alain -- Rozenberg, Flore -- Vivier, Eric -- Geissmann, Frederic -- Tardieu, Marc -- Abel, Laurent -- Casanova, Jean-Laurent -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 14;317(5844):1522-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, Institut National de la Sante et de la Recherche Medicale (INSERM), U550, Faculty Necker, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872438" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; CD8-Positive T-Lymphocytes/immunology ; Cell Line ; Child, Preschool ; Dendritic Cells/immunology ; Encephalitis, Herpes Simplex/*genetics/*immunology ; Female ; Fibroblasts/immunology/metabolism/virology ; Genes, Dominant ; *Herpesvirus 1, Human/physiology ; Heterozygote ; Humans ; Immunity, Innate ; Infant ; Interferons/biosynthesis ; Keratinocytes/immunology ; Killer Cells, Natural/immunology ; Leukocytes, Mononuclear/immunology ; Mutation ; Poly I-C/pharmacology ; Toll-Like Receptor 3/chemistry/*deficiency/*genetics/physiology
    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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  • 2
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    Ethics. The ISSCR guidelines for human embryonic stem cell research (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daley, George Q -- Ahrlund Richter, Lars -- Auerbach, Jonathan M -- Benvenisty, Nissim -- Charo, R Alta -- Chen, Grace -- Deng, Hong-Kui -- Goldstein, Lawrence S -- Hudson, Kathy L -- Hyun, Insoo -- Junn, Sung Chull -- Love, Jane -- Lee, Eng Hin -- McLaren, Anne -- Mummery, Christine L -- Nakatsuji, Norio -- Racowsky, Catherine -- Rooke, Heather -- Rossant, Janet -- Scholer, Hans R -- Solbakk, Jan Helge -- Taylor, Patrick -- Trounson, Alan O -- Weissman, Irving L -- Wilmut, Ian -- Yu, John -- Zoloth, Laurie -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):603-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital, Boston, Massachusetts, USA. george.daley@childrens.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272706" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chimera ; *Embryo Research/ethics/legislation & jurisprudence ; Embryonic Development ; *Embryonic Stem Cells ; *Guidelines as Topic ; Humans ; Informed Consent ; International Cooperation ; Oocyte Donation/economics/ethics ; Pluripotent Stem Cells ; Societies, Scientific ; Tissue Donors/ethics
    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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  • 3
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    DNA double-strand breaks activate a multi-functional genetic program in developing lymphocytes (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-14
    Description: DNA double-strand breaks are generated by genotoxic agents and by cellular endonucleases as intermediates of several important physiological processes. The cellular response to genotoxic DNA breaks includes the activation of transcriptional programs known primarily to regulate cell-cycle checkpoints and cell survival. DNA double-strand breaks are generated in all developing lymphocytes during the assembly of antigen receptor genes, a process that is essential for normal lymphocyte development. Here we show that in murine lymphocytes these physiological DNA breaks activate a broad transcriptional program. This program transcends the canonical DNA double-strand break response and includes many genes that regulate diverse cellular processes important for lymphocyte development. Moreover, the expression of several of these genes is regulated similarly in response to genotoxic DNA damage. Thus, physiological DNA double-strand breaks provide cues that can regulate cell-type-specific processes not directly involved in maintaining the integrity of the genome, and genotoxic DNA breaks could disrupt normal cellular functions by corrupting these processes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605662/" 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/PMC2605662/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bredemeyer, Andrea L -- Helmink, Beth A -- Innes, Cynthia L -- Calderon, Boris -- McGinnis, Lisa M -- Mahowald, Grace K -- Gapud, Eric J -- Walker, Laura M -- Collins, Jennifer B -- Weaver, Brian K -- Mandik-Nayak, Laura -- Schreiber, Robert D -- Allen, Paul M -- May, Michael J -- Paules, Richard S -- Bassing, Craig H -- Sleckman, Barry P -- R01 AI047829/AI/NIAID NIH HHS/ -- R01 AI047829-09/AI/NIAID NIH HHS/ -- R01 CA125195/CA/NCI NIH HHS/ -- R01 CA125195-02/CA/NCI NIH HHS/ -- England -- Nature. 2008 Dec 11;456(7223):819-23. doi: 10.1038/nature07392. Epub 2008 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18849970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/drug effects/*metabolism ; Cell Cycle Proteins/drug effects ; Cell Line ; *DNA Breaks, Double-Stranded ; DNA-Binding Proteins/drug effects ; Enzyme Inhibitors/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental/drug effects/*genetics ; Homeodomain Proteins/metabolism ; Mice ; Mice, Knockout ; Mice, SCID ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/drug effects ; Tumor Suppressor Proteins/drug effects
    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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  • 4
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    A paracrine requirement for hedgehog signalling in cancer (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-30
    Description: Ligand-dependent activation of the hedgehog (Hh) signalling pathway has been associated with tumorigenesis in a number of human tissues. Here we show that, although previous reports have described a cell-autonomous role for Hh signalling in these tumours, Hh ligands fail to activate signalling in tumour epithelial cells. In contrast, our data support ligand-dependent activation of the Hh pathway in the stromal microenvironment. Specific inhibition of Hh signalling using small molecule inhibitors, a neutralizing anti-Hh antibody or genetic deletion of smoothened (Smo) in the mouse stroma results in growth inhibition in xenograft tumour models. Taken together, these studies demonstrate a paracrine requirement for Hh ligand signalling in the tumorigenesis of Hh-expressing cancers and have important implications for the development of Hh pathway antagonists in cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yauch, Robert L -- Gould, Stephen E -- Scales, Suzie J -- Tang, Tracy -- Tian, Hua -- Ahn, Christina P -- Marshall, Derek -- Fu, Ling -- Januario, Thomas -- Kallop, Dara -- Nannini-Pepe, Michelle -- Kotkow, Karen -- Marsters, James C -- Rubin, Lee L -- de Sauvage, Frederic J -- England -- Nature. 2008 Sep 18;455(7211):406-10. doi: 10.1038/nature07275. Epub 2008 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18754008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Hedgehog Proteins/*metabolism ; Humans ; Ligands ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms/genetics/*metabolism ; Paracrine Communication/*physiology ; Receptors, G-Protein-Coupled/deficiency/genetics/metabolism ; Stromal Cells/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Wnt3a-mediated formation of phosphatidylinositol 4,5-bisphosphate regulates LRP6 phosphorylation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: The canonical Wnt-beta-catenin signaling pathway is initiated by inducing phosphorylation of one of the Wnt receptors, low-density lipoprotein receptor-related protein 6 (LRP6), at threonine residue 1479 (Thr1479) and serine residue 1490 (Ser1490). By screening a human kinase small interfering RNA library, we identified phosphatidylinositol 4-kinase type II alpha and phosphatidylinositol-4-phosphate 5-kinase type I (PIP5KI) as required for Wnt3a-induced LRP6 phosphorylation at Ser1490 in mammalian cells and confirmed that these kinases are important for Wnt signaling in Xenopus embryos. Wnt3a stimulates the formation of phosphatidylinositol 4,5-bisphosphates [PtdIns (4,5)P2] through frizzled and dishevelled, the latter of which directly interacted with and activated PIP5KI. In turn, PtdIns (4,5)P2 regulated phosphorylation of LRP6 at Thr1479 and Ser1490. Therefore, our study reveals a signaling mechanism for Wnt to regulate LRP6 phosphorylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" 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/PMC2532521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Weijun -- Choi, Sun-Cheol -- Wang, He -- Qin, Yuanbo -- Volpicelli-Daley, Laura -- Swan, Laura -- Lucast, Louise -- Khoo, Cynthia -- Zhang, Xiaowu -- Li, Lin -- Abrams, Charles S -- Sokol, Sergei Y -- Wu, Dianqing -- AR051476/AR/NIAMS NIH HHS/ -- CA132317/CA/NCI NIH HHS/ -- DA018343/DA/NIDA NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- P30 DA018343/DA/NIDA NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 CA132317-01A2/CA/NCI NIH HHS/ -- R01 CA139395/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1350-3. doi: 10.1126/science.1160741.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772438" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Axin Protein ; Cell Line ; Frizzled Receptors/metabolism ; Humans ; LDL-Receptor Related Proteins/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; Repressor Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Wnt3A Protein ; Xenopus/embryology ; Xenopus Proteins
    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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  • 6
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    An overlapping protein-coding region in influenza A virus segment 3 modulates the host response (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-30
    Description: Influenza A virus (IAV) infection leads to variable and imperfectly understood pathogenicity. We report that segment 3 of the virus contains a second open reading frame ("X-ORF"), accessed via ribosomal frameshifting. The frameshift product, termed PA-X, comprises the endonuclease domain of the viral PA protein with a C-terminal domain encoded by the X-ORF and functions to repress cellular gene expression. PA-X also modulates IAV virulence in a mouse infection model, acting to decrease pathogenicity. Loss of PA-X expression leads to changes in the kinetics of the global host response, which notably includes increases in inflammatory, apoptotic, and T lymphocyte-signaling pathways. Thus, we have identified a previously unknown IAV protein that modulates the host response to infection, a finding with important implications for understanding IAV pathogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552242/" 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/PMC3552242/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jagger, B W -- Wise, H M -- Kash, J C -- Walters, K-A -- Wills, N M -- Xiao, Y-L -- Dunfee, R L -- Schwartzman, L M -- Ozinsky, A -- Bell, G L -- Dalton, R M -- Lo, A -- Efstathiou, S -- Atkins, J F -- Firth, A E -- Taubenberger, J K -- Digard, P -- 073126/Wellcome Trust/United Kingdom -- 088789/Wellcome Trust/United Kingdom -- G0700815/Medical Research Council/United Kingdom -- G0700815(82260)/Medical Research Council/United Kingdom -- G9800943/Medical Research Council/United Kingdom -- MR/J002232/1/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):199-204. doi: 10.1126/science.1222213. Epub 2012 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745253" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon ; Conserved Sequence ; Female ; *Frameshifting, Ribosomal ; Gene Expression Regulation ; Genome, Viral ; HEK293 Cells ; Humans ; Influenza A Virus, H1N1 Subtype/*genetics/growth & development/pathogenicity ; Influenza A virus/*genetics/metabolism ; Lung/pathology/virology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutation ; *Open Reading Frames ; Orthomyxoviridae Infections/genetics/immunology/pathology/*virology ; Protein Interaction Domains and Motifs ; Proteome ; RNA Replicase/chemistry/*genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Viral/genetics/metabolism ; Reassortant Viruses/genetics ; Repressor Proteins/chemistry/*genetics/*metabolism ; Viral Nonstructural Proteins/chemistry/*genetics/*metabolism ; Viral Proteins/biosynthesis/chemistry/*genetics/*metabolism ; Virus Replication
    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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  • 7
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    MR1 presents microbial vitamin B metabolites to MAIT cells (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-12
    Description: Antigen-presenting molecules, encoded by the major histocompatibility complex (MHC) and CD1 family, bind peptide- and lipid-based antigens, respectively, for recognition by T cells. Mucosal-associated invariant T (MAIT) cells are an abundant population of innate-like T cells in humans that are activated by an antigen(s) bound to the MHC class I-like molecule MR1. Although the identity of MR1-restricted antigen(s) is unknown, it is present in numerous bacteria and yeast. Here we show that the structure and chemistry within the antigen-binding cleft of MR1 is distinct from the MHC and CD1 families. MR1 is ideally suited to bind ligands originating from vitamin metabolites. The structure of MR1 in complex with 6-formyl pterin, a folic acid (vitamin B9) metabolite, shows the pterin ring sequestered within MR1. Furthermore, we characterize related MR1-restricted vitamin derivatives, originating from the bacterial riboflavin (vitamin B2) biosynthetic pathway, which specifically and potently activate MAIT cells. Accordingly, we show that metabolites of vitamin B represent a class of antigen that are presented by MR1 for MAIT-cell immunosurveillance. As many vitamin biosynthetic pathways are unique to bacteria and yeast, our data suggest that MAIT cells use these metabolites to detect microbial infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kjer-Nielsen, Lars -- Patel, Onisha -- Corbett, Alexandra J -- Le Nours, Jerome -- Meehan, Bronwyn -- Liu, Ligong -- Bhati, Mugdha -- Chen, Zhenjun -- Kostenko, Lyudmila -- Reantragoon, Rangsima -- Williamson, Nicholas A -- Purcell, Anthony W -- Dudek, Nadine L -- McConville, Malcolm J -- O'Hair, Richard A J -- Khairallah, George N -- Godfrey, Dale I -- Fairlie, David P -- Rossjohn, Jamie -- McCluskey, James -- England -- Nature. 2012 Nov 29;491(7426):717-23. doi: 10.1038/nature11605. Epub 2012 Oct 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology & Immunology, University of Melbourne, Parkville, Victoria 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23051753" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen Presentation ; Bacterial Infections/immunology/microbiology ; Binding Sites ; Cell Line ; Crystallography, X-Ray ; Folic Acid/chemistry/immunology/*metabolism ; Histocompatibility Antigens/chemistry/immunology ; Histocompatibility Antigens Class I/*chemistry/*immunology/metabolism ; Humans ; Immunologic Surveillance/immunology ; Jurkat Cells ; Ligands ; Lymphocyte Activation ; Models, Molecular ; Protein Refolding/drug effects ; Pterins/*chemistry/*immunology/metabolism/pharmacology ; Salmonella/immunology/metabolism ; Salmonella Infections/immunology/microbiology ; Static Electricity ; T-Lymphocytes/*immunology ; beta 2-Microglobulin/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    A novel retinoblastoma therapy from genomic and epigenetic analyses (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-01-13
    Description: Retinoblastoma is an aggressive childhood cancer of the developing retina that is initiated by the biallelic loss of RB1. Tumours progress very quickly following RB1 inactivation but the underlying mechanism is not known. Here we show that the retinoblastoma genome is stable, but that multiple cancer pathways can be epigenetically deregulated. To identify the mutations that cooperate with RB1 loss, we performed whole-genome sequencing of retinoblastomas. The overall mutational rate was very low; RB1 was the only known cancer gene mutated. We then evaluated the role of RB1 in genome stability and considered non-genetic mechanisms of cancer pathway deregulation. For example, the proto-oncogene SYK is upregulated in retinoblastoma and is required for tumour cell survival. Targeting SYK with a small-molecule inhibitor induced retinoblastoma tumour cell death in vitro and in vivo. Thus, retinoblastomas may develop quickly as a result of the epigenetic deregulation of key cancer pathways as a direct or indirect result of RB1 loss.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3289956/" 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/PMC3289956/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jinghui -- Benavente, Claudia A -- McEvoy, Justina -- Flores-Otero, Jacqueline -- Ding, Li -- Chen, Xiang -- Ulyanov, Anatoly -- Wu, Gang -- Wilson, Matthew -- Wang, Jianmin -- Brennan, Rachel -- Rusch, Michael -- Manning, Amity L -- Ma, Jing -- Easton, John -- Shurtleff, Sheila -- Mullighan, Charles -- Pounds, Stanley -- Mukatira, Suraj -- Gupta, Pankaj -- Neale, Geoff -- Zhao, David -- Lu, Charles -- Fulton, Robert S -- Fulton, Lucinda L -- Hong, Xin -- Dooling, David J -- Ochoa, Kerri -- Naeve, Clayton -- Dyson, Nicholas J -- Mardis, Elaine R -- Bahrami, Armita -- Ellison, David -- Wilson, Richard K -- Downing, James R -- Dyer, Michael A -- CA21765/CA/NCI NIH HHS/ -- CA64402/CA/NCI NIH HHS/ -- EY014867/EY/NEI NIH HHS/ -- EY018599/EY/NEI NIH HHS/ -- GM81607/GM/NIGMS NIH HHS/ -- R01 CA155202/CA/NCI NIH HHS/ -- R01 EY014867/EY/NEI NIH HHS/ -- R01 EY014867-02/EY/NEI NIH HHS/ -- R01 EY018599/EY/NEI NIH HHS/ -- R01 EY018599-03/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jan 11;481(7381):329-34. doi: 10.1038/nature10733.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Computational Biology and Bioinformatics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22237022" target="_blank"〉PubMed〈/a〉
    Keywords: Aneuploidy ; Animals ; Cell Death/drug effects ; Cell Line ; Cell Survival/drug effects ; Chromosomal Instability/genetics ; Epigenesis, Genetic/*genetics ; Gene Expression Regulation, Neoplastic ; Genes, Retinoblastoma/genetics ; *Genomics ; Humans ; Intracellular Signaling Peptides and Proteins/antagonists & ; inhibitors/genetics/metabolism ; Mice ; *Molecular Targeted Therapy ; Mutation/genetics ; Protein Kinase Inhibitors/*pharmacology/therapeutic use ; Protein-Tyrosine Kinases/antagonists & inhibitors/genetics/metabolism ; Retinoblastoma/*drug therapy/*genetics/pathology ; Retinoblastoma Protein/deficiency/genetics ; Sequence Analysis, DNA ; Xenograft Model Antitumor Assays
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-24
    Description: The identification of somatic activating mutations in JAK2 (refs 1-4) and in the thrombopoietin receptor gene (MPL) in most patients with myeloproliferative neoplasm (MPN) led to the clinical development of JAK2 kinase inhibitors. JAK2 inhibitor therapy improves MPN-associated splenomegaly and systemic symptoms but does not significantly decrease or eliminate the MPN clone in most patients with MPN. We therefore sought to characterize mechanisms by which MPN cells persist despite chronic inhibition of JAK2. Here we show that JAK2 inhibitor persistence is associated with reactivation of JAK-STAT signalling and with heterodimerization between activated JAK2 and JAK1 or TYK2, consistent with activation of JAK2 in trans by other JAK kinases. Further, this phenomenon is reversible: JAK2 inhibitor withdrawal is associated with resensitization to JAK2 kinase inhibitors and with reversible changes in JAK2 expression. We saw increased JAK2 heterodimerization and sustained JAK2 activation in cell lines, in murine models and in patients treated with JAK2 inhibitors. RNA interference and pharmacological studies show that JAK2-inhibitor-persistent cells remain dependent on JAK2 protein expression. Consequently, therapies that result in JAK2 degradation retain efficacy in persistent cells and may provide additional benefit to patients with JAK2-dependent malignancies treated with JAK2 inhibitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991463/" 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/PMC3991463/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koppikar, Priya -- Bhagwat, Neha -- Kilpivaara, Outi -- Manshouri, Taghi -- Adli, Mazhar -- Hricik, Todd -- Liu, Fan -- Saunders, Lindsay M -- Mullally, Ann -- Abdel-Wahab, Omar -- Leung, Laura -- Weinstein, Abby -- Marubayashi, Sachie -- Goel, Aviva -- Gonen, Mithat -- Estrov, Zeev -- Ebert, Benjamin L -- Chiosis, Gabriela -- Nimer, Stephen D -- Bernstein, Bradley E -- Verstovsek, Srdan -- Levine, Ross L -- 1R01CA151949-01/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- R01 CA151949/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Sep 6;489(7414):155-9. doi: 10.1038/nature11303.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22820254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Disease Models, Animal ; Drug Resistance, Neoplasm/drug effects ; Enzyme Activation/drug effects ; Gene Knockdown Techniques ; Granulocytes/drug effects/enzymology/metabolism ; HSP90 Heat-Shock Proteins/antagonists & inhibitors/metabolism ; Humans ; Janus Kinase 1/biosynthesis/deficiency/genetics/metabolism ; Janus Kinase 2/*antagonists & inhibitors/deficiency/genetics/*metabolism ; Mice ; Myeloproliferative Disorders/*drug therapy/enzymology/metabolism/pathology ; Phosphorylation ; Protein Biosynthesis ; *Protein Multimerization ; RNA Interference ; STAT Transcription Factors/*metabolism ; *Signal Transduction/drug effects ; TYK2 Kinase/biosynthesis/deficiency/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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    Androgenetic haploid embryonic stem cells produce live transgenic mice (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-02
    Description: Haploids and double haploids are important resources for studying recessive traits and have large impacts on crop breeding, but natural haploids are rare in animals. Mammalian haploids are restricted to germline cells and are occasionally found in tumours with massive chromosome loss. Recent success in establishing haploid embryonic stem (ES) cells in medaka fish and mice raised the possibility of using engineered mammalian haploid cells in genetic studies. However, the availability and functional characterization of mammalian haploid ES cells are still limited. Here we show that mouse androgenetic haploid ES (ahES) cell lines can be established by transferring sperm into an enucleated oocyte. The ahES cells maintain haploidy and stable growth over 30 passages, express pluripotent markers, possess the ability to differentiate into all three germ layers in vitro and in vivo, and contribute to germlines of chimaeras when injected into blastocysts. Although epigenetically distinct from sperm cells, the ahES cells can produce viable and fertile progenies after intracytoplasmic injection into mature oocytes. The oocyte-injection procedure can also produce viable transgenic mice from genetically engineered ahES cells. Our findings show the developmental pluripotency of androgenentic haploids and provide a new tool to quickly produce genetic models for recessive traits. They may also shed new light on assisted reproduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Wei -- Shuai, Ling -- Wan, Haifeng -- Dong, Mingzhu -- Wang, Meng -- Sang, Lisi -- Feng, Chunjing -- Luo, Guan-Zheng -- Li, Tianda -- Li, Xin -- Wang, Libin -- Zheng, Qin-Yuan -- Sheng, Chao -- Wu, Hua-Jun -- Liu, Zhonghua -- Liu, Lei -- Wang, Liu -- Wang, Xiu-Jie -- Zhao, Xiao-Yang -- Zhou, Qi -- England -- Nature. 2012 Oct 18;490(7420):407-11. doi: 10.1038/nature11435. Epub 2012 Sep 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23023130" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/*metabolism ; Animals ; Biomarkers/metabolism ; Blastocyst/cytology ; Cell Line ; Cell Nucleus ; Chimera/embryology/genetics ; Embryonic Stem Cells/cytology/*physiology ; Epigenesis, Genetic ; Female ; *Haploidy ; Male ; Mice ; Mice, Transgenic/embryology/genetics/*growth & development ; Models, Animal ; Models, Genetic ; Oocytes/cytology/growth & development/metabolism ; Pluripotent Stem Cells/cytology/physiology ; Sperm Injections, Intracytoplasmic ; Spermatozoa/metabolism/transplantation
    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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