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  • Cell Line  (59)
  • American Association for the Advancement of Science (AAAS)  (59)
  • American Physical Society
  • EMBO Press
  • Essen : Verl. Glückauf
  • Institute of Physics
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • 2005-2009  (59)
  • 2008  (59)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (59)
  • American Physical Society
  • EMBO Press
  • Essen : Verl. Glückauf
  • Institute of Physics
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Years
  • 2005-2009  (59)
Year
  • 1
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    Medicine. The cart before the horse (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rowley, Janet D -- Blumenthal, Thomas -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1302-4. doi: 10.1126/science.1163791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, 5841 South Maryland Avenue, MC 2115, Chicago, IL 60637, USA. jrowley@medicine.bsd.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772424" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosomes, Human, Pair 17/genetics ; Chromosomes, Human, Pair 7/genetics ; Endometrial Neoplasms/genetics ; Endometrium/cytology/*metabolism ; Female ; Gene Fusion ; Gene Rearrangement ; Humans ; Macaca mulatta ; Menstrual Cycle ; Neoplasm Proteins/*genetics ; RNA, Guide/genetics ; RNA, Messenger/*genetics ; *Trans-Splicing ; Transcription Factors/*genetics ; *Translocation, 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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  • 2
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    Molecular coupling of Xist regulation and pluripotency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-20
    Description: During mouse embryogenesis, reversion of imprinted X chromosome inactivation in the pluripotent inner cell mass of the female blastocyst is initiated by the repression of Xist from the paternal X chromosome. Here we report that key factors supporting pluripotency-Nanog, Oct3/4, and Sox2-bind within Xist intron 1 in undifferentiated embryonic stem (ES) cells. Whereas Nanog null ES cells display a reversible and moderate up-regulation of Xist in the absence of any apparent modification of Oct3/4 and Sox2 binding, the drastic release of all three factors from Xist intron 1 triggers rapid ectopic accumulation of Xist RNA. We conclude that the three main genetic factors underlying pluripotency cooperate to repress Xist and thus couple X inactivation reprogramming to the control of pluripotency during embryogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Navarro, Pablo -- Chambers, Ian -- Karwacki-Neisius, Violetta -- Chureau, Corinne -- Morey, Celine -- Rougeulle, Claire -- Avner, Philip -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1693-5. doi: 10.1126/science.1160952.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Unite de Genetique Moleculaire Murine, CNRS, URA2578, F-75015, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18802003" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst Inner Cell Mass/metabolism ; Cell Differentiation ; Cell Line ; DNA-Binding Proteins/*metabolism ; Embryonic Stem Cells/cytology/*metabolism ; Female ; HMGB Proteins/*metabolism ; Homeodomain Proteins/genetics/*metabolism ; Introns ; Male ; Mice ; Octamer Transcription Factor-3/genetics/*metabolism ; Pluripotent Stem Cells/cytology/*metabolism ; RNA, Long Noncoding ; RNA, Untranslated/*genetics/metabolism ; SOXB1 Transcription Factors ; Transcription Factors/*metabolism ; Up-Regulation ; X Chromosome/physiology ; *X Chromosome Inactivation
    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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    Regulation of CD45 alternative splicing by heterogeneous ribonucleoprotein, hnRNPLL (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: The transition from naive to activated T cells is marked by alternative splicing of pre-mRNA encoding the transmembrane phosphatase CD45. Using a short hairpin RNA interference screen, we identified heterogeneous ribonucleoprotein L-like (hnRNPLL) as a critical inducible regulator of CD45 alternative splicing. HnRNPLL was up-regulated in stimulated T cells, bound CD45 transcripts, and was both necessary and sufficient for CD45 alternative splicing. Depletion or overexpression of hnRNPLL in B and T cell lines and primary T cells resulted in reciprocal alteration of CD45RA and RO expression. Exon array analysis suggested that hnRNPLL acts as a global regulator of alternative splicing in activated T cells. Induction of hnRNPLL during hematopoietic cell activation and differentiation may allow cells to rapidly shift their transcriptomes to favor proliferation and inhibit cell death.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791692/" 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/PMC2791692/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oberdoerffer, Shalini -- Moita, Luis Ferreira -- Neems, Daniel -- Freitas, Rui P -- Hacohen, Nir -- Rao, Anjana -- AI40127/AI/NIAID NIH HHS/ -- AI44432/AI/NIAID NIH HHS/ -- CA42471/CA/NCI NIH HHS/ -- R01 AI040127/AI/NIAID NIH HHS/ -- R01 AI040127-18/AI/NIAID NIH HHS/ -- R01 AI040127-19/AI/NIAID NIH HHS/ -- R01 AI044432/AI/NIAID NIH HHS/ -- R01 AI044432-09/AI/NIAID NIH HHS/ -- R01 AI044432-10/AI/NIAID NIH HHS/ -- R01 AI080875/AI/NIAID NIH HHS/ -- R01 AI080875-01/AI/NIAID NIH HHS/ -- R01 CA042471/CA/NCI NIH HHS/ -- R01 CA042471-23/CA/NCI NIH HHS/ -- R21 AI071060/AI/NIAID NIH HHS/ -- R21 AI071060-01/AI/NIAID NIH HHS/ -- R21 AI071060-02/AI/NIAID NIH HHS/ -- T32 HL066987/HL/NHLBI NIH HHS/ -- U19 AI070352/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):686-91. doi: 10.1126/science.1157610. Epub 2008 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669861" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Antigens, CD45/chemistry/*genetics ; B-Lymphocytes/immunology/metabolism ; CD4-Positive T-Lymphocytes/*immunology/*metabolism ; Cell Line ; Cell Line, Tumor ; Heterogeneous-Nuclear Ribonucleoproteins/genetics/*metabolism ; Humans ; Lentivirus/genetics/physiology ; *Lymphocyte Activation ; Protein Isoforms/chemistry/genetics ; RNA Interference ; STAT5 Transcription Factor/genetics ; T-Lymphocytes/*immunology/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic ; Transduction, Genetic ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 4
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    ERdj5 is required as a disulfide reductase for degradation of misfolded proteins in the ER (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-26
    Description: Membrane and secretory proteins cotranslationally enter and are folded in the endoplasmic reticulum (ER). Misfolded or unassembled proteins are discarded by a process known as ER-associated degradation (ERAD), which involves their retrotranslocation into the cytosol. ERAD substrates frequently contain disulfide bonds that must be cleaved before their retrotranslocation. Here, we found that an ER-resident protein ERdj5 had a reductase activity, cleaved the disulfide bonds of misfolded proteins, and accelerated ERAD through its physical and functional associations with EDEM (ER degradation-enhancing alpha-mannosidase-like protein) and an ER-resident chaperone BiP. Thus, ERdj5 is a member of a supramolecular ERAD complex that recognizes and unfolds misfolded proteins for their efficient retrotranslocation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ushioda, Ryo -- Hoseki, Jun -- Araki, Kazutaka -- Jansen, Gregor -- Thomas, David Y -- Nagata, Kazuhiro -- New York, N.Y. -- Science. 2008 Jul 25;321(5888):569-72. doi: 10.1126/science.1159293.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18653895" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cell Line ; Endoplasmic Reticulum/*metabolism ; Glutathione/metabolism ; HSP40 Heat-Shock Proteins/chemistry/genetics/*metabolism ; Heat-Shock Proteins/metabolism ; Humans ; Immunoglobulin J-Chains/chemistry/metabolism ; Membrane Proteins/metabolism ; Mice ; Molecular Chaperones/chemistry/genetics/*metabolism ; Mutation ; Oxidation-Reduction ; Protein Disulfide Reductase (Glutathione)/metabolism ; Protein Disulfide-Isomerases/metabolism ; Protein Folding ; Protein Structure, Tertiary ; Proteins/chemistry/*metabolism ; Recombinant Proteins/chemistry/metabolism ; Transfection ; Two-Hybrid System Techniques ; alpha 1-Antitrypsin/chemistry/metabolism
    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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    Ceramide triggers budding of exosome vesicles into multivesicular endosomes (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-01
    Description: Intraluminal vesicles of multivesicular endosomes are either sorted for cargo degradation into lysosomes or secreted as exosomes into the extracellular milieu. The mechanisms underlying the sorting of membrane into the different populations of intraluminal vesicles are unknown. Here, we find that cargo is segregated into distinct subdomains on the endosomal membrane and that the transfer of exosome-associated domains into the lumen of the endosome did not depend on the function of the ESCRT (endosomal sorting complex required for transport) machinery, but required the sphingolipid ceramide. Purified exosomes were enriched in ceramide, and the release of exosomes was reduced after the inhibition of neutral sphingomyelinases. These results establish a pathway in intraendosomal membrane transport and exosome formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trajkovic, Katarina -- Hsu, Chieh -- Chiantia, Salvatore -- Rajendran, Lawrence -- Wenzel, Dirk -- Wieland, Felix -- Schwille, Petra -- Brugger, Britta -- Simons, Mikael -- New York, N.Y. -- Science. 2008 Feb 29;319(5867):1244-7. doi: 10.1126/science.1153124.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Biochemistry and Molecular Cell Biology, University of Gottingen, 37073 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18309083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Line, Tumor ; Ceramides/analysis/*metabolism ; Cytoplasmic Vesicles/chemistry/*metabolism/ultrastructure ; Endosomes/*metabolism/ultrastructure ; Humans ; Intracellular Membranes/*metabolism/ultrastructure ; Membrane Microdomains/*metabolism/ultrastructure ; Mice ; Myelin Proteolipid Protein/*metabolism ; Oligodendroglia/metabolism/ultrastructure ; Protein Transport ; Receptor, Epidermal Growth Factor/metabolism ; Recombinant Fusion Proteins/metabolism ; Sphingomyelin Phosphodiesterase/antagonists & inhibitors/metabolism
    Print ISSN: 0036-8075
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  • 6
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    Evidence for editing of human papillomavirus DNA by APOBEC3 in benign and precancerous lesions (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-12
    Description: Cytidine deaminases of the APOBEC3 family all have specificity for single-stranded DNA, which may become exposed during replication or transcription of double-stranded DNA. Three human APOBEC3A (hA3A), hA3B, and hA3H genes are expressed in keratinocytes and skin, leading us to determine whether genetic editing of human papillomavirus (HPV) DNA occurred. In a study of HPV1a plantar warts and HPV16 precancerous cervical biopsies, hyperedited HPV1a and HPV16 genomes were found. Strictly analogous results were obtained from transfection experiments with HPV plasmid DNA and the three nuclear localized enzymes: hA3A, hA3C, and hA3H. Thus, stochastic or transient overexpression of APOBEC3 genes may expose the genome to a broad spectrum of mutations that could influence the development of tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vartanian, Jean-Pierre -- Guetard, Denise -- Henry, Michel -- Wain-Hobson, Simon -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):230-3. doi: 10.1126/science.1153201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Retrovirology Unit, Institut Pasteur, 28 Rue de Docteur Roux, 75724 Paris cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403710" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cervix Uteri/virology ; Cytidine/metabolism ; Cytosine Deaminase/*metabolism ; DNA Mismatch Repair ; DNA, Viral/genetics/*metabolism ; Female ; Genome, Viral ; Human papillomavirus 16/*genetics ; Humans ; Mupapillomavirus/*genetics ; Mutation ; Papillomavirus Infections/enzymology/virology ; Precancerous Conditions/enzymology/*virology ; Transfection ; Uterine Cervical Neoplasms/enzymology/*virology ; Warts/enzymology/*virology
    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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    Asymmetric tethering of flat and curved lipid membranes by a golgin (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-03
    Description: Golgins, long stringlike proteins, tether cisternae and transport vesicles at the Golgi apparatus. We examined the attachment of golgin GMAP-210 to lipid membranes. GMAP-210 connected highly curved liposomes to flatter ones. This asymmetric tethering relied on motifs that sensed membrane curvature both in the N terminus of GMAP-210 and in ArfGAP1, which controlled the interaction of the C terminus of GMAP-210 with the small guanine nucleotide-binding protein Arf1. Because membrane curvature constantly changes during vesicular trafficking, this mode of tethering suggests a way to maintain the Golgi architecture without compromising membrane flow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drin, Guillaume -- Morello, Vincent -- Casella, Jean-Francois -- Gounon, Pierre -- Antonny, Bruno -- New York, N.Y. -- Science. 2008 May 2;320(5876):670-3. doi: 10.1126/science.1155821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Pharmacologie Moleculaire et Cellulaire, Universite de Nice Sophia Antipolis and CNRS, 660 route des lucioles, 06560 Valbonne, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451304" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factor 1/metabolism ; Binding Sites ; Cell Line ; GTPase-Activating Proteins/metabolism ; Golgi Apparatus/chemistry/metabolism ; HeLa Cells ; Humans ; Intracellular Membranes/*chemistry/metabolism ; Liposomes ; Membrane Lipids/*chemistry ; Nuclear Proteins/*chemistry/metabolism ; Recombinant Proteins/chemistry/metabolism
    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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  • 8
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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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  • 9
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    Reversible compartmentalization of de novo purine biosynthetic complexes in living cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-05
    Description: Purines are synthesized de novo in 10 chemical steps that are catalyzed by six enzymes in eukaryotes. Studies in vitro have provided little evidence of anticipated protein-protein interactions that would enable substrate channeling and regulation of the metabolic flux. We applied fluorescence microscopy to HeLa cells and discovered that all six enzymes colocalize to form clusters in the cellular cytoplasm. The association and dissociation of these enzyme clusters can be regulated dynamically, by either changing the purine levels of or adding exogenous agents to the culture media. Collectively, the data provide strong evidence for the formation of a multi-enzyme complex, the "purinosome," to carry out de novo purine biosynthesis in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉An, Songon -- Kumar, Ravindra -- Sheets, Erin D -- Benkovic, Stephen J -- R21 AG030949/AG/NIA NIH HHS/ -- R21 AG030949-01/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 4;320(5872):103-6. doi: 10.1126/science.1152241.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Pennsylvania State University, University Park, PA 16802, USA. sua13@psu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18388293" target="_blank"〉PubMed〈/a〉
    Keywords: Azaserine/pharmacology ; Binding Sites ; Carbon-Nitrogen Ligases/genetics/*metabolism ; Carbon-Nitrogen Ligases with Glutamine as Amide-N-Donor/genetics/*metabolism ; Cell Compartmentation ; Cell Line ; Cell Line, Tumor ; Culture Media ; Cytoplasm/*enzymology ; Fluorescent Antibody Technique ; HeLa Cells ; Humans ; Hypoxanthine/pharmacology ; Microscopy, Fluorescence ; Multienzyme Complexes/genetics/*metabolism ; Phosphoribosylglycinamide Formyltransferase/genetics/*metabolism ; Purines/*biosynthesis ; Recombinant Fusion Proteins/metabolism ; Transfection
    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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  • 10
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    The antisense transcriptomes of human cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Transcription in mammalian cells can be assessed at a genome-wide level, but it has been difficult to reliably determine whether individual transcripts are derived from the plus or minus strands of chromosomes. This distinction can be critical for understanding the relationship between known transcripts (sense) and the complementary antisense transcripts that may regulate them. Here, we describe a technique that can be used to (i) identify the DNA strand of origin for any particular RNA transcript, and (ii) quantify the number of sense and antisense transcripts from expressed genes at a global level. We examined five different human cell types and in each case found evidence for antisense transcripts in 2900 to 6400 human genes. The distribution of antisense transcripts was distinct from that of sense transcripts, was nonrandom across the genome, and differed among cell types. Antisense transcripts thus appear to be a pervasive feature of human cells, which suggests that they are a fundamental component of gene regulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824178/" 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/PMC2824178/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yiping -- Vogelstein, Bert -- Velculescu, Victor E -- Papadopoulos, Nickolas -- Kinzler, Kenneth W -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- R37 CA057345-18/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1855-7. doi: 10.1126/science.1163853. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056939" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Line, Tumor ; Exons ; Gene Expression ; *Gene Expression Profiling ; *Genome, Human ; Humans ; Introns ; Leukocytes, Mononuclear/metabolism ; Promoter Regions, Genetic ; RNA, Antisense/*genetics/metabolism ; RNA, Messenger/genetics/metabolism ; *Transcription, Genetic
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  • 11
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    Induced pluripotent stem cells generated without viral integration (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-27
    Description: Pluripotent stem cells have been generated from mouse and human somatic cells by viral expression of the transcription factors Oct4, Sox2, Klf4, and c-Myc. A major limitation of this technology is the use of potentially harmful genome-integrating viruses. We generated mouse induced pluripotent stem (iPS) cells from fibroblasts and liver cells by using nonintegrating adenoviruses transiently expressing Oct4, Sox2, Klf4, and c-Myc. These adenoviral iPS (adeno-iPS) cells show DNA demethylation characteristic of reprogrammed cells, express endogenous pluripotency genes, form teratomas, and contribute to multiple tissues, including the germ line, in chimeric mice. Our results provide strong evidence that insertional mutagenesis is not required for in vitro reprogramming. Adenoviral reprogramming may provide an improved method for generating and studying patient-specific stem cells and for comparing embryonic stem cells and iPS cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987909/" 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/PMC3987909/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stadtfeld, Matthias -- Nagaya, Masaki -- Utikal, Jochen -- Weir, Gordon -- Hochedlinger, Konrad -- DP2 OD003266/OD/NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):945-9. doi: 10.1126/science.1162494. Epub 2008 Sep 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, 185 Cambridge Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18818365" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/*genetics/physiology ; Animals ; Cell Differentiation ; Cell Line ; *Cellular Reprogramming ; Chimera ; Cloning, Molecular ; Female ; Fibroblasts/*cytology/metabolism/virology ; Genes, myc ; *Genetic Vectors ; Hepatocytes/*cytology/metabolism/virology ; Kruppel-Like Transcription Factors/genetics/metabolism ; Liver/cytology/embryology ; Male ; Mice ; Mice, SCID ; Octamer Transcription Factor-3/genetics/metabolism ; *Pluripotent Stem Cells/cytology/metabolism/transplantation ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; SOXB1 Transcription Factors/genetics/metabolism ; Teratoma/etiology ; Transgenes ; Virus Integration
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Medicine. Sidestepping mutational meltdown (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shoubridge, Eric A -- Wai, Timothy -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):914-5. doi: 10.1126/science.1154515.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Montreal Neurological Institute and Department of Human Genetics, McGill University, Montreal, Quebec H3A 2B4, Canada. eric@ericpc.mni.mcgill.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Cell Line ; DNA, Mitochondrial/*genetics ; DNA-Directed DNA Polymerase/genetics ; Electron Transport Complex IV/*genetics ; Embryonic Stem Cells ; Female ; Frameshift Mutation ; *Germ-Line Mutation ; Male ; Mice ; Mitochondria/physiology ; NADH Dehydrogenase/*genetics ; Oocytes/*physiology ; Oogenesis ; *Selection, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    A mouse model of mitochondrial disease reveals germline selection against severe mtDNA mutations (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: The majority of mitochondrial DNA (mtDNA) mutations that cause human disease are mild to moderately deleterious, yet many random mtDNA mutations would be expected to be severe. To determine the fate of the more severe mtDNA mutations, we introduced mtDNAs containing two mutations that affect oxidative phosphorylation into the female mouse germ line. The severe ND6 mutation was selectively eliminated during oogenesis within four generations, whereas the milder COI mutation was retained throughout multiple generations even though the offspring consistently developed mitochondrial myopathy and cardiomyopathy. Thus, severe mtDNA mutations appear to be selectively eliminated from the female germ line, thereby minimizing their impact on population fitness.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3049809/" 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/PMC3049809/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, Weiwei -- Waymire, Katrina G -- Narula, Navneet -- Li, Peng -- Rocher, Christophe -- Coskun, Pinar E -- Vannan, Mani A -- Narula, Jagat -- Macgregor, Grant R -- Wallace, Douglas C -- AG13154/AG/NIA NIH HHS/ -- AG16573/AG/NIA NIH HHS/ -- AG24373/AG/NIA NIH HHS/ -- DK73691/DK/NIDDK NIH HHS/ -- HD45913/HD/NICHD NIH HHS/ -- NS21328/NS/NINDS NIH HHS/ -- U01 HD045913-01/HD/NICHD NIH HHS/ -- U01 HD045913-02/HD/NICHD NIH HHS/ -- U01 HD045913-03/HD/NICHD NIH HHS/ -- U01 HD045913-04/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):958-62. doi: 10.1126/science.1147786.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular and Mitochondrial Medicine and Genetics, University of California, Irvine, CA 92697, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276892" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathies/genetics/pathology ; Cell Line ; Crosses, Genetic ; DNA, Mitochondrial/*genetics ; Electron Transport Complex I/metabolism ; Electron Transport Complex IV/*genetics/metabolism ; Embryonic Stem Cells ; Female ; Frameshift Mutation ; *Germ-Line Mutation ; Litter Size ; Male ; Mice ; Mitochondria/physiology ; Mitochondrial Myopathies/*genetics/pathology ; Mutation, Missense ; Myocardium/pathology ; NADH Dehydrogenase/*genetics ; Oocytes/*physiology ; Oogenesis ; Oxidative Phosphorylation ; Oxygen Consumption ; Point Mutation ; *Selection, Genetic
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  • 14
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    Adenovirus small e1a alters global patterns of histone modification (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-23
    Description: Adenovirus small early region 1a (e1a) protein drives cells into S phase by binding RB family proteins and the closely related histone acetyl transferases p300 and CBP. The interaction with RB proteins displaces them from DNA-bound E2F transcription factors, reversing their repression of cell cycle genes. However, it has been unclear how the e1a interaction with p300 and CBP promotes passage through the cell cycle. We show that this interaction causes a threefold reduction in total cellular histone H3 lysine 18 acetylation (H3K18ac). CBP and p300 are required for acetylation at this site because their knockdown causes specific hypoacetylation at H3K18. SV40 T antigen also induces H3K18 hypoacetylation. Because global hypoacetylation at this site is observed in prostate carcinomas with poor prognosis, this suggests that processes resulting in global H3K18 hypoacetylation may be linked to oncogenic transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756290/" 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/PMC2756290/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horwitz, Gregory A -- Zhang, Kangling -- McBrian, Matthew A -- Grunstein, Michael -- Kurdistani, Siavash K -- Berk, Arnold J -- CA25235/CA/NCI NIH HHS/ -- R37 CA025235/CA/NCI NIH HHS/ -- R37 CA025235-30/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1084-5. doi: 10.1126/science.1155544.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719283" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Adenovirus E1A Proteins/genetics/*metabolism ; Adenoviruses, Human/*metabolism ; Antigens, Polyomavirus Transforming/metabolism ; CREB-Binding Protein/metabolism ; *Cell Cycle ; Cell Line ; Cell Transformation, Viral ; Cells, Cultured ; HeLa Cells ; Histones/*metabolism ; Humans ; Lysine/metabolism ; Mutation ; p300-CBP Transcription Factors/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Phosphorylation of retinoblastoma protein by viral protein with cyclin-dependent kinase function (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-10
    Description: As obligate intracellular parasites, viruses expertly modify cellular processes to facilitate their replication and spread, often by encoding genes that mimic the functions of cellular proteins while lacking regulatory features that modify their activity. We show that the human cytomegalovirus UL97 protein has activities similar to cellular cyclin-cyclin-dependent kinase (CDK) complexes. UL97 phosphorylated and inactivated the retinoblastoma tumor suppressor, stimulated cell cycle progression in mammalian cells, and rescued proliferation of Saccharomyces cerevisiae lacking CDK activity. UL97 is not inhibited by the CDK inhibitor p21 and lacks amino acid residues conserved in the CDKs that permit the attenuation of kinase activity. Thus, UL97 represents a functional ortholog of cellular CDKs that is immune from normal CDK control mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hume, Adam J -- Finkel, Jonathan S -- Kamil, Jeremy P -- Coen, Donald M -- Culbertson, Michael R -- Kalejta, Robert F -- AI26077/AI/NIAID NIH HHS/ -- GM65172/GM/NIGMS NIH HHS/ -- R56-AI064703/AI/NIAID NIH HHS/ -- T32 AI07245/AI/NIAID NIH HHS/ -- T32 CA009135-31/CA/NCI NIH HHS/ -- T32 GM007215/GM/NIGMS NIH HHS/ -- T32 GM077078-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 9;320(5877):797-9. doi: 10.1126/science.1152095.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Virology and McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18467589" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; Cell Line ; Cyclin-Dependent Kinases/antagonists & inhibitors/*metabolism ; Cytomegalovirus/enzymology/*physiology ; Humans ; Molecular Mimicry ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors/*metabolism ; Protein Kinase Inhibitors/pharmacology ; Retinoblastoma Protein/*metabolism
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  • 16
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    Phosphorylation networks regulating JNK activity in diverse genetic backgrounds (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-10-18
    Description: Cellular signaling networks have evolved to enable swift and accurate responses, even in the face of genetic or environmental perturbation. Thus, genetic screens may not identify all the genes that regulate different biological processes. Moreover, although classical screening approaches have succeeded in providing parts lists of the essential components of signaling networks, they typically do not provide much insight into the hierarchical and functional relations that exist among these components. We describe a high-throughput screen in which we used RNA interference to systematically inhibit two genes simultaneously in 17,724 combinations to identify regulators of Drosophila JUN NH(2)-terminal kinase (JNK). Using both genetic and phosphoproteomics data, we then implemented an integrative network algorithm to construct a JNK phosphorylation network, which provides structural and mechanistic insights into the systems architecture of JNK signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581798/" 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/PMC2581798/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakal, Chris -- Linding, Rune -- Llense, Flora -- Heffern, Elleard -- Martin-Blanco, Enrique -- Pawson, Tony -- Perrimon, Norbert -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):453-6. doi: 10.1126/science.1158739.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02215, USA. cbakal@receptor.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927396" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Line ; Computational Biology ; Drosophila/*enzymology/genetics ; Drosophila Proteins/genetics/*metabolism ; Fluorescence Resonance Energy Transfer ; *Genes, Insect ; JNK Mitogen-Activated Protein Kinases/genetics/*metabolism ; *MAP Kinase Signaling System ; Metabolic Networks and Pathways ; Phosphorylation ; Proteomics ; RNA Interference ; Signal Transduction
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  • 17
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    Four-jointed is a Golgi kinase that phosphorylates a subset of cadherin domains (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-19
    Description: The atypical cadherin Fat acts as a receptor for a signaling pathway that regulates growth, gene expression, and planar cell polarity. Genetic studies in Drosophila identified the four-jointed gene as a regulator of Fat signaling. We show that four-jointed encodes a protein kinase that phosphorylates serine or threonine residues within extracellular cadherin domains of Fat and its transmembrane ligand, Dachsous. Four-jointed functions in the Golgi and is the first molecularly defined kinase that phosphorylates protein domains destined to be extracellular. An acidic sequence motif (Asp-Asn-Glu) within Four-jointed was essential for its kinase activity in vitro and for its biological activity in vivo. Our results indicate that Four-jointed regulates Fat signaling by phosphorylating cadherin domains of Fat and Dachsous as they transit through the Golgi.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562711/" 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/PMC2562711/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishikawa, Hiroyuki O -- Takeuchi, Hideyuki -- Haltiwanger, Robert S -- Irvine, Kenneth D -- CA123071/CA/NCI NIH HHS/ -- GM061126/GM/NIGMS NIH HHS/ -- GM078620/GM/NIGMS NIH HHS/ -- R01 CA123071/CA/NCI NIH HHS/ -- R01 CA123071-02/CA/NCI NIH HHS/ -- R01 GM061126/GM/NIGMS NIH HHS/ -- R01 GM061126-08/GM/NIGMS NIH HHS/ -- R01 GM078620/GM/NIGMS NIH HHS/ -- R01 GM078620-02/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jul 18;321(5887):401-4. doi: 10.1126/science.1158159.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18635802" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cadherins/chemistry/*metabolism ; Cell Adhesion Molecules/chemistry/*metabolism ; Cell Line ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster ; Electrophoretic Mobility Shift Assay ; Glycosylation ; Golgi Apparatus/enzymology/*metabolism ; Kinetics ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Phosphorylation ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism
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  • 18
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    Global protein stability profiling in mammalian cells (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-08
    Description: The abundance of cellular proteins is determined largely by the rate of transcription and translation coupled with the stability of individual proteins. Although we know a great deal about global transcript abundance, little is known about global protein stability. We present a highly parallel multiplexing strategy to monitor protein turnover on a global scale by coupling flow cytometry with microarray technology to track the stability of individual proteins within a complex mixture. We demonstrated the feasibility of this approach by measuring the stability of approximately 8000 human proteins and identifying proteasome substrates. The technology provides a general platform for proteome-scale analysis of protein turnover under various physiological and disease conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yen, Hsueh-Chi Sherry -- Xu, Qikai -- Chou, Danny M -- Zhao, Zhenming -- Elledge, Stephen J -- AG11085/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):918-23. doi: 10.1126/science.1160489.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Center for Genetics and Genomics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988847" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/analysis ; Cell Cycle ; Cell Line ; DNA, Complementary ; Flow Cytometry ; Green Fluorescent Proteins/analysis/metabolism ; Half-Life ; Humans ; Luminescent Proteins/analysis/metabolism ; Oligonucleotide Array Sequence Analysis ; Open Reading Frames ; Proteasome Endopeptidase Complex/*metabolism ; Protein Biosynthesis ; *Protein Stability ; Proteins/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Transcription, Genetic
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  • 19
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    Membrane phosphatidylserine regulates surface charge and protein localization (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-01-12
    Description: Electrostatic interactions with negatively charged membranes contribute to the subcellular targeting of proteins with polybasic clusters or cationic domains. Although the anionic phospholipid phosphatidylserine is comparatively abundant, its contribution to the surface charge of individual cellular membranes is unknown, partly because of the lack of reagents to analyze its distribution in intact cells. We developed a biosensor to study the subcellular distribution of phosphatidylserine and found that it binds the cytosolic leaflets of the plasma membrane, as well as endosomes and lysosomes. The negative charge associated with the presence of phosphatidylserine directed proteins with moderately positive charge to the endocytic pathway. More strongly cationic proteins, normally associated with the plasma membrane, relocalized to endocytic compartments when the plasma membrane surface charge decreased on calcium influx.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Tony -- Gilbert, Gary E -- Shi, Jialan -- Silvius, John -- Kapus, Andras -- Grinstein, Sergio -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):210-3. doi: 10.1126/science.1152066.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Hospital for Sick Children, Toronto M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biosensing Techniques ; Cell Line ; Cell Membrane/*metabolism ; Endocytosis ; Endosomes/*metabolism ; Fluorescence ; Fluorescence Resonance Energy Transfer ; Humans ; Hydrophobic and Hydrophilic Interactions ; Intracellular Membranes/*metabolism ; Lysosomes/*metabolism ; Microscopy, Confocal ; Milk Proteins/metabolism ; Organelles/metabolism ; Phosphatidylserines/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/metabolism ; Signal Transduction ; Static Electricity ; Surface Properties
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  • 20
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    Regulated protein denitrosylation by cytosolic and mitochondrial thioredoxins (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-24
    Description: Nitric oxide acts substantially in cellular signal transduction through stimulus-coupled S-nitrosylation of cysteine residues. The mechanisms that might subserve protein denitrosylation in cellular signaling remain uncharacterized. Our search for denitrosylase activities focused on caspase-3, an exemplar of stimulus-dependent denitrosylation, and identified thioredoxin and thioredoxin reductase in a biochemical screen. In resting human lymphocytes, thioredoxin-1 actively denitrosylated cytosolic caspase-3 and thereby maintained a low steady-state amount of S-nitrosylation. Upon stimulation of Fas, thioredoxin-2 mediated denitrosylation of mitochondria-associated caspase-3, a process required for caspase-3 activation, and promoted apoptosis. Inhibition of thioredoxin-thioredoxin reductases enabled identification of additional substrates subject to endogenous S-nitrosylation. Thus, specific enzymatic mechanisms may regulate basal and stimulus-induced denitrosylation in mammalian cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754768/" 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/PMC2754768/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benhar, Moran -- Forrester, Michael T -- Hess, Douglas T -- Stamler, Jonathan S -- P01 HL075443/HL/NHLBI NIH HHS/ -- P01 HL075443-050003/HL/NHLBI NIH HHS/ -- R01 HL059130/HL/NHLBI NIH HHS/ -- R01 HL059130-11/HL/NHLBI NIH HHS/ -- U19 ES012496/ES/NIEHS NIH HHS/ -- U19 ES012496-05/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 23;320(5879):1050-4. doi: 10.1126/science.1158265.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/metabolism ; Apoptosis ; Auranofin/pharmacology ; Binding Sites ; Caspase 3/metabolism ; Caspase Inhibitors ; Cell Line ; Cytosol/*metabolism ; Dinitrochlorobenzene/pharmacology ; HeLa Cells ; Humans ; Jurkat Cells ; Macrophages/metabolism ; Mitochondria/enzymology/*metabolism ; Mitochondrial Proteins/*metabolism ; Nitric Oxide/*metabolism ; Rats ; Recombinant Proteins/metabolism ; S-Nitrosothiols/*metabolism ; T-Lymphocytes/metabolism ; Thioredoxin-Disulfide Reductase/*metabolism ; Thioredoxins/*metabolism
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    Human CHN1 mutations hyperactivate alpha2-chimaerin and cause Duane's retraction syndrome (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-07-26
    Description: Duane's retraction syndrome (DRS) is a complex congenital eye movement disorder caused by aberrant innervation of the extraocular muscles by axons of brainstem motor neurons. Studying families with a variant form of the disorder (DURS2-DRS), we have identified causative heterozygous missense mutations in CHN1, a gene on chromosome 2q31 that encodes alpha2-chimaerin, a Rac guanosine triphosphatase-activating protein (RacGAP) signaling protein previously implicated in the pathfinding of corticospinal axons in mice. We found that these are gain-of-function mutations that increase alpha2-chimaerin RacGAP activity in vitro. Several of the mutations appeared to enhance alpha2-chimaerin translocation to the cell membrane or enhance its ability to self-associate. Expression of mutant alpha2-chimaerin constructs in chick embryos resulted in failure of oculomotor axons to innervate their target extraocular muscles. We conclude that alpha2-chimaerin has a critical developmental function in ocular motor axon pathfinding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593867/" 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/PMC2593867/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyake, Noriko -- Chilton, John -- Psatha, Maria -- Cheng, Long -- Andrews, Caroline -- Chan, Wai-Man -- Law, Krystal -- Crosier, Moira -- Lindsay, Susan -- Cheung, Michelle -- Allen, James -- Gutowski, Nick J -- Ellard, Sian -- Young, Elizabeth -- Iannaccone, Alessandro -- Appukuttan, Binoy -- Stout, J Timothy -- Christiansen, Stephen -- Ciccarelli, Maria Laura -- Baldi, Alfonso -- Campioni, Mara -- Zenteno, Juan C -- Davenport, Dominic -- Mariani, Laura E -- Sahin, Mustafa -- Guthrie, Sarah -- Engle, Elizabeth C -- G9900837/Medical Research Council/United Kingdom -- G9900989/Medical Research Council/United Kingdom -- R01 EY015298/EY/NEI NIH HHS/ -- R01 EY015298-01/EY/NEI NIH HHS/ -- R01 EY015298-02/EY/NEI NIH HHS/ -- R01 EY015298-03/EY/NEI NIH HHS/ -- R01 EY015298-04/EY/NEI NIH HHS/ -- R01 EY015298-05/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 8;321(5890):839-43. doi: 10.1126/science.1156121. Epub 2008 Jul 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine (Genetics), Children's Hospital Boston, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18653847" target="_blank"〉PubMed〈/a〉
    Keywords: Abducens Nerve/abnormalities ; Amino Acid Sequence ; Animals ; Axons/physiology ; Cell Line ; Cell Membrane/metabolism ; Chick Embryo ; Chimerin 1/chemistry/*genetics/*metabolism ; Duane Retraction Syndrome/*genetics ; Female ; Gene Expression Profiling ; Heterozygote ; Humans ; Male ; Molecular Sequence Data ; *Mutation, Missense ; Oculomotor Muscles/embryology/innervation/metabolism ; Oculomotor Nerve/abnormalities/embryology ; Pedigree
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    Polycomb proteins targeted by a short repeat RNA to the mouse X chromosome (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-01
    Description: To equalize X-chromosome dosages between the sexes, the female mammal inactivates one of her two X chromosomes. X-chromosome inactivation (XCI) is initiated by expression of Xist, a 17-kb noncoding RNA (ncRNA) that accumulates on the X in cis. Because interacting factors have not been isolated, the mechanism by which Xist induces silencing remains unknown. We discovered a 1.6-kilobase ncRNA (RepA) within Xist and identified the Polycomb complex, PRC2, as its direct target. PRC2 is initially recruited to the X by RepA RNA, with Ezh2 serving as the RNA binding subunit. The antisense Tsix RNA inhibits this interaction. RepA depletion abolishes full-length Xist induction and trimethylation on lysine 27 of histone H3 of the X. Likewise, PRC2 deficiency compromises Xist up-regulation. Therefore, RepA, together with PRC2, is required for the initiation and spread of XCI. We conclude that a ncRNA cofactor recruits Polycomb complexes to their target locus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748911/" 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/PMC2748911/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Jing -- Sun, Bryan K -- Erwin, Jennifer A -- Song, Ji-Joon -- Lee, Jeannie T -- R01 GM058839/GM/NIGMS NIH HHS/ -- R01 GM058839-10/GM/NIGMS NIH HHS/ -- R01 GM110090/GM/NIGMS NIH HHS/ -- R01GM58839/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Oct 31;322(5902):750-6. doi: 10.1126/science.1163045.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18974356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chromatin Immunoprecipitation ; Electrophoretic Mobility Shift Assay ; Embryonic Stem Cells ; Female ; Fibroblasts ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Polycomb-Group Proteins ; Polymerase Chain Reaction ; RNA, Long Noncoding ; RNA, Untranslated/genetics/*metabolism ; Repetitive Sequences, Nucleic Acid ; Repressor Proteins/*metabolism ; Up-Regulation ; X Chromosome/*metabolism ; X Chromosome Inactivation
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    Research ethics. When embryonic stem cell lines fail to meet consent standards (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugarman, Jeremy -- Siegel, Andrew W -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):379. doi: 10.1126/science.1164441.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Berman Institute of Bioethics, Johns Hopkins University, Baltimore, MD 21205, USA. jsugarm1@jhmi.edu .〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927375" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Disposition ; Embryo Research/*ethics/legislation & jurisprudence ; *Embryo, Mammalian ; *Embryonic Stem Cells ; Female ; Germ Cells ; Guidelines as Topic ; Humans ; *Informed Consent ; *Tissue Donors
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  • 24
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    A global view of gene activity and alternative splicing by deep sequencing of the human transcriptome (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-07-05
    Description: The functional complexity of the human transcriptome is not yet fully elucidated. We report a high-throughput sequence of the human transcriptome from a human embryonic kidney and a B cell line. We used shotgun sequencing of transcripts to generate randomly distributed reads. Of these, 50% mapped to unique genomic locations, of which 80% corresponded to known exons. We found that 66% of the polyadenylated transcriptome mapped to known genes and 34% to nonannotated genomic regions. On the basis of known transcripts, RNA-Seq can detect 25% more genes than can microarrays. A global survey of messenger RNA splicing events identified 94,241 splice junctions (4096 of which were previously unidentified) and showed that exon skipping is the most prevalent form of alternative splicing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sultan, Marc -- Schulz, Marcel H -- Richard, Hugues -- Magen, Alon -- Klingenhoff, Andreas -- Scherf, Matthias -- Seifert, Martin -- Borodina, Tatjana -- Soldatov, Aleksey -- Parkhomchuk, Dmitri -- Schmidt, Dominic -- O'Keeffe, Sean -- Haas, Stefan -- Vingron, Martin -- Lehrach, Hans -- Yaspo, Marie-Laure -- New York, N.Y. -- Science. 2008 Aug 15;321(5891):956-60. doi: 10.1126/science.1160342. Epub 2008 Jul 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Vertebrate Genomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 73, 14195 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18599741" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Cell Line ; Cell Line, Tumor ; Computational Biology ; DNA, Complementary ; DNA, Intergenic ; Exons ; *Gene Expression Profiling ; *Genome, Human ; Humans ; Introns ; Oligonucleotide Array Sequence Analysis ; RNA Polymerase II/metabolism ; *RNA Splice Sites ; RNA, Messenger/*genetics ; *Sequence Analysis, RNA
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    Nascent RNA sequencing reveals widespread pausing and divergent initiation at human promoters (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-12-06
    Description: RNA polymerases are highly regulated molecular machines. We present a method (global run-on sequencing, GRO-seq) that maps the position, amount, and orientation of transcriptionally engaged RNA polymerases genome-wide. In this method, nuclear run-on RNA molecules are subjected to large-scale parallel sequencing and mapped to the genome. We show that peaks of promoter-proximal polymerase reside on approximately 30% of human genes, transcription extends beyond pre-messenger RNA 3' cleavage, and antisense transcription is prevalent. Additionally, most promoters have an engaged polymerase upstream and in an orientation opposite to the annotated gene. This divergent polymerase is associated with active genes but does not elongate effectively beyond the promoter. These results imply that the interplay between polymerases and regulators over broad promoter regions dictates the orientation and efficiency of productive transcription.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833333/" 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/PMC2833333/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Core, Leighton J -- Waterfall, Joshua J -- Lis, John T -- GM25232/GM/NIGMS NIH HHS/ -- R01 GM025232/GM/NIGMS NIH HHS/ -- R01 GM025232-32/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1845-8. doi: 10.1126/science.1162228. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056941" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; CpG Islands ; DNA-Directed RNA Polymerases/*metabolism ; Genome, Human ; Humans ; Nucleosomes/metabolism ; *Promoter Regions, Genetic ; RNA Polymerase II/*metabolism ; RNA, Antisense/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; *Sequence Analysis, RNA ; Transcription Initiation Site ; *Transcription, Genetic
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    A neoplastic gene fusion mimics trans-splicing of RNAs in normal human cells (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-09-06
    Description: Chromosomal rearrangements that create gene fusions are common features of human tumors. The prevailing view is that the resultant chimeric transcripts and proteins are abnormal, tumor-specific products that provide tumor cells with a growth and/or survival advantage. We show that normal endometrial stromal cells contain a specific chimeric RNA joining 5' exons of the JAZF1 gene on chromosome 7p15 to 3' exons of the Polycomb group gene JJAZ1/SUZ12 on chromosome 17q11 and that this RNA is translated into JAZF1-JJAZ1, a protein with anti-apoptotic activity. The JAZF1-JJAZ1 RNA appears to arise from physiologically regulated trans-splicing between precursor messenger RNAs for JAZF1 and JJAZ1. The chimeric RNA and protein are identical to those produced from a gene fusion found in human endometrial stromal tumors. These observations suggest that certain gene fusions may be pro-neoplastic owing to constitutive expression of chimeric gene products normally generated by trans-splicing of RNAs in developing tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Hui -- Wang, Jinglan -- Mor, Gil -- Sklar, Jeffrey -- R01 CA85995/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1357-61. doi: 10.1126/science.1156725.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772439" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; Chromosome Aberrations ; Chromosomes, Human, Pair 17/genetics ; Chromosomes, Human, Pair 7/genetics ; Deferoxamine/pharmacology ; Endometrial Neoplasms/genetics ; Endometrium/cytology/*metabolism ; Exons ; Female ; *Gene Fusion ; Humans ; Menstrual Cycle ; Mutant Chimeric Proteins/genetics ; Neoplasm Proteins/biosynthesis/*genetics ; Progesterone/pharmacology ; Protein Biosynthesis ; RNA Precursors/*genetics ; RNA, Messenger/genetics ; Stromal Cells/*metabolism ; *Trans-Splicing ; Transcription Factors/biosynthesis/*genetics ; Translocation, Genetic
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    The Rag GTPases bind raptor and mediate amino acid signaling to mTORC1 (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-05-24
    Description: The multiprotein mTORC1 protein kinase complex is the central component of a pathway that promotes growth in response to insulin, energy levels, and amino acids and is deregulated in common cancers. We find that the Rag proteins--a family of four related small guanosine triphosphatases (GTPases)--interact with mTORC1 in an amino acid-sensitive manner and are necessary for the activation of the mTORC1 pathway by amino acids. A Rag mutant that is constitutively bound to guanosine triphosphate interacted strongly with mTORC1, and its expression within cells made the mTORC1 pathway resistant to amino acid deprivation. Conversely, expression of a guanosine diphosphate-bound Rag mutant prevented stimulation of mTORC1 by amino acids. The Rag proteins do not directly stimulate the kinase activity of mTORC1, but, like amino acids, promote the intracellular localization of mTOR to a compartment that also contains its activator Rheb.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475333/" 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/PMC2475333/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sancak, Yasemin -- Peterson, Timothy R -- Shaul, Yoav D -- Lindquist, Robert A -- Thoreen, Carson C -- Bar-Peled, Liron -- Sabatini, David M -- AI47389/AI/NIAID NIH HHS/ -- R01 AI047389/AI/NIAID NIH HHS/ -- R01 AI047389-09/AI/NIAID NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA103866-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 13;320(5882):1496-501. doi: 10.1126/science.1157535. Epub 2008 May 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology (MIT), Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497260" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acids/*metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Dimerization ; Guanosine Triphosphate/metabolism ; Humans ; Insulin/metabolism ; Leucine/metabolism ; Monomeric GTP-Binding Proteins/genetics/*metabolism ; Multiprotein Complexes ; Mutant Proteins/metabolism ; Mutation ; Neuropeptides/metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/metabolism ; Proteins/*metabolism ; *Signal Transduction ; TOR Serine-Threonine Kinases ; Transcription Factors/*metabolism
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    Proliferating cells express mRNAs with shortened 3' untranslated regions and fewer microRNA target sites (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-21
    Description: Messenger RNA (mRNA) stability, localization, and translation are largely determined by sequences in the 3' untranslated region (3'UTR). We found a conserved increase in expression of mRNAs terminating at upstream polyadenylation sites after activation of primary murine CD4+ T lymphocytes. This program, resulting in shorter 3'UTRs, is a characteristic of gene expression during immune cell activation and correlates with proliferation across diverse cell types and tissues. Forced expression of full-length 3'UTRs conferred reduced protein expression. In some cases the reduction in protein expression could be reversed by deletion of predicted microRNA target sites in the variably included region. Our data indicate that gene expression is coordinately regulated, such that states of increased proliferation are associated with widespread reductions in the 3'UTR-based regulatory capacity of mRNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587246/" 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/PMC2587246/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandberg, Rickard -- Neilson, Joel R -- Sarma, Arup -- Sharp, Phillip A -- Burge, Christopher B -- P01 CA042063/CA/NCI NIH HHS/ -- P01 CA042063-22/CA/NCI NIH HHS/ -- P01-CA42063/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 GM034277/GM/NIGMS NIH HHS/ -- R01 GM034277-23/GM/NIGMS NIH HHS/ -- R01 HG002439/HG/NHGRI NIH HHS/ -- R01 HG002439-07/HG/NHGRI NIH HHS/ -- R01-GM34277/GM/NIGMS NIH HHS/ -- R01-HG002439/HG/NHGRI NIH HHS/ -- U19 AI056900/AI/NIAID NIH HHS/ -- U19 AI056900-010001/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 20;320(5883):1643-7. doi: 10.1126/science.1155390.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18566288" target="_blank"〉PubMed〈/a〉
    Keywords: *3' Untranslated Regions ; Animals ; CD4-Positive T-Lymphocytes/cytology/immunology/*metabolism ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cells, Cultured ; *Gene Expression Regulation ; Humans ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*metabolism ; Oligonucleotide Array Sequence Analysis ; Polyadenylation ; RNA Splicing ; RNA, Messenger/chemistry/genetics/*metabolism
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    Control of the reversibility of cellular quiescence by the transcriptional repressor HES1 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-23
    Description: The mechanisms by which quiescent cells, including adult stem cells, preserve their ability to resume proliferation after weeks or even years of cell cycle arrest are not known. We report that reversibility is not a passive property of nondividing cells, because enforced cell cycle arrest for a period as brief as 4 days initiates spontaneous, premature, and irreversible senescence. Increased expression of the gene encoding the basic helix-loop-helix protein HES1 was required for quiescence to be reversible, because HES1 prevented both premature senescence and inappropriate differentiation in quiescent fibroblasts. In some human tumors, the HES1 pathway was activated, which allowed these cells to evade differentiation and irreversible cell cycle arrest. We conclude that HES1 safeguards against irreversible cell cycle exit both during normal cellular quiescence and pathologically in the setting of tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721335/" 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/PMC2721335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sang, Liyun -- Coller, Hilary A -- Roberts, James M -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50 GM071508-05/GM/NIGMS NIH HHS/ -- R01 CA118043/CA/NCI NIH HHS/ -- R01 CA118043-03/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1095-100. doi: 10.1126/science.1155998.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719287" target="_blank"〉PubMed〈/a〉
    Keywords: Basic Helix-Loop-Helix Transcription Factors/genetics/*metabolism ; Cell Aging ; *Cell Cycle ; Cell Differentiation ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Fibroblasts/*cytology/metabolism ; Homeodomain Proteins/genetics/*metabolism ; Humans ; Muscle Development ; MyoD Protein/metabolism ; Receptors, Notch/metabolism ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Rhabdomyosarcoma/metabolism/pathology ; Signal Transduction ; Transduction, Genetic
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    Self-assembled water-soluble nucleic acid probe tiles for label-free RNA hybridization assays (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-12
    Description: The DNA origami method, in which long, single-stranded DNA segments are folded into shapes by short staple segments, was used to create nucleic acid probe tiles that are molecular analogs of macroscopic DNA chips. One hundred trillion probe tiles were fabricated in one step and bear pairs of 20-nucleotide-long single-stranded DNA segments that act as probe sequences. These tiles can hybridize to their targets in solution and, after adsorption onto mica surfaces, can be examined by atomic force microscopy in order to quantify binding events, because the probe segments greatly increase in stiffness upon hybridization. The nucleic acid probe tiles have been used to study position-dependent hybridization on the nanoscale and have also been used for label-free detection of RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ke, Yonggang -- Lindsay, Stuart -- Chang, Yung -- Liu, Yan -- Yan, Hao -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):180-3. doi: 10.1126/science.1150082.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Single Molecule Biophysics, Arizona State University, Tempe, AZ 85287, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187649" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Adsorption ; Aluminum Silicates ; Animals ; Cell Line ; DNA, Single-Stranded ; Gene Expression Profiling/*methods ; Genes, RAG-1 ; Genes, myc ; Mice ; Microscopy, Atomic Force ; *Molecular Probe Techniques ; *Nanostructures ; Nucleic Acid Hybridization/*methods ; *Oligonucleotide Probes ; RNA/*analysis/genetics ; Sensitivity and Specificity ; Solubility
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    Recognition of a ubiquitous self antigen by prostate cancer-infiltrating CD8+ T lymphocytes (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-01-12
    Description: Substantial evidence exists that many tumors can be specifically recognized by CD8+ T lymphocytes. The definition of antigens targeted by these cells is paramount for the development of effective immunotherapeutic strategies for treating human cancers. In a screen for endogenous tumor-associated T cell responses in a primary mouse model of prostatic adenocarcinoma, we identified a naturally arising CD8+ T cell response that is reactive to a peptide derived from histone H4. Despite the ubiquitous nature of histones, T cell recognition of histone H4 peptide was specifically associated with the presence of prostate cancer in these mice. Thus, the repertoire of antigens recognized by tumor-infiltrating T cells is broader than previously thought and includes peptides derived from ubiquitous self antigens that are normally sequestered from immune detection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savage, Peter A -- Vosseller, Keith -- Kang, Chulho -- Larimore, Kevin -- Riedel, Elyn -- Wojnoonski, Kathleen -- Jungbluth, Achim A -- Allison, James P -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):215-20. doi: 10.1126/science.1148886.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Howard Hughes Medical Institute, and Ludwig Center for Cancer Immunotherapy, Memorial Sloan-Kettering Cancer Center (MSKCC), New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187659" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*immunology ; Adoptive Transfer ; Animals ; Antigen Presentation ; Antigens, Neoplasm/*immunology ; Autoantigens/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Line ; Epitopes, T-Lymphocyte/immunology ; Histones/*immunology ; Hybridomas ; Lymphocytes, Tumor-Infiltrating/*immunology ; Male ; Mice ; Mice, Transgenic ; Peptide Fragments/immunology ; Prostatic Neoplasms/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology
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    Arabidopsis CLV3 peptide directly binds CLV1 ectodomain (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-19
    Description: CLV1, which encodes a leucine-rich repeat receptor kinase, and CLV3, which encodes a secreted peptide, function in the same genetic pathway to maintain stem cell populations in Arabidopsis shoot apical meristem. Here, we show biochemical evidence, by ligand binding assay and photoaffinity labeling, that the CLV3 peptide directly binds the CLV1 ectodomain with a dissociation constant of 17.5 nM. The CLV1 ectodomain also interacts with the structurally related CLE peptides, with distinct affinities depending on the specific amino acid sequence. Our results provide direct evidence that CLV3 and CLV1 function as a ligand-receptor pair involved in stem cell maintenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogawa, Mari -- Shinohara, Hidefumi -- Sakagami, Youji -- Matsubayashi, Yoshikatsu -- New York, N.Y. -- Science. 2008 Jan 18;319(5861):294. doi: 10.1126/science.1150083.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Bio-Agricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18202283" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/cytology/genetics/*metabolism ; Arabidopsis Proteins/chemistry/*metabolism ; Cell Line ; Genes, Plant ; Ligands ; Meristem/cytology/metabolism ; Peptides/chemistry/metabolism ; Plants, Genetically Modified ; Protein Binding ; Protein Structure, Tertiary ; Receptor Protein-Tyrosine Kinases/chemistry/*metabolism ; Tobacco
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    A cholesterol biosynthesis inhibitor blocks Staphylococcus aureus virulence (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-16
    Description: Staphylococcus aureus produces hospital- and community-acquired infections, with methicillin-resistant S. aureus posing a serious public health threat. The golden carotenoid pigment of S. aureus, staphyloxanthin, promotes resistance to reactive oxygen species and host neutrophil-based killing, and early enzymatic steps in staphyloxanthin production resemble those for cholesterol biosynthesis. We determined the crystal structures of S. aureus dehydrosqualene synthase (CrtM) at 1.58 angstrom resolution, finding structural similarity to human squalene synthase (SQS). We screened nine SQS inhibitors and determined the structures of three, bound to CrtM. One, previously tested for cholesterol-lowering activity in humans, blocked staphyloxanthin biosynthesis in vitro (median inhibitory concentration approximately 100 nM), resulting in colorless bacteria with increased susceptibility to killing by human blood and to innate immune clearance in a mouse infection model. This finding represents proof of principle for a virulence factor-based therapy against S. aureus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747771/" 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/PMC2747771/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Chia-I -- Liu, George Y -- Song, Yongcheng -- Yin, Fenglin -- Hensler, Mary E -- Jeng, Wen-Yih -- Nizet, Victor -- Wang, Andrew H-J -- Oldfield, Eric -- AI07482/AI/NIAID NIH HHS/ -- GM073216/GM/NIGMS NIH HHS/ -- GM65307/GM/NIGMS NIH HHS/ -- HD051796/HD/NICHD NIH HHS/ -- R01 GM065307/GM/NIGMS NIH HHS/ -- R01 GM065307-07/GM/NIGMS NIH HHS/ -- R01 GM073216/GM/NIGMS NIH HHS/ -- R01 GM073216-29/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 7;319(5868):1391-4. doi: 10.1126/science.1153018. Epub 2008 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biological Chemistry, Academia Sinica, Nankang, Taipei 11529, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276850" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Bacterial Agents/chemical synthesis/chemistry/*pharmacology/therapeutic use ; Bacterial Proteins/*antagonists & inhibitors/chemistry/isolation & ; purification/metabolism ; Cell Line ; Cell Proliferation/drug effects ; Cholesterol/biosynthesis ; Crystallography, X-Ray ; Enzyme Inhibitors/chemical synthesis/metabolism/*pharmacology ; Farnesyl-Diphosphate Farnesyltransferase/*antagonists & ; inhibitors/chemistry/isolation & purification/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Organothiophosphorus Compounds/chemical ; synthesis/metabolism/*pharmacology/therapeutic use ; Polyisoprenyl Phosphates/chemistry/metabolism ; Protein Structure, Secondary ; Sesquiterpenes/chemistry/metabolism ; Staphylococcal Infections/*drug therapy/microbiology ; Staphylococcus aureus/drug effects/growth & development/metabolism/*pathogenicity ; Virulence/drug effects ; Xanthophylls/biosynthesis
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    Germline allele-specific expression of TGFBR1 confers an increased risk of colorectal cancer (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: Much of the genetic predisposition to colorectal cancer (CRC) in humans is unexplained. Studying a Caucasian-dominated population in the United States, we showed that germline allele-specific expression (ASE) of the gene encoding transforming growth factor-beta (TGF-beta) type I receptor, TGFBR1, is a quantitative trait that occurs in 10 to 20% of CRC patients and 1 to 3% of controls. ASE results in reduced expression of the gene, is dominantly inherited, segregates in families, and occurs in sporadic CRC cases. Although subtle, the reduction in constitutive TGFBR1 expression alters SMAD-mediated TGF-beta signaling. Two major TGFBR1 haplotypes are predominant among ASE cases, which suggests ancestral mutations, but causative germline changes have not been identified. Conservative estimates suggest that ASE confers a substantially increased risk of CRC (odds ratio, 8.7; 95% confidence interval, 2.6 to 29.1), but these estimates require confirmation and will probably show ethnic differences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672914/" 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/PMC2672914/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valle, Laura -- Serena-Acedo, Tarsicio -- Liyanarachchi, Sandya -- Hampel, Heather -- Comeras, Ilene -- Li, Zhongyuan -- Zeng, Qinghua -- Zhang, Hong-Tao -- Pennison, Michael J -- Sadim, Maureen -- Pasche, Boris -- Tanner, Stephan M -- de la Chapelle, Albert -- CA108741/CA/NCI NIH HHS/ -- CA112520/CA/NCI NIH HHS/ -- CA16058/CA/NCI NIH HHS/ -- CA67941/CA/NCI NIH HHS/ -- R01 CA108741/CA/NCI NIH HHS/ -- R01 CA108741-01A2/CA/NCI NIH HHS/ -- R01 CA112520/CA/NCI NIH HHS/ -- R01 CA112520-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1361-5. doi: 10.1126/science.1159397. Epub 2008 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703712" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Adult ; Aged ; Aged, 80 and over ; Alleles ; Cell Line ; Colorectal Neoplasms/*genetics ; Female ; *Gene Expression ; *Genetic Predisposition to Disease ; Haplotypes ; Heterozygote ; Humans ; Linkage Disequilibrium ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Protein-Serine-Threonine Kinases/*genetics ; Quantitative Trait, Heritable ; Receptors, Transforming Growth Factor beta/*genetics ; Risk Factors ; Signal Transduction ; Smad3 Protein/metabolism ; Transforming Growth Factor beta/metabolism
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    Subdiffraction multicolor imaging of the nuclear periphery with 3D structured illumination microscopy (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-06-07
    Description: Fluorescence light microscopy allows multicolor visualization of cellular components with high specificity, but its utility has until recently been constrained by the intrinsic limit of spatial resolution. We applied three-dimensional structured illumination microscopy (3D-SIM) to circumvent this limit and to study the mammalian nucleus. By simultaneously imaging chromatin, nuclear lamina, and the nuclear pore complex (NPC), we observed several features that escape detection by conventional microscopy. We could resolve single NPCs that colocalized with channels in the lamin network and peripheral heterochromatin. We could differentially localize distinct NPC components and detect double-layered invaginations of the nuclear envelope in prophase as previously seen only by electron microscopy. Multicolor 3D-SIM opens new and facile possibilities to analyze subcellular structures beyond the diffraction limit of the emitted light.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916659/" 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/PMC2916659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schermelleh, Lothar -- Carlton, Peter M -- Haase, Sebastian -- Shao, Lin -- Winoto, Lukman -- Kner, Peter -- Burke, Brian -- Cardoso, M Cristina -- Agard, David A -- Gustafsson, Mats G L -- Leonhardt, Heinrich -- Sedat, John W -- GM-2501-25/GM/NIGMS NIH HHS/ -- R01 GM025101/GM/NIGMS NIH HHS/ -- R01 GM025101-25/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 6;320(5881):1332-6. doi: 10.1126/science.1156947.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Integrated Protein Science, Department of Biology, Ludwig Maximilians University Munich, 82152 Planegg-Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18535242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/*ultrastructure ; Chromatin/*ultrastructure ; Fluorescent Dyes ; Heterochromatin/ultrastructure ; Imaging, Three-Dimensional/instrumentation/*methods ; Indoles ; Interphase ; Lamins/ultrastructure ; Mice ; Microscopy, Confocal ; Microscopy, Fluorescence/instrumentation/*methods ; Myoblasts ; Nuclear Envelope/*ultrastructure ; Nuclear Lamina/ultrastructure ; Nuclear Pore/ultrastructure ; Optics and Photonics
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    Plastin 3 is a protective modifier of autosomal recessive spinal muscular atrophy (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-29
    Description: Homozygous deletion of the survival motor neuron 1 gene (SMN1) causes spinal muscular atrophy (SMA), the most frequent genetic cause of early childhood lethality. In rare instances, however, individuals are asymptomatic despite carrying the same SMN1 mutations as their affected siblings, thereby suggesting the influence of modifier genes. We discovered that unaffected SMN1-deleted females exhibit significantly higher expression of plastin 3 (PLS3) than their SMA-affected counterparts. We demonstrated that PLS3 is important for axonogenesis through increasing the F-actin level. Overexpression of PLS3 rescued the axon length and outgrowth defects associated with SMN down-regulation in motor neurons of SMA mouse embryos and in zebrafish. Our study suggests that defects in axonogenesis are the major cause of SMA, thereby opening new therapeutic options for SMA and similar neuromuscular diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oprea, Gabriela E -- Krober, Sandra -- McWhorter, Michelle L -- Rossoll, Wilfried -- Muller, Stefan -- Krawczak, Michael -- Bassell, Gary J -- Beattie, Christine E -- Wirth, Brunhilde -- HD055835/HD/NICHD NIH HHS/ -- R01 HD055835/HD/NICHD NIH HHS/ -- R01NS50414/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):524-7. doi: 10.1126/science.1155085.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Human Genetics, University of Cologne, 50931 Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18440926" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/blood/*genetics/*metabolism ; Animals ; Axons/metabolism/*physiology/ultrastructure ; Cell Differentiation ; Cell Line ; Cyclic AMP Response Element-Binding Protein/genetics/metabolism ; Female ; Gene Expression ; Growth Cones/metabolism/ultrastructure ; Humans ; Male ; Membrane Glycoproteins ; Mice ; Microfilament Proteins ; Muscular Atrophy, Spinal/*genetics ; Nerve Tissue Proteins/genetics/metabolism ; Pedigree ; Phosphoproteins/blood/*genetics/*metabolism ; RNA-Binding Proteins/genetics/metabolism ; SMN Complex Proteins ; Spinal Cord/metabolism ; Survival of Motor Neuron 1 Protein ; Transcription, Genetic ; Zebrafish/embryology/genetics
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    Bora and the kinase Aurora a cooperatively activate the kinase Plk1 and control mitotic entry (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-06-21
    Description: A central question in the study of cell proliferation is, what controls cell-cycle transitions? Although the accumulation of mitotic cyclins drives the transition from the G2 phase to the M phase in embryonic cells, the trigger for mitotic entry in somatic cells remains unknown. We report that the synergistic action of Bora and the kinase Aurora A (Aur-A) controls the G2-M transition. Bora accumulates in the G2 phase and promotes Aur-A-mediated activation of Polo-like kinase 1 (Plk1), leading to the activation of cyclin-dependent kinase 1 and mitotic entry. Mechanistically, Bora interacts with Plk1 and controls the accessibility of its activation loop for phosphorylation and activation by Aur-A. Thus, Bora and Aur-A control mitotic entry, which provides a mechanism for one of the most important yet ill-defined events in the cell cycle.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834883/" 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/PMC2834883/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seki, Akiko -- Coppinger, Judith A -- Jang, Chang-Young -- Yates, John R -- Fang, Guowei -- GM062852/GM/NIGMS NIH HHS/ -- HL079442/HL/NHLBI NIH HHS/ -- P41 RR011823/RR/NCRR NIH HHS/ -- P41 RR011823-10/RR/NCRR NIH HHS/ -- R01 GM062852-05/GM/NIGMS NIH HHS/ -- R01 HL079442/HL/NHLBI NIH HHS/ -- R01 HL079442-04/HL/NHLBI NIH HHS/ -- RR11823-10/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 20;320(5883):1655-8. doi: 10.1126/science.1157425.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18566290" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aurora Kinases ; CDC2 Protein Kinase/metabolism ; Cell Cycle Proteins/chemistry/*metabolism ; Cell Line ; Enzyme Activation ; Feedback, Physiological ; G2 Phase ; HeLa Cells ; Humans ; Kinetics ; *Mitosis ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/chemistry/*metabolism ; Proto-Oncogene Proteins/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Xenopus ; Xenopus Proteins/metabolism
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    Cancer proliferation gene discovery through functional genomics (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-02
    Description: Retroviral short hairpin RNA (shRNA)-mediated genetic screens in mammalian cells are powerful tools for discovering loss-of-function phenotypes. We describe a highly parallel multiplex methodology for screening large pools of shRNAs using half-hairpin barcodes for microarray deconvolution. We carried out dropout screens for shRNAs that affect cell proliferation and viability in cancer cells and normal cells. We identified many shRNAs to be antiproliferative that target core cellular processes, such as the cell cycle and protein translation, in all cells examined. Moreover, we identified genes that are selectively required for proliferation and survival in different cell lines. Our platform enables rapid and cost-effective genome-wide screens to identify cancer proliferation and survival genes for target discovery. Such efforts are complementary to the Cancer Genome Atlas and provide an alternative functional view of cancer cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981870/" 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/PMC2981870/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlabach, Michael R -- Luo, Ji -- Solimini, Nicole L -- Hu, Guang -- Xu, Qikai -- Li, Mamie Z -- Zhao, Zhenming -- Smogorzewska, Agata -- Sowa, Mathew E -- Ang, Xiaolu L -- Westbrook, Thomas F -- Liang, Anthony C -- Chang, Kenneth -- Hackett, Jennifer A -- Harper, J Wade -- Hannon, Gregory J -- Elledge, Stephen J -- F31 NS054507-01/NS/NINDS NIH HHS/ -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-36/CA/NCI NIH HHS/ -- P01 CA013106-37/CA/NCI NIH HHS/ -- R01 AG011085/AG/NIA NIH HHS/ -- T32CA09216/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):620-4. doi: 10.1126/science.1149200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Genetics, Center for Genetics and Genomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239126" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics/pathology ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cell Survival/genetics ; Colonic Neoplasms/*genetics/pathology ; Gene Library ; *Genes, Neoplasm ; Genetic Vectors ; Genome, Human ; Genomics/*methods ; Humans ; MicroRNAs ; Oligonucleotide Array Sequence Analysis ; RNA, Small Interfering ; Retroviridae/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    TMEM16A, a membrane protein associated with calcium-dependent chloride channel activity (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: Calcium-dependent chloride channels are required for normal electrolyte and fluid secretion, olfactory perception, and neuronal and smooth muscle excitability. The molecular identity of these membrane proteins is still unclear. Treatment of bronchial epithelial cells with interleukin-4 (IL-4) causes increased calcium-dependent chloride channel activity, presumably by regulating expression of the corresponding genes. We performed a global gene expression analysis to identify membrane proteins that are regulated by IL-4. Transfection of epithelial cells with specific small interfering RNA against each of these proteins shows that TMEM16A, a member of a family of putative plasma membrane proteins with unknown function, is associated with calcium-dependent chloride current, as measured with halide-sensitive fluorescent proteins, short-circuit current, and patch-clamp techniques. Our results indicate that TMEM16A is an intrinsic constituent of the calcium-dependent chloride channel. Identification of a previously unknown family of membrane proteins associated with chloride channel function will improve our understanding of chloride transport physiopathology and allow for the development of pharmacological tools useful for basic research and drug development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caputo, Antonella -- Caci, Emanuela -- Ferrera, Loretta -- Pedemonte, Nicoletta -- Barsanti, Cristina -- Sondo, Elvira -- Pfeffer, Ulrich -- Ravazzolo, Roberto -- Zegarra-Moran, Olga -- Galietta, Luis J V -- GGP05103/Telethon/Italy -- New York, N.Y. -- Science. 2008 Oct 24;322(5901):590-4. doi: 10.1126/science.1163518. Epub 2008 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratorio di Genetica Molecolare, Istituto Giannina Gaslini, Genova 16148, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772398" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Bronchi/cytology/*metabolism ; Calcium/*metabolism ; Cell Line ; Cell Membrane/*metabolism ; Cells, Cultured ; Chloride Channels/*metabolism ; Chlorides/*metabolism ; Epithelial Cells/metabolism ; Humans ; Interleukin-4/metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Neoplasm Proteins/chemistry/genetics/*metabolism ; Oligonucleotide Array Sequence Analysis ; Patch-Clamp Techniques ; RNA, Small Interfering ; Respiratory Mucosa/cytology/metabolism ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Detection of GTP-tubulin conformation in vivo reveals a role for GTP remnants in microtubule rescues (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-10-18
    Description: Microtubules display dynamic instability, with alternating phases of growth and shrinkage separated by catastrophe and rescue events. The guanosine triphosphate (GTP) cap at the growing end of microtubules, whose presence is essential to prevent microtubule catastrophes in vitro, has been difficult to observe in vivo. We selected a recombinant antibody that specifically recognizes GTP-bound tubulin in microtubules and found that GTP-tubulin was indeed present at the plus end of growing microtubules. Unexpectedly, GTP-tubulin remnants were also present in older parts of microtubules, which suggests that GTP hydrolysis is sometimes incomplete during polymerization. Observations in living cells suggested that these GTP remnants may be responsible for the rescue events in which microtubules recover from catastrophe.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dimitrov, Ariane -- Quesnoit, Melanie -- Moutel, Sandrine -- Cantaloube, Isabelle -- Pous, Christian -- Perez, Franck -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1353-6. doi: 10.1126/science.1165401. Epub 2008 Oct 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR144, Institut Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Cell Line ; Computer Simulation ; Dimerization ; Fluorescent Antibody Technique ; Guanosine Triphosphate/*analysis/metabolism ; HeLa Cells ; Humans ; Microtubules/*chemistry/metabolism/ultrastructure ; Models, Biological ; Monte Carlo Method ; Protein Conformation ; Recombinant Fusion Proteins/metabolism ; Tubulin/analysis/*chemistry/immunology/metabolism
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    Breakthrough of the year. Reprogramming Cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1766-7. doi: 10.1126/science.322.5909.1766.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cellular Reprogramming ; Embryonic Stem Cells/cytology/physiology ; Humans ; Keratinocytes/cytology ; Pluripotent Stem Cells/cytology/physiology
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    Induced pluripotent stem cells generated from patients with ALS can be differentiated into motor neurons (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: The generation of pluripotent stem cells from an individual patient would enable the large-scale production of the cell types affected by that patient's disease. These cells could in turn be used for disease modeling, drug discovery, and eventually autologous cell replacement therapies. Although recent studies have demonstrated the reprogramming of human fibroblasts to a pluripotent state, it remains unclear whether these induced pluripotent stem (iPS) cells can be produced directly from elderly patients with chronic disease. We have generated iPS cells from an 82-year-old woman diagnosed with a familial form of amyotrophic lateral sclerosis (ALS). These patient-specific iPS cells possess properties of embryonic stem cells and were successfully directed to differentiate into motor neurons, the cell type destroyed in ALS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dimos, John T -- Rodolfa, Kit T -- Niakan, Kathy K -- Weisenthal, Laurin M -- Mitsumoto, Hiroshi -- Chung, Wendy -- Croft, Gist F -- Saphier, Genevieve -- Leibel, Rudy -- Goland, Robin -- Wichterle, Hynek -- Henderson, Christopher E -- Eggan, Kevin -- New York, N.Y. -- Science. 2008 Aug 29;321(5893):1218-21. doi: 10.1126/science.1158799. Epub 2008 Jul 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Stem Cell Institute, Stowers Medical Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669821" target="_blank"〉PubMed〈/a〉
    Keywords: Aged, 80 and over ; Amyotrophic Lateral Sclerosis/genetics/*pathology/physiopathology ; *Cell Differentiation ; Cell Line ; *Cellular Reprogramming ; Embryonic Stem Cells/cytology ; Female ; Fibroblasts/*cytology ; Gene Expression ; Humans ; Motor Neurons/*cytology/metabolism ; Neuroglia/cytology ; Pluripotent Stem Cells/*cytology ; Retroviridae/genetics ; Spinal Cord/cytology ; Superoxide Dismutase/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transduction, Genetic
    Print ISSN: 0036-8075
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    Cell biology. No ESCRTs for exosomes (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsh, Mark -- van Meer, Gerrit -- MC_U122665002/Medical Research Council/United Kingdom -- U.1226.00.003.00001.01(65002)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 Feb 29;319(5867):1191-2. doi: 10.1126/science.1155750.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology Unit, MRC Laboratory for Molecular Cell Biology and Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK. m.marsh@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18309064" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/metabolism ; Antigens, CD63 ; Cell Line ; Ceramides/analysis/*metabolism ; Cytoplasmic Vesicles/chemistry/*metabolism/ultrastructure ; Endosomes/*metabolism/ultrastructure ; Intracellular Membranes/*metabolism/ultrastructure ; Lysosomes/metabolism ; Membrane Microdomains/*metabolism ; Myelin Proteolipid Protein/*metabolism ; Oligodendroglia/metabolism/ultrastructure ; Platelet Membrane Glycoproteins/metabolism ; Protein Transport ; Receptor, Epidermal Growth Factor/metabolism ; Sphingomyelin Phosphodiesterase/antagonists & inhibitors/metabolism
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    FBXW7 targets mTOR for degradation and cooperates with PTEN in tumor suppression (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-13
    Description: The enzyme mTOR (mammalian target of rapamycin) is a major target for therapeutic intervention to treat many human diseases, including cancer, but very little is known about the processes that control levels of mTOR protein. Here, we show that mTOR is targeted for ubiquitination and consequent degradation by binding to the tumor suppressor protein FBXW7. Human breast cancer cell lines and primary tumors showed a reciprocal relation between loss of FBXW7 and deletion or mutation of PTEN (phosphatase and tensin homolog), which also activates mTOR. Tumor cell lines harboring deletions or mutations in FBXW7 are particularly sensitive to rapamycin treatment, which suggests that loss of FBXW7 may be a biomarker for human cancers susceptible to treatment with inhibitors of the mTOR pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849753/" 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/PMC2849753/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Jian-Hua -- Kim, Il-Jin -- Wu, Di -- Climent, Joan -- Kang, Hio Chung -- DelRosario, Reyno -- Balmain, Allan -- R01 CA116481/CA/NCI NIH HHS/ -- U01 CA084244/CA/NCI NIH HHS/ -- U01 CA084244-08/CA/NCI NIH HHS/ -- U01 CA084244-09/CA/NCI NIH HHS/ -- U01 CA084244-10/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 12;321(5895):1499-502. doi: 10.1126/science.1162981.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Institute, University of California at San Francisco, 2340 Sutter Street, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18787170" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/drug therapy/genetics/*metabolism/pathology ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; F-Box Proteins/genetics/*metabolism ; Gene Deletion ; Gene Dosage ; Gene Silencing ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Nude ; Mutation ; Neoplasm Transplantation ; PTEN Phosphohydrolase/genetics/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/pharmacology/therapeutic use ; TOR Serine-Threonine Kinases ; Transfection ; Tumor Suppressor Proteins/*metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism ; Ubiquitination
    Print ISSN: 0036-8075
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    Scientific misconduct. Fraud charges cast doubt on claims of DNA damage from cell phone fields (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2008 Aug 29;321(5893):1144-5. doi: 10.1126/science.321.5893.1144a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18755946" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Cell Phones ; *DNA Breaks ; Electromagnetic Fields/*adverse effects ; Ethics Committees, Research ; Humans ; Research Design/standards ; Retraction of Publication as Topic ; *Scientific Misconduct
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    Adapting proteostasis for disease intervention (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-16
    Description: The protein components of eukaryotic cells face acute and chronic challenges to their integrity. Eukaryotic protein homeostasis, or proteostasis, enables healthy cell and organismal development and aging and protects against disease. Here, we describe the proteostasis network, a set of interacting activities that maintain the health of proteome and the organism. Deficiencies in proteostasis lead to many metabolic, oncological, neurodegenerative, and cardiovascular disorders. Small-molecule or biological proteostasis regulators that manipulate the concentration, conformation, quaternary structure, and/or the location of protein(s) have the potential to ameliorate some of the most challenging diseases of our era.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balch, William E -- Morimoto, Richard I -- Dillin, Andrew -- Kelly, Jeffery W -- AG 18917/AG/NIA NIH HHS/ -- AG026647/AG/NIA NIH HHS/ -- AG04342/AG/NIA NIH HHS/ -- DK46336/DK/NIDDK NIH HHS/ -- DK75295/DK/NIDDK NIH HHS/ -- GM38109/GM/NIGMS NIH HHS/ -- NS50636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):916-9. doi: 10.1126/science.1141448.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Institute for Childhood and Neglected Diseases, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276881" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Line ; *Cell Physiological Phenomena ; *Drug Therapy ; Homeostasis ; Humans ; Infection/drug therapy/metabolism ; Metabolic Diseases/drug therapy/metabolism ; Metabolic Networks and Pathways ; Neoplasms/drug therapy/metabolism ; Protein Conformation ; Protein Folding ; Protein Transport ; Proteins/*chemistry/*metabolism/therapeutic use ; Signal Transduction
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    Aneuploidy affects proliferation and spontaneous immortalization in mammalian cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-01
    Description: Aneuploidy, an incorrect number of chromosomes, is the leading cause of miscarriages and mental retardation in humans and is a hallmark of cancer. We examined the effects of aneuploidy on primary mouse cells by generating a series of cell lines that carry an extra copy of one of four mouse chromosomes. In all four trisomic lines, proliferation was impaired and metabolic properties were altered. Immortalization, the acquisition of the ability to proliferate indefinitely, was also affected by the presence of an additional copy of certain chromosomes. Our data indicate that aneuploidy decreases not only organismal but also cellular fitness and elicits traits that are shared between different aneuploid cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701511/" 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/PMC2701511/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, Bret R -- Prabhu, Vineet R -- Hunter, Karen E -- Glazier, Christina M -- Whittaker, Charles A -- Housman, David E -- Amon, Angelika -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Oct 31;322(5902):703-9. doi: 10.1126/science.1160058.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18974345" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Animals ; Cell Aging ; Cell Cycle ; Cell Line ; *Cell Proliferation ; Cell Size ; Cell Transformation, Neoplastic ; Culture Media ; Embryo, Mammalian ; Fibroblasts ; Gene Dosage ; *Gene Expression ; Genomic Instability ; Glucose/*metabolism ; Glutamine/*metabolism ; Metabolic Networks and Pathways ; Mice ; Serial Passage ; Translocation, Genetic ; *Trisomy
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    Cell biology. A seismic shift for stem cell research (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- Vogel, Gretchen -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):560-3. doi: 10.1126/science.319.5863.560.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239100" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Research/legislation & jurisprudence ; Cell Differentiation ; Cell Line ; *Cellular Reprogramming ; Embryo Research/legislation & jurisprudence ; *Embryonic Stem Cells/cytology/physiology ; Genetic Vectors ; Humans ; Nuclear Transfer Techniques ; *Pluripotent Stem Cells/cytology/physiology ; Politics ; Skin/cytology
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    Cancer. Aneuploidy advantages? (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hernando, Eva -- New York, N.Y. -- Science. 2008 Oct 31;322(5902):692-3. doi: 10.1126/science.1166151.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, New York University School of Medicine, New York, NY 10016, USA. eva.hernando@med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18974340" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Animals ; Cell Line ; Cell Movement ; Cell Proliferation ; Cell Survival ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Gene Amplification ; Genomic Instability ; Humans ; Mice ; Models, Biological ; Mutation ; Neoplasms/*genetics ; *Trisomy
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    Profiling essential genes in human mammary cells by multiplex RNAi screening (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-02
    Description: By virtue of their accumulated genetic alterations, tumor cells may acquire vulnerabilities that create opportunities for therapeutic intervention. We have devised a massively parallel strategy for screening short hairpin RNA (shRNA) collections for stable loss-of-function phenotypes. We assayed from 6000 to 20,000 shRNAs simultaneously to identify genes important for the proliferation and survival of five cell lines derived from human mammary tissue. Lethal shRNAs common to these cell lines targeted many known cell-cycle regulatory networks. Cell line-specific sensitivities to suppression of protein complexes and biological pathways also emerged, and these could be validated by RNA interference (RNAi) and pharmacologically. These studies establish a practical platform for genome-scale screening of complex phenotypes in mammalian cells and demonstrate that RNAi can be used to expose genotype-specific sensitivities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981861/" 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/PMC2981861/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silva, Jose M -- Marran, Krista -- Parker, Joel S -- Silva, Javier -- Golding, Michael -- Schlabach, Michael R -- Elledge, Stephen J -- Hannon, Gregory J -- Chang, Kenneth -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-36/CA/NCI NIH HHS/ -- P01 CA013106-37/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):617-20. doi: 10.1126/science.1149185.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Watson School of Biological Sciences, Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239125" target="_blank"〉PubMed〈/a〉
    Keywords: Breast/*cytology/*metabolism ; Breast Neoplasms/*genetics/pathology ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; *Cell Survival ; Gene Expression Profiling ; *Genes, Essential ; Genomics ; Humans ; Metabolic Networks and Pathways/*genetics ; Oligonucleotide Array Sequence Analysis ; Phenotype ; *RNA Interference ; RNA, Small Interfering
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    Three-dimensional super-resolution imaging by stochastic optical reconstruction microscopy (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-05
    Description: Recent advances in far-field fluorescence microscopy have led to substantial improvements in image resolution, achieving a near-molecular resolution of 20 to 30 nanometers in the two lateral dimensions. Three-dimensional (3D) nanoscale-resolution imaging, however, remains a challenge. We demonstrated 3D stochastic optical reconstruction microscopy (STORM) by using optical astigmatism to determine both axial and lateral positions of individual fluorophores with nanometer accuracy. Iterative, stochastic activation of photoswitchable probes enables high-precision 3D localization of each probe, and thus the construction of a 3D image, without scanning the sample. Using this approach, we achieved an image resolution of 20 to 30 nanometers in the lateral dimensions and 50 to 60 nanometers in the axial dimension. This development allowed us to resolve the 3D morphology of nanoscopic cellular structures.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633023/" 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/PMC2633023/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Bo -- Wang, Wenqin -- Bates, Mark -- Zhuang, Xiaowei -- GM 068518/GM/NIGMS NIH HHS/ -- R01 GM068518/GM/NIGMS NIH HHS/ -- R01 GM068518-05/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Feb 8;319(5864):810-3. doi: 10.1126/science.1153529. Epub 2008 Jan 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18174397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbocyanines ; Cell Line ; Cercopithecus aethiops ; Clathrin ; Coated Pits, Cell-Membrane/*ultrastructure ; Cyclic AMP/analogs & derivatives ; Fluorescent Antibody Technique ; Fluorescent Dyes ; Image Processing, Computer-Assisted ; *Imaging, Three-Dimensional/instrumentation/methods ; *Microscopy, Fluorescence/instrumentation/methods ; Microtubules/*ultrastructure ; *Nanotechnology ; Quantum Dots ; Stochastic Processes ; Streptavidin
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    Obama transition. A fresh start for embryonic stem cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2008 Dec 12;322(5908):1619. doi: 10.1126/science.322.5908.1619.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074316" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Embryo Research/economics/legislation & jurisprudence ; *Embryonic Stem Cells ; Financing, Government ; Guidelines as Topic ; Humans ; Nuclear Transfer Techniques/legislation & jurisprudence ; Research Support as Topic/legislation & jurisprudence ; United States
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    NFAT binding and regulation of T cell activation by the cytoplasmic scaffolding Homer proteins (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-26
    Description: T cell receptor (TCR) and costimulatory receptor (CD28) signals cooperate in activating T cells, although understanding of how these pathways are themselves regulated is incomplete. We found that Homer2 and Homer3, members of the Homer family of cytoplasmic scaffolding proteins, are negative regulators of T cell activation. This is achieved through binding of nuclear factor of activated T cells (NFAT) and by competing with calcineurin. Homer-NFAT binding was also antagonized by active serine-threonine kinase AKT, thereby enhancing TCR signaling via calcineurin-dependent dephosphorylation of NFAT. This corresponded with changes in cytokine expression and an increase in effector-memory T cell populations in Homer-deficient mice, which also developed autoimmune-like pathology. These results demonstrate a further means by which costimulatory signals are regulated to control self-reactivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3602998/" 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/PMC3602998/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Guo N -- Huso, David L -- Bouyain, Samuel -- Tu, Jianchen -- McCorkell, Kelly A -- May, Michael J -- Zhu, Yuwen -- Lutz, Michael -- Collins, Samuel -- Dehoff, Marlin -- Kang, Shin -- Whartenby, Katharine -- Powell, Jonathan -- Leahy, Daniel -- Worley, Paul F -- DA00266/DA/NIDA NIH HHS/ -- DA10309/DA/NIDA NIH HHS/ -- P30 CA006973/CA/NCI NIH HHS/ -- R01 CA098109/CA/NCI NIH HHS/ -- T32 CA009140/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Jan 25;319(5862):476-81. doi: 10.1126/science.1151227.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Biochemistry, Cellular and Molecular Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18218901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD28/immunology ; Antigens, CD3/immunology ; Calcineurin/metabolism ; Calcium/metabolism ; Carrier Proteins/chemistry/*metabolism ; Cell Line ; Cells, Cultured ; Crystallography, X-Ray ; Humans ; Jurkat Cells ; *Lymphocyte Activation ; Mice ; Mice, Knockout ; NFATC Transcription Factors/chemistry/*metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Proto-Oncogene Proteins c-akt/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism
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    Developmental biology. From genetic association to genetic switch (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michelson, Alan M -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1803-4. doi: 10.1126/science.1169216.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Heart, Lung and Blood Institute, National Institutes of Health, 31 Center Drive, Bethesda, MD 20892, USA. michelsonam@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095932" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Carrier Proteins/*genetics/metabolism ; Cell Line ; Erythroid Cells/*metabolism ; Erythropoiesis ; Fetal Hemoglobin/biosynthesis/*genetics ; *Gene Expression Regulation ; Genome, Human ; *Genome-Wide Association Study ; Hemoglobinopathies/therapy ; Humans ; Introns ; Nuclear Proteins/*genetics/metabolism ; Polymorphism, Single Nucleotide ; Transcription, Genetic ; beta-Globins/genetics ; gamma-Globins/*genetics
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    Identification of SCF ubiquitin ligase substrates by global protein stability profiling (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-08
    Description: Ubiquitin-mediated proteolysis regulates all aspects of cellular function, and defects in this process are associated with human diseases. The limited number of identified ubiquitin ligase-substrate pairs is a major bottleneck in the ubiquitin field. We established and applied genetic technologies that combine global protein stability (GPS) profiling and genetic perturbation of E3 activity to screen for substrates of the Skp1-cullin-F-box (SCF) ubiquitin ligase in mammalian cells. Among the 〉350 potential substrates identified, we found most known SCF targets and many previously unknown substrates involved in cell cycle, apoptosis, and signaling pathways. Exploring cell cycle-stage stability, we found that several substrates used the SCF and other E3s in different cell cycle stages. Our results demonstrate the potential of these technologies as general platforms for the global discovery of E3-substrate regulatory networks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yen, Hsueh-Chi Sherry -- Elledge, Stephen J -- AG 11085/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):923-9. doi: 10.1126/science.1160462.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Center for Genetics and Genomics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988848" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Cell Cycle ; Cell Cycle Proteins/isolation & purification/metabolism ; Cell Line ; Cullin Proteins/genetics/metabolism ; Green Fluorescent Proteins/analysis/metabolism ; Half-Life ; Humans ; Luminescent Proteins/analysis/metabolism ; Oligonucleotide Array Sequence Analysis ; Open Reading Frames ; *Protein Stability ; Proteins/genetics/isolation & purification/*metabolism ; Recombinant Fusion Proteins/metabolism ; SKP Cullin F-Box Protein Ligases/antagonists & inhibitors/genetics/*metabolism ; Signal Transduction ; Substrate Specificity ; cdc25 Phosphatases/isolation & purification/metabolism
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    Mutations in the pericentrin (PCNT) gene cause primordial dwarfism (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-05
    Description: Fundamental processes influencing human growth can be revealed by studying extreme short stature. Using genetic linkage analysis, we find that biallelic loss-of-function mutations in the centrosomal pericentrin (PCNT) gene on chromosome 21q22.3 cause microcephalic osteodysplastic primordial dwarfism type II (MOPD II) in 25 patients. Adults with this rare inherited condition have an average height of 100 centimeters and a brain size comparable to that of a 3-month-old baby, but are of near-normal intelligence. Absence of PCNT results in disorganized mitotic spindles and missegregation of chromosomes. Mutations in related genes are known to cause primary microcephaly (MCPH1, CDK5RAP2, ASPM, and CENPJ).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rauch, Anita -- Thiel, Christian T -- Schindler, Detlev -- Wick, Ursula -- Crow, Yanick J -- Ekici, Arif B -- van Essen, Anthonie J -- Goecke, Timm O -- Al-Gazali, Lihadh -- Chrzanowska, Krystyna H -- Zweier, Christiane -- Brunner, Han G -- Becker, Kristin -- Curry, Cynthia J -- Dallapiccola, Bruno -- Devriendt, Koenraad -- Dorfler, Arnd -- Kinning, Esther -- Megarbane, Andre -- Meinecke, Peter -- Semple, Robert K -- Spranger, Stephanie -- Toutain, Annick -- Trembath, Richard C -- Voss, Egbert -- Wilson, Louise -- Hennekam, Raoul -- de Zegher, Francis -- Dorr, Helmuth-Gunther -- Reis, Andre -- 062346/Z/00/Z/Wellcome Trust/United Kingdom -- 080952/Z/06/Z/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Feb 8;319(5864):816-9. doi: 10.1126/science.1151174. Epub 2008 Jan 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Human Genetics, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany. Anita.Rauch@humgenet.uni-erlangen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18174396" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens/*genetics/metabolism/*physiology ; Apoptosis ; Cell Line ; Centrosome/physiology ; Dwarfism/*genetics/pathology/physiopathology ; Female ; Fibroblasts/cytology ; Humans ; Lod Score ; Lymphocytes/metabolism ; Male ; Microcephaly/*genetics/pathology/physiopathology ; Mitosis ; *Mutation ; Pedigree ; RNA, Messenger/genetics/metabolism ; Spindle Apparatus/physiology/ultrastructure ; Syndrome
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    In vivo imaging of membrane-associated glycans in developing zebrafish (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-03
    Description: Glycans are attractive targets for molecular imaging but have been inaccessible because of their incompatibility with genetically encoded reporters. We demonstrated the noninvasive imaging of glycans in live developing zebrafish, using a chemical reporter strategy. Zebrafish embryos were treated with an unnatural sugar to metabolically label their cell-surface glycans with azides. Subsequently, the embryos were reacted with fluorophore conjugates by means of copper-free click chemistry, enabling the visualization of glycans in vivo at subcellular resolution during development. At 60 hours after fertilization, we observed an increase in de novo glycan biosynthesis in the jaw region, pectoral fins, and olfactory organs. Using a multicolor detection strategy, we performed a spatiotemporal analysis of glycan expression and trafficking and identified patterns that would be undetectable with conventional molecular imaging approaches.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701225/" 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/PMC2701225/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laughlin, Scott T -- Baskin, Jeremy M -- Amacher, Sharon L -- Bertozzi, Carolyn R -- GM058867/GM/NIGMS NIH HHS/ -- GM061952/GM/NIGMS NIH HHS/ -- R01 GM058867/GM/NIGMS NIH HHS/ -- R01 GM058867-11/GM/NIGMS NIH HHS/ -- R01 GM061952/GM/NIGMS NIH HHS/ -- R01 GM061952-06A2S1/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 May 2;320(5876):664-7. doi: 10.1126/science.1155106.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451302" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylgalactosamine/chemistry ; Affinity Labels ; Animals ; Cell Line ; Cell Membrane/*chemistry ; Fluorescent Dyes/chemistry ; Polysaccharides/*analysis/biosynthesis ; *Zebrafish/embryology
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    Endogenous siRNAs derived from transposons and mRNAs in Drosophila somatic cells (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-12
    Description: Small interfering RNAs (siRNAs) direct RNA interference (RNAi) in eukaryotes. In flies, somatic cells produce siRNAs from exogenous double-stranded RNA (dsRNA) as a defense against viral infection. We identified endogenous siRNAs (endo-siRNAs), 21 nucleotides in length, that correspond to transposons and heterochromatic sequences in the somatic cells of Drosophila melanogaster. We also detected endo-siRNAs complementary to messenger RNAs (mRNAs); these siRNAs disproportionately mapped to the complementary regions of overlapping mRNAs predicted to form double-stranded RNA in vivo. Normal accumulation of somatic endo-siRNAs requires the siRNA-generating ribonuclease Dicer-2 and the RNAi effector protein Argonaute2 (Ago2). We propose that endo-siRNAs generated by the fly RNAi pathway silence selfish genetic elements in the soma, much as Piwi-interacting RNAs do in the germ line.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2953241/" 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/PMC2953241/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghildiyal, Megha -- Seitz, Herve -- Horwich, Michael D -- Li, Chengjian -- Du, Tingting -- Lee, Soohyun -- Xu, Jia -- Kittler, Ellen L W -- Zapp, Maria L -- Weng, Zhiping -- Zamore, Phillip D -- F30 AG030283-02/AG/NIA NIH HHS/ -- F30 AG030283-03/AG/NIA NIH HHS/ -- F30 AG030283-04/AG/NIA NIH HHS/ -- F30AG030283/AG/NIA NIH HHS/ -- GM080625/GM/NIGMS NIH HHS/ -- GM62862/GM/NIGMS NIH HHS/ -- GM65236/GM/NIGMS NIH HHS/ -- HG003367/HG/NHGRI NIH HHS/ -- P30 AI042845/AI/NIAID NIH HHS/ -- P30 AI042845-119008/AI/NIAID NIH HHS/ -- R01 AI043208/AI/NIAID NIH HHS/ -- R01 AI043208-08/AI/NIAID NIH HHS/ -- R01 GM062862/GM/NIGMS NIH HHS/ -- R01 GM062862-08/GM/NIGMS NIH HHS/ -- R01 GM062862-09/GM/NIGMS NIH HHS/ -- R01 GM065236/GM/NIGMS NIH HHS/ -- R01 GM065236-07/GM/NIGMS NIH HHS/ -- R01 GM065236-08/GM/NIGMS NIH HHS/ -- R01 GM080625/GM/NIGMS NIH HHS/ -- R01 GM080625-02/GM/NIGMS NIH HHS/ -- R01 GM080625-03/GM/NIGMS NIH HHS/ -- R01 HG003367/HG/NHGRI NIH HHS/ -- R01 HG003367-03/HG/NHGRI NIH HHS/ -- R37 GM062862/GM/NIGMS NIH HHS/ -- R37 GM062862-11/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 May 23;320(5879):1077-81. doi: 10.1126/science.1157396. Epub 2008 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403677" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Base Sequence ; Cell Line ; *DNA Transposable Elements ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/*genetics/metabolism ; Mutation ; RNA Helicases/genetics/metabolism ; *RNA Interference ; RNA, Double-Stranded/metabolism ; RNA, Messenger/*genetics ; RNA, Small Interfering/*genetics/*metabolism ; RNA-Induced Silencing Complex/genetics/metabolism ; Retroelements ; Ribonuclease III
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    Local positive feedback regulation determines cell shape in root hair cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-01
    Description: The specification and maintenance of growth sites are tightly regulated during cell morphogenesis in all organisms. ROOT HAIR DEFECTIVE 2 reduced nicotinamide adenine dinucleotide phosphate (RHD2 NADPH) oxidase-derived reactive oxygen species (ROS) stimulate a Ca2+ influx into the cytoplasm that is required for root hair growth in Arabidopsis thaliana. We found that Ca2+, in turn, activated the RHD2 NADPH oxidase to produce ROS at the growing point in the root hair. Together, these components could establish a means of positive feedback regulation that maintains an active growth site in expanding root hair cells. Because the location and stability of growth sites predict the ultimate form of a plant cell, our findings demonstrate how a positive feedback mechanism involving RHD2, ROS, and Ca2+ can determine cell shape.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Seiji -- Gapper, Catherine -- Kaya, Hidetaka -- Bell, Elizabeth -- Kuchitsu, Kazuyuki -- Dolan, Liam -- BBS/B/04498/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 Feb 29;319(5867):1241-4. doi: 10.1126/science.1152505.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18309082" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Arabidopsis/cytology/growth & development/*metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Calcium/*metabolism ; Cation Transport Proteins/metabolism ; Cell Line ; Cell Shape ; EF Hand Motifs ; Endocytosis ; *Feedback, Physiological ; Humans ; Mutant Proteins/chemistry/metabolism ; NADPH Oxidase/chemistry/genetics/*metabolism ; Oxazoles/pharmacology ; Phosphorylation ; Plant Roots/*cytology/metabolism ; Protein Structure, Tertiary ; Reactive Oxygen Species/*metabolism ; Recombinant Fusion Proteins/metabolism
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