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  • Cell Line  (686)
  • American Association for the Advancement of Science (AAAS)  (686)
  • Cell Press
  • EMBO Press
  • Essen : Verl. Glückauf
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • PANGAEA
  • 2005-2009  (341)
  • 2000-2004  (345)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (686)
  • Cell Press
  • EMBO Press
  • Essen : Verl. Glückauf
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
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Years
Year
  • 101
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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)
    Details
    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
    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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  • 102
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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)
    Details
    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
    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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  • 103
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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)
    Details
    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
    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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  • 104
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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
    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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  • 105
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 106
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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
    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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  • 107
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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
    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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  • 108
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 109
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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
    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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  • 110
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 111
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Adapting proteostasis for disease intervention (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Cell biology. A seismic shift for stem cell research (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 115
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    Cancer. Aneuploidy advantages? (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 119
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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)
    Details
    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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    Counting low-copy number proteins in a single cell (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-06
    Description: We have designed a microfluidic device in which we can manipulate, lyse, label, separate, and quantify the protein contents of a single cell using single-molecule fluorescence counting. Generic labeling of proteins is achieved through fluorescent-antibody binding. The use of cylindrical optics enables high-efficiency (approximately 60%) counting of molecules in micrometer-sized channels. We used this microfluidic device to quantify beta2 adrenergic receptors expressed in insect cells (SF9). We also analyzed phycobiliprotein contents in individual cyanobacterial cells (Synechococcus sp. PCC 7942) and observed marked differences in the levels of specific complexes in cell populations that were grown under nitrogen-depleted conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Bo -- Wu, Hongkai -- Bhaya, Devaki -- Grossman, Arthur -- Granier, Sebastien -- Kobilka, Brian K -- Zare, Richard N -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):81-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, Stanford, CA 94305-5080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Bacterial Proteins/*analysis ; Bacteriolysis ; Carbocyanines ; Cell Line ; Culture Media ; Fluorescence ; Fluorescent Antibody Technique ; Fluorescent Dyes ; Humans ; Lasers ; *Microfluidic Analytical Techniques/instrumentation ; Microfluidics ; Nitrogen/metabolism ; Optics and Photonics ; Phycobilisomes/metabolism ; Phycocyanin/*analysis ; Receptors, Adrenergic, beta-2/*analysis ; Synechococcus/*chemistry/growth & development/metabolism
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    Multicolor super-resolution imaging with photo-switchable fluorescent probes (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-19
    Description: Recent advances in far-field optical nanoscopy have enabled fluorescence imaging with a spatial resolution of 20 to 50 nanometers. Multicolor super-resolution imaging, however, remains a challenging task. Here, we introduce a family of photo-switchable fluorescent probes and demonstrate multicolor stochastic optical reconstruction microscopy (STORM). Each probe consists of a photo-switchable "reporter" fluorophore that can be cycled between fluorescent and dark states, and an "activator" that facilitates photo-activation of the reporter. Combinatorial pairing of reporters and activators allows the creation of probes with many distinct colors. Iterative, color-specific activation of sparse subsets of these probes allows their localization with nanometer accuracy, enabling the construction of a super-resolution STORM image. Using this approach, we demonstrate multicolor imaging of DNA model samples and mammalian cells with 20- to 30-nanometer resolution. This technique will facilitate direct visualization of molecular interactions at the nanometer scale.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633025/" 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/PMC2633025/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bates, Mark -- Huang, Bo -- Dempsey, Graham T -- Zhuang, Xiaowei -- GM 068518/GM/NIGMS NIH HHS/ -- R01 GM068518/GM/NIGMS NIH HHS/ -- R01 GM068518-05/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1749-53. Epub 2007 Aug 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702910" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cercopithecus aethiops ; Clathrin-Coated Vesicles ; DNA/*analysis ; *DNA Probes ; *Fluorescent Dyes ; Microscopy, Fluorescence/methods ; Microtubules ; Nanotechnology
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    Differential transmission of actin motion within focal adhesions (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-01-06
    Description: Cell migration requires the transmission of motion generated in the actin cytoskeleton to the extracellular environment through a complex assembly of proteins in focal adhesions. We developed correlational fluorescent speckle microscopy to measure the coupling of focal-adhesion proteins to actin filaments. Different classes of focal-adhesion structural and regulatory molecules exhibited varying degrees of correlated motions with actin filaments, indicating hierarchical transmission of actin motion through focal adhesions. Interactions between vinculin, talin, and actin filaments appear to constitute a slippage interface between the cytoskeleton and integrins, generating a molecular clutch that is regulated during the morphodynamic transitions of cell migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Ke -- Ji, Lin -- Applegate, Kathryn T -- Danuser, Gaudenz -- Waterman-Storer, Clare M -- GM67230/GM/NIGMS NIH HHS/ -- U54GM64346/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):111-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204653" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*metabolism ; Actinin/metabolism ; Actins/*metabolism ; Animals ; Cell Line ; Cell Movement ; Extracellular Matrix/metabolism ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Focal Adhesions/*metabolism ; Integrin alphaVbeta3/metabolism ; Microfilament Proteins/*metabolism ; Microscopy, Fluorescence ; Monte Carlo Method ; Paxillin/metabolism ; Potoroidae ; Recombinant Fusion Proteins/metabolism ; Talin/metabolism ; Vinculin/metabolism
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    Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-10
    Description: A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willis, Simon N -- Fletcher, Jamie I -- Kaufmann, Thomas -- van Delft, Mark F -- Chen, Lin -- Czabotar, Peter E -- Ierino, Helen -- Lee, Erinna F -- Fairlie, W Douglas -- Bouillet, Philippe -- Strasser, Andreas -- Kluck, Ruth M -- Adams, Jerry M -- Huang, David C S -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):856-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; Tumor Suppressor Proteins/genetics/metabolism ; bcl-2 Homologous Antagonist-Killer Protein/metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism ; bcl-Associated Death Protein/metabolism ; bcl-X Protein/metabolism
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    The slit receptor EVA-1 coactivates a SAX-3/Robo mediated guidance signal in C. elegans (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-29
    Description: The SAX-3/roundabout (Robo) receptor has SLT-1/Slit-dependent and -independent functions in guiding cell and axon migrations. We identified enhancer of ventral-axon guidance defects of unc-40 mutants (EVA-1) as a Caenorhabditis elegans transmembrane receptor for SLT-1. EVA-1 has two predicted galactose-binding ectodomains, acts cell-autonomously for SLT-1/Slit-dependent axon migration functions of SAX-3/Robo, binds to SLT-1 and SAX-3, colocalizes with SAX-3 on cells, and provides cell specificity to the activation of SAX-3 signaling by SLT-1. Double mutants of eva-1 or slt-1 with sax-3 mutations suggest that SAX-3 can (when slt-1 or eva-1 function is reduced) inhibit a parallel-acting guidance mechanism, which involves UNC-40/deleted in colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujisawa, Kazuko -- Wrana, Jeffrey L -- Culotti, Joseph G -- NS41397/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1934-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute of Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Axons/*physiology ; Caenorhabditis elegans/cytology/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/*chemistry/genetics/*metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Movement ; Cloning, Molecular ; Humans ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/*metabolism ; Nervous System/growth & development/metabolism ; Neurons/physiology ; Protein Structure, Tertiary ; Receptors, Immunologic/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
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    RAP80 targets BRCA1 to specific ubiquitin structures at DNA damage sites (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-05-26
    Description: Mutations affecting the BRCT domains of the breast cancer-associated tumor suppressor BRCA1 disrupt the recruitment of this protein to DNA double-strand breaks (DSBs). The molecular structures at DSBs recognized by BRCA1 are presently unknown. We report the interaction of the BRCA1 BRCT domain with RAP80, a ubiquitin-binding protein. RAP80 targets a complex containing the BRCA1-BARD1 (BRCA1-associated ring domain protein 1) E3 ligase and the deubiquitinating enzyme (DUB) BRCC36 to MDC1-gammaH2AX-dependent lysine(6)- and lysine(63)-linked ubiquitin polymers at DSBs. These events are required for cell cycle checkpoint and repair responses to ionizing radiation, implicating ubiquitin chain recognition and turnover in the BRCA1-mediated repair of DSBs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706583/" 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/PMC2706583/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sobhian, Bijan -- Shao, Genze -- Lilli, Dana R -- Culhane, Aedin C -- Moreau, Lisa A -- Xia, Bing -- Livingston, David M -- Greenberg, Roger A -- K08 CA106597/CA/NCI NIH HHS/ -- K08 CA106597-01A2/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1198-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Genetics and Department of Medicine, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525341" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; BRCA1 Protein/*metabolism ; Binding Sites ; Carrier Proteins/*metabolism ; Cell Line ; DNA/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair/physiology ; HeLa Cells ; Humans ; Mice ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Nucleic Acid Conformation ; Protein Structure, Tertiary ; Tumor Suppressor Proteins/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligases/metabolism
    Print ISSN: 0036-8075
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    A melanocortin 1 receptor allele suggests varying pigmentation among Neanderthals (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-27
    Description: The melanocortin 1 receptor (MC1R) regulates pigmentation in humans and other vertebrates. Variants of MC1R with reduced function are associated with pale skin color and red hair in humans of primarily European origin. We amplified and sequenced a fragment of the MC1R gene (mc1r) from two Neanderthal remains. Both specimens have a mutation that was not found in approximately 3700 modern humans analyzed. Functional analyses show that this variant reduces MC1R activity to a level that alters hair and/or skin pigmentation in humans. The impaired activity of this variant suggests that Neanderthals varied in pigmentation levels, potentially on the scale observed in modern humans. Our data suggest that inactive MC1R variants evolved independently in both modern humans and Neanderthals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lalueza-Fox, Carles -- Rompler, Holger -- Caramelli, David -- Staubert, Claudia -- Catalano, Giulio -- Hughes, David -- Rohland, Nadin -- Pilli, Elena -- Longo, Laura -- Condemi, Silvana -- de la Rasilla, Marco -- Fortea, Javier -- Rosas, Antonio -- Stoneking, Mark -- Schoneberg, Torsten -- Bertranpetit, Jaume -- Hofreiter, Michael -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1453-5. Epub 2007 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departament de Biologia Animal, Universitat de Barcelona, Spain. clalueza@ub.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17962522" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Substitution ; Animals ; Biological Evolution ; Cell Line ; DNA/genetics ; *Fossils ; Hair Color/*genetics ; Hominidae/*genetics ; Humans ; Molecular Sequence Data ; *Mutation ; Polymerase Chain Reaction ; Receptor, Melanocortin, Type 1/chemistry/*genetics/metabolism ; Sequence Analysis, DNA ; Skin Pigmentation/*genetics
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    The genomic landscapes of human breast and colorectal cancers (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-13
    Description: Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, Laura D -- Parsons, D Williams -- Jones, Sian -- Lin, Jimmy -- Sjoblom, Tobias -- Leary, Rebecca J -- Shen, Dong -- Boca, Simina M -- Barber, Thomas -- Ptak, Janine -- Silliman, Natalie -- Szabo, Steve -- Dezso, Zoltan -- Ustyanksky, Vadim -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Karchin, Rachel -- Wilson, Paul A -- Kaminker, Joshua S -- Zhang, Zemin -- Croshaw, Randal -- Willis, Joseph -- Dawson, Dawn -- Shipitsin, Michail -- Willson, James K V -- Sukumar, Saraswati -- Polyak, Kornelia -- Park, Ben Ho -- Pethiyagoda, Charit L -- Pant, P V Krishna -- Ballinger, Dennis G -- Sparks, Andrew B -- Hartigan, James -- Smith, Douglas R -- Suh, Erick -- Papadopoulos, Nickolas -- Buckhaults, Phillip -- Markowitz, Sanford D -- Parmigiani, Giovanni -- Kinzler, Kenneth W -- Velculescu, Victor E -- Vogelstein, Bert -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA109274/CA/NCI NIH HHS/ -- CA112828/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM070219/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- P30-CA43703/CA/NCI NIH HHS/ -- RR017698/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1108-13. Epub 2007 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at 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/17932254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*genetics/metabolism ; Cell Line ; Chromosome Mapping ; Colorectal Neoplasms/*genetics/metabolism ; Computational Biology ; DNA, Neoplasm ; Databases, Genetic ; Genes, Neoplasm ; Genome, Human ; Humans ; Metabolic Networks and Pathways/genetics ; Mice ; Mutation ; Neoplasm Proteins/genetics/metabolism ; Sequence Analysis, DNA
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    Polymerizing actin fibers position integrins primed to probe for adhesion sites (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-17
    Description: Migrating cells extend protrusions, probing the surrounding matrix in search of permissive sites to form adhesions. We found that actin fibers polymerizing along the leading edge directed local protrusions and drove synchronous sideways movement of beta1 integrin adhesion receptors. These movements lead to the clustering and positioning of conformationally activated, but unligated, beta1 integrins along the leading edge of fibroblast lamellae and growth cone filopodia. Thus, rapid actin-based movement of primed integrins along the leading edge suggests a "sticky fingers" mechanism to probe for new adhesion sites and to direct migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galbraith, Catherine G -- Yamada, Kenneth M -- Galbraith, James A -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):992-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17303755" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*physiology ; Animals ; Antigens, CD29/*physiology ; Cell Adhesion/*physiology ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Movement/*physiology ; Extracellular Matrix/metabolism ; Fibroblasts/physiology ; Fibronectins/metabolism ; Green Fluorescent Proteins/metabolism ; Mice ; Microfilament Proteins/metabolism ; NIH 3T3 Cells ; Phosphoproteins/metabolism ; Protein Binding ; Pseudopodia/metabolism
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    Mechanism of two classes of cancer mutations in the phosphoinositide 3-kinase catalytic subunit (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-14
    Description: Many human cancers involve up-regulation of the phosphoinositide 3-kinase PI3Kalpha, with oncogenic mutations identified in both the p110alpha catalytic and the p85alpha regulatory subunits. We used crystallographic and biochemical approaches to gain insight into activating mutations in two noncatalytic p110alpha domains-the adaptor-binding and the helical domains. A structure of the adaptor-binding domain of p110alpha in a complex with the p85alpha inter-Src homology 2 (inter-SH2) domain shows that oncogenic mutations in the adaptor-binding domain are not at the inter-SH2 interface but in a polar surface patch that is a plausible docking site for other domains in the holo p110/p85 complex. We also examined helical domain mutations and found that the Glu545 to Lys545 (E545K) oncogenic mutant disrupts an inhibitory charge-charge interaction with the p85 N-terminal SH2 domain. These studies extend our understanding of the architecture of PI3Ks and provide insight into how two classes of mutations that cause a gain in function can lead to cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miled, Nabil -- Yan, Ying -- Hon, Wai-Ching -- Perisic, Olga -- Zvelebil, Marketa -- Inbar, Yuval -- Schneidman-Duhovny, Dina -- Wolfson, Haim J -- Backer, Jonathan M -- Williams, Roger L -- GM55692/GM/NIGMS NIH HHS/ -- MC_U105184308/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):239-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626883" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; *Catalytic Domain ; Cattle ; Cell Line ; Cell Transformation, Neoplastic ; Crystallography, X-Ray ; Dimerization ; Humans ; Models, Molecular ; Molecular Sequence Data ; *Mutation ; Neoplasms/*genetics ; Phosphatidylinositol 3-Kinases/antagonists & ; inhibitors/chemistry/*genetics/*metabolism ; Protein Structure, Secondary ; Protein Structure, Tertiary ; src Homology Domains
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    Protein composition of catalytically active human telomerase from immortal cells (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-31
    Description: Telomerase is a ribonucleoprotein enzyme complex that adds 5'-TTAGGG-3' repeats onto the ends of human chromosomes, providing a telomere maintenance mechanism for approximately 90% of human cancers. We have purified human telomerase approximately 10(8)-fold, with the final elution dependent on the enzyme's ability to catalyze nucleotide addition onto a DNA oligonucleotide of telomeric sequence, thereby providing specificity for catalytically active telomerase. Mass spectrometric sequencing of the protein components and molecular size determination indicated an enzyme composition of two molecules each of telomerase reverse transcriptase, telomerase RNA, and dyskerin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Scott B -- Graham, Mark E -- Lovrecz, George O -- Bache, Nicolai -- Robinson, Phillip J -- Reddel, Roger R -- New York, N.Y. -- Science. 2007 Mar 30;315(5820):1850-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Unit, Children's Medical Research Institute, 214 Hawkesbury Road, Westmead NSW 2145, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17395830" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Cycle Proteins/*chemistry/isolation & purification ; Cell Line ; Cell Line, Tumor ; Centrifugation, Density Gradient ; Humans ; Molecular Sequence Data ; Molecular Weight ; Multienzyme Complexes/chemistry ; Nuclear Proteins/*chemistry/isolation & purification ; RNA/*chemistry/isolation & purification ; Tandem Mass Spectrometry ; Telomerase/*chemistry/isolation & purification/metabolism
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    Network analysis of oncogenic Ras activation in cancer (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-20
    Description: To investigate the unregulated Ras activation associated with cancer, we developed and validated a mathematical model of Ras signaling. The model-based predictions and associated experiments help explain why only one of two classes of activating Ras point mutations with in vitro transformation potential is commonly found in cancers. Model-based analysis of these mutants uncovered a systems-level process that contributes to total Ras activation in cells. This predicted behavior was supported by experimental observations. We also used the model to identify a strategy in which a drug could cause stronger inhibition on the cancerous Ras network than on the wild-type network. This system-level analysis of the oncogenic Ras network provides new insights and potential therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stites, Edward C -- Trampont, Paul C -- Ma, Zhong -- Ravichandran, Kodi S -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):463-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beirne B. Carter Center for Immunology Research and the Department of Microbiology, University of Virginia, Charlottesville, VA 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947584" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/metabolism/pharmacology ; Cell Line ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; *Computer Simulation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; GTP Phosphohydrolases/metabolism ; GTPase-Activating Proteins/antagonists & inhibitors/metabolism ; Genes, ras ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Mathematics ; *Metabolic Networks and Pathways ; *Models, Biological ; Neoplasms/*metabolism ; Phosphorylation ; Point Mutation ; *Signal Transduction ; ras Proteins/antagonists & inhibitors/genetics/*metabolism
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    Histone replacement marks the boundaries of cis-regulatory domains (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-10
    Description: Cellular memory is maintained at homeotic genes by cis-regulatory elements whose mechanism of action is unknown. We have examined chromatin at Drosophila homeotic gene clusters by measuring, at high resolution, levels of histone replacement and nucleosome occupancy. Homeotic gene clusters display conspicuous peaks of histone replacement at boundaries of cis-regulatory domains superimposed over broad regions of low replacement. Peaks of histone replacement closely correspond to nuclease-hypersensitive sites, binding sites for Polycomb and trithorax group proteins, and sites of nucleosome depletion. Our results suggest the existence of a continuous process that disrupts nucleosomes and maintains accessibility of cis-regulatory elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mito, Yoshiko -- Henikoff, Jorja G -- Henikoff, Steven -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic Sciences Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17347439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Line ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/metabolism ; Drosophila Proteins/metabolism ; Drosophila melanogaster ; Genes, Homeobox ; Genes, Insect ; HSP70 Heat-Shock Proteins/genetics ; Histones/*metabolism ; Multigene Family ; Nuclear Proteins/metabolism ; Nucleosomes/*metabolism ; Oligonucleotide Array Sequence Analysis ; Polycomb Repressive Complex 1 ; Polycomb Repressive Complex 2 ; Protein Binding ; *Regulatory Sequences, Nucleic Acid ; Repressor Proteins/metabolism ; Response Elements ; Transcription Factors/metabolism
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    LeuT-desipramine structure reveals how antidepressants block neurotransmitter reuptake (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-11
    Description: Tricyclic antidepressants exert their pharmacological effect-inhibiting the reuptake of serotonin, norepinephrine, and dopamine-by directly blocking neurotransmitter transporters (SERT, NET, and DAT, respectively) in the presynaptic membrane. The drug-binding site and the mechanism of this inhibition are poorly understood. We determined the crystal structure at 2.9 angstroms of the bacterial leucine transporter (LeuT), a homolog of SERT, NET, and DAT, in complex with leucine and the antidepressant desipramine. Desipramine binds at the inner end of the extracellular cavity of the transporter and is held in place by a hairpin loop and by a salt bridge. This binding site is separated from the leucine-binding site by the extracellular gate of the transporter. By directly locking the gate, desipramine prevents conformational changes and blocks substrate transport. Mutagenesis experiments on human SERT and DAT indicate that both the desipramine-binding site and its inhibition mechanism are probably conserved in the human neurotransmitter transporters.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711652/" 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/PMC3711652/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Zheng -- Zhen, Juan -- Karpowich, Nathan K -- Goetz, Regina M -- Law, Christopher J -- Reith, Maarten E A -- Wang, Da-Neng -- DA013261/DA/NIDA NIH HHS/ -- DA019676/DA/NIDA NIH HHS/ -- GM075026/GM/NIGMS NIH HHS/ -- GM075936/GM/NIGMS NIH HHS/ -- R01 DA013261/DA/NIDA NIH HHS/ -- R01 DA019676/DA/NIDA NIH HHS/ -- R01 DK053973/DK/NIDDK NIH HHS/ -- R21 DK060841/DK/NIDDK NIH HHS/ -- R21 GM075936/GM/NIGMS NIH HHS/ -- U54 GM075026/GM/NIGMS NIH HHS/ -- U54 GM095315/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1390-3. Epub 2007 Aug 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine and Department of Cell Biology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17690258" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antidepressive Agents, Tricyclic/chemistry/*metabolism ; Bacterial Proteins/chemistry/*metabolism ; Binding Sites ; Caenorhabditis elegans Proteins/chemistry/metabolism ; Cell Line ; Conserved Sequence ; Crystallography, X-Ray ; Desipramine/chemistry/*metabolism ; Dopamine/chemistry/metabolism ; Dopamine Uptake Inhibitors/chemistry/metabolism ; Drosophila Proteins/chemistry/metabolism ; Humans ; Leucine/chemistry/metabolism ; Models, Molecular ; Molecular Sequence Data ; Neurotransmitter Uptake Inhibitors/chemistry/*metabolism ; Norepinephrine/chemistry/metabolism ; Norepinephrine Plasma Membrane Transport Proteins/antagonists & ; inhibitors/chemistry/metabolism ; Plasma Membrane Neurotransmitter Transport Proteins/chemistry/*metabolism ; Protein Binding ; Protein Conformation ; Sequence Homology, Amino Acid ; Serotonin/chemistry/metabolism ; Serotonin Uptake Inhibitors/chemistry/metabolism
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    Demethylation of H3K27 regulates polycomb recruitment and H2A ubiquitination (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-01
    Description: Methylation of histone H3 lysine 27 (H3K27) is a posttranslational modification that is highly correlated with genomic silencing. Here we show that human UTX, a member of the Jumonji C family of proteins, is a di- and trimethyl H3K27 demethylase. UTX occupies the promoters of HOX gene clusters and regulates their transcriptional output by modulating the recruitment of polycomb repressive complex 1 and the monoubiquitination of histone H2A. Moreover, UTX associates with mixed-lineage leukemia (MLL) 2/3 complexes, and during retinoic acid signaling events, the recruitment of the UTX complex to HOX genes results in H3K27 demethylation and a concomitant methylation of H3K4. Our results suggest a concerted mechanism for transcriptional activation in which cycles of H3K4 methylation by MLL2/3 are linked with the demethylation of H3K27 through UTX.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Min Gyu -- Villa, Raffaella -- Trojer, Patrick -- Norman, Jessica -- Yan, Kai-Ping -- Reinberg, Danny -- Di Croce, Luciano -- Shiekhattar, Ramin -- R01CA090758/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):447-50. Epub 2007 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761849" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Line ; Cell Line, Tumor ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells ; *Genes, Homeobox ; Histone Demethylases ; Histones/*metabolism ; Humans ; Lysine/*metabolism ; Methylation ; Multigene Family ; Neoplasm Proteins/metabolism ; Nuclear Proteins/genetics/*metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism ; Repressor Proteins/*metabolism ; Signal Transduction ; Transcription, Genetic ; Transcriptional Activation ; Tretinoin/metabolism/pharmacology ; Ubiquitin/metabolism
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    A membrane receptor for retinol binding protein mediates cellular uptake of vitamin A (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-01-27
    Description: Vitamin A has diverse biological functions. It is transported in the blood as a complex with retinol binding protein (RBP), but the molecular mechanism by which vitamin A is absorbed by cells from the vitamin A-RBP complex is not clearly understood. We identified in bovine retinal pigment epithelium cells STRA6, a multitransmembrane domain protein, as a specific membrane receptor for RBP. STRA6 binds to RBP with high affinity and has robust vitamin A uptake activity from the vitamin A-RBP complex. It is widely expressed in embryonic development and in adult organ systems. The RBP receptor represents a major physiological mediator of cellular vitamin A uptake.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawaguchi, Riki -- Yu, Jiamei -- Honda, Jane -- Hu, Jane -- Whitelegge, Julian -- Ping, Peipei -- Wiita, Patrick -- Bok, Dean -- Sun, Hui -- 5T32EY07026/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):820-5. Epub 2007 Jan 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, David Geffen School of Medicine at UCLA, 650 Charles E. Young Drive South, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17255476" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/metabolism ; Amino Acid Sequence ; Animals ; Blood-Retinal Barrier ; COS Cells ; Cattle ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cercopithecus aethiops ; Embryonic Development ; Endocytosis ; Humans ; Molecular Sequence Data ; Mutation, Missense ; Pigment Epithelium of Eye/*metabolism ; Placenta/metabolism ; Receptors, Cell Surface/*metabolism ; Retinal Vessels/metabolism ; Retinol-Binding Proteins/*metabolism ; Spleen/metabolism ; Transfection ; Vitamin A/*metabolism
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    2008 budget. Senators offer sympathetic ear to complaints on NIH's fiscal slide (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2007 Mar 23;315(5819):1646.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17379778" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*economics ; *Budgets ; Cell Line ; Embryo Research/*economics ; *Embryonic Stem Cells ; Financing, Government ; Humans ; National Institutes of Health (U.S.)/*economics ; Politics ; *Research Support as Topic ; United States
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    Widespread monoallelic expression on human autosomes (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-17
    Description: Monoallelic expression with random choice between the maternal and paternal alleles defines an unusual class of genes comprising X-inactivated genes and a few autosomal gene families. Using a genome-wide approach, we assessed allele-specific transcription of about 4000 human genes in clonal cell lines and found that more than 300 were subject to random monoallelic expression. For a majority of monoallelic genes, we also observed some clonal lines displaying biallelic expression. Clonal cell lines reflect an independent choice to express the maternal, the paternal, or both alleles for each of these genes. This can lead to differences in expressed protein sequence and to differences in levels of gene expression. Unexpectedly widespread monoallelic expression suggests a mechanism that generates diversity in individual cells and their clonal descendants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gimelbrant, Alexander -- Hutchinson, John N -- Thompson, Benjamin R -- Chess, Andrew -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1136-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Human Genetic Research and Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006746" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Apoptosis Regulatory Proteins/genetics ; Calcium-Calmodulin-Dependent Protein Kinases/genetics ; Cell Line ; Clone Cells ; DNA-Binding Proteins/genetics ; Death-Associated Protein Kinases ; Dosage Compensation, Genetic ; Female ; *Gene Expression ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Genotype ; Humans ; In Situ Hybridization, Fluorescence ; Polymerase Chain Reaction ; Trans-Activators/genetics
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    DUBA: a deubiquitinase that regulates type I interferon production (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: Production of type I interferon (IFN-I) is a critical host defense triggered by pattern-recognition receptors (PRRs) of the innate immune system. Deubiquitinating enzyme A (DUBA), an ovarian tumor domain-containing deubiquitinating enzyme, was discovered in a small interfering RNA-based screen as a regulator of IFN-I production. Reduction of DUBA augmented the PRR-induced IFN-I response, whereas ectopic expression of DUBA had the converse effect. DUBA bound tumor necrosis factor receptor-associated factor 3 (TRAF3), an adaptor protein essential for the IFN-I response. TRAF3 is an E3 ubiquitin ligase that preferentially assembled lysine-63-linked polyubiquitin chains. DUBA selectively cleaved the lysine-63-linked polyubiquitin chains on TRAF3, resulting in its dissociation from the downstream signaling complex containing TANK-binding kinase 1. A discrete ubiquitin interaction motif within DUBA was required for efficient deubiquitination of TRAF3 and optimal suppression of IFN-I. Our data identify DUBA as a negative regulator of innate immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kayagaki, Nobuhiko -- Phung, Qui -- Chan, Salina -- Chaudhari, Ruchir -- Quan, Casey -- O'Rourke, Karen M -- Eby, Michael -- Pietras, Eric -- Cheng, Genhong -- Bazan, J Fernando -- Zhang, Zemin -- Arnott, David -- Dixit, Vishva M -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1628-32. Epub 2007 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991829" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Line ; Endopeptidases/*metabolism ; Humans ; Interferon Type I/*biosynthesis/genetics ; Interferon-alpha/genetics ; Molecular Sequence Data ; NF-kappa B/metabolism ; Protein Structure, Tertiary ; RNA, Small Interfering ; Signal Transduction ; TNF Receptor-Associated Factor 3/metabolism ; Toll-Like Receptor 3/metabolism ; Ubiquitin/metabolism ; Ubiquitination
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    Cysteine redox sensor in PKGIa enables oxidant-induced activation (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-25
    Description: Changes in the concentration of oxidants in cells can regulate biochemical signaling mechanisms that control cell function. We have found that guanosine 3',5'-monophosphate (cGMP)-dependent protein kinase (PKG) functions directly as a redox sensor. The Ialpha isoform, PKGIalpha, formed an interprotein disulfide linking its two subunits in cells exposed to exogenous hydrogen peroxide. This oxidation directly activated the kinase in vitro, and in rat cells and tissues. The affinity of the kinase for substrates it phosphorylates was enhanced by disulfide formation. This oxidation-induced activation represents an alternate mechanism for regulation along with the classical activation involving nitric oxide and cGMP. This mechanism underlies cGMP-independent vasorelaxation in response to oxidants in the cardiovascular system and provides a molecular explantion for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burgoyne, Joseph R -- Madhani, Melanie -- Cuello, Friederike -- Charles, Rebecca L -- Brennan, Jonathan P -- Schroder, Ewald -- Browning, Darren D -- Eaton, Philip -- G0700320/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1393-7. Epub 2007 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Cardiovascular Division, King's College London, Rayne Institute, St. Thomas' Hospital, London SE1 7EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta ; Cell Line ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/genetics/*metabolism ; Cysteine/*metabolism ; Disulfides/metabolism ; Enzyme Activation ; Humans ; Hydrogen Peroxide/metabolism ; Male ; Nitric Oxide/metabolism ; Oxidants/*metabolism ; Oxidation-Reduction ; Oxidative Stress ; Rats ; Rats, Wistar ; Signal Transduction ; Tissue Culture Techniques ; Transfection ; Vasodilation/physiology
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    Molecular biology. Do Watson and Crick motor from X to Z? (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapienza, Carmen -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):46-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fels Institute for Cancer Research and Department of Pathology, Temple University Medical School, 3307 North Broad Street, Philadelphia, PA 19140, USA. sapienza@temple.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonemal Dyneins ; Body Patterning ; Cell Line ; Cells, Cultured ; Chromatids/*physiology ; *Chromosome Segregation ; DNA Replication ; Dyneins/*genetics/*physiology ; Ectoderm/*cytology ; Embryonic Stem Cells/*cytology ; Endoderm/*cytology ; Interphase ; Mice ; Mitosis ; Recombination, Genetic ; Spindle Apparatus/physiology/ultrastructure
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    A MicroRNA feedback circuit in midbrain dopamine neurons (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-01
    Description: MicroRNAs (miRNAs) are evolutionarily conserved, 18- to 25-nucleotide, non-protein coding transcripts that posttranscriptionally regulate gene expression during development. miRNAs also occur in postmitotic cells, such as neurons in the mammalian central nervous system, but their function is less well characterized. We investigated the role of miRNAs in mammalian midbrain dopaminergic neurons (DNs). We identified a miRNA, miR-133b, that is specifically expressed in midbrain DNs and is deficient in midbrain tissue from patients with Parkinson's disease. miR-133b regulates the maturation and function of midbrain DNs within a negative feedback circuit that includes the paired-like homeodomain transcription factor Pitx3. We propose a role for this feedback circuit in the fine-tuning of dopaminergic behaviors such as locomotion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782470/" 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/PMC2782470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jongpil -- Inoue, Keiichi -- Ishii, Jennifer -- Vanti, William B -- Voronov, Sergey V -- Murchison, Elizabeth -- Hannon, Gregory -- Abeliovich, Asa -- R01 NS064433/NS/NINDS NIH HHS/ -- R01 NS064433-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 31;317(5842):1220-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pathology and Neurology, Center for Neurobiology and Behavior, and Taub Institute, Columbia University, College of Physicians and Surgeons 15-403, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761882" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/metabolism ; Aged ; Aged, 80 and over ; Animals ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Dopamine/*metabolism ; Embryonic Stem Cells ; *Feedback, Physiological ; Female ; Gene Expression Regulation ; Homeodomain Proteins/*metabolism ; Humans ; Locomotion ; Male ; Mesencephalon/cytology/*metabolism ; Mice ; MicroRNAs/*metabolism ; Middle Aged ; Models, Biological ; Neurons/cytology/*metabolism ; Parkinson Disease/metabolism ; Rats ; Ribonuclease III/genetics/metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
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    Negative regulation of toll-like receptor signaling by NF-kappaB p50 ubiquitination blockade (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: Toll-like receptors (TLRs) trigger the production of inflammatory cytokines and shape adaptive and innate immunity to pathogens. We report the identification of B cell leukemia (Bcl)-3 as an essential negative regulator of TLR signaling. By blocking ubiquitination of p50, a member of the nuclear factor (NF)-kappaB family, Bcl-3 stabilizes a p50 complex that inhibits gene transcription. As a consequence, Bcl-3-deficient mice and cells were found to be hypersensitive to TLR activation and unable to control responses to lipopolysaccharides. Thus, p50 ubiquitination blockade by Bcl-3 limits the strength of TLR responses and maintains innate immune homeostasis. These findings indicate that the p50 ubiquitination pathway can be selectively targeted to control deleterious inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carmody, Ruaidhri J -- Ruan, Qingguo -- Palmer, Scott -- Hilliard, Brendan -- Chen, Youhai H -- AI069289/AI/NIAID NIH HHS/ -- AI50059/AI/NIAID NIH HHS/ -- DK070691/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):675-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673665" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; DNA/metabolism ; Female ; Half-Life ; Immune Tolerance ; Immunity, Innate ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages, Peritoneal/*immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B p50 Subunit/*metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics/*metabolism ; *Signal Transduction ; Toll-Like Receptors/*metabolism ; Transcription Factor RelA/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/genetics/metabolism ; Ubiquitin/metabolism
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    Gene body-specific methylation on the active X chromosome (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-27
    Description: Differential DNA methylation is important for the epigenetic regulation of gene expression. Allele-specific methylation of the inactive X chromosome has been demonstrated at promoter CpG islands, but the overall pattern of methylation on the active X(Xa) and inactive X (Xi) chromosomes is unknown. We performed allele-specific analysis of more than 1000 informative loci along the human X chromosome. The Xa displays more than two times as much allele-specific methylation as Xi. This methylation is concentrated at gene bodies, affecting multiple neighboring CpGs. Before X inactivation, all of these Xa gene body-methylated sites are biallelically methylated. Thus, a bipartite methylation-demethylation program results in Xa-specific hypomethylation at gene promoters and hypermethylation at gene bodies. These results suggest a relationship between global methylation and expression potentiality.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hellman, Asaf -- Chess, Andrew -- New York, N.Y. -- Science. 2007 Feb 23;315(5815):1141-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Human Genetic Research and Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA. hellman@chgr.mgh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17322062" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cell Line ; Chromosomes, Human, X/*genetics/metabolism ; CpG Islands ; *DNA Methylation ; Embryonic Stem Cells ; Epigenesis, Genetic ; Female ; Gene Expression Regulation ; Gene Silencing ; Heterozygote ; Humans ; Male ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; X Chromosome Inactivation
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    Switching from repression to activation: microRNAs can up-regulate translation (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-12-01
    Description: AU-rich elements (AREs) and microRNA target sites are conserved sequences in messenger RNA (mRNA) 3' untranslated regions (3'UTRs) that control gene expression posttranscriptionally. Upon cell cycle arrest, the ARE in tumor necrosis factor-alpha (TNFalpha) mRNA is transformed into a translation activation signal, recruiting Argonaute (AGO) and fragile X mental retardation-related protein 1 (FXR1), factors associated with micro-ribonucleoproteins (microRNPs). We show that human microRNA miR369-3 directs association of these proteins with the AREs to activate translation. Furthermore, we document that two well-studied microRNAs-Let-7 and the synthetic microRNA miRcxcr4-likewise induce translation up-regulation of target mRNAs on cell cycle arrest, yet they repress translation in proliferating cells. Thus, activation is a common function of microRNPs on cell cycle arrest. We propose that translation regulation by microRNPs oscillates between repression and activation during the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vasudevan, Shobha -- Tong, Yingchun -- Steitz, Joan A -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1931-4. Epub 2007 Nov 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048652" target="_blank"〉PubMed〈/a〉
    Keywords: *3' Untranslated Regions ; Argonaute Proteins ; Base Pairing ; Cell Cycle ; Cell Line ; Cell Proliferation ; Computational Biology ; Eukaryotic Initiation Factor-2/genetics/metabolism ; *Gene Expression Regulation ; HMGA2 Protein/genetics ; HeLa Cells ; Humans ; Interphase ; MicroRNAs/*metabolism ; *Protein Biosynthesis ; RNA, Messenger/genetics/metabolism ; RNA-Binding Proteins/genetics/metabolism ; Ribonucleoproteins/metabolism ; Transfection ; Tumor Necrosis Factor-alpha/biosynthesis/*genetics ; *Up-Regulation
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    Requirement of inositol pyrophosphates for full exocytotic capacity in pancreatic beta cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-24
    Description: Inositol pyrophosphates are recognized components of cellular processes that regulate vesicle trafficking, telomere length, and apoptosis. We observed that pancreatic beta cells maintain high basal concentrations of the pyrophosphate diphosphoinositol pentakisphosphate (InsP7 or IP7). Inositol hexakisphosphate kinases (IP6Ks) that can generate IP7 were overexpressed. This overexpression stimulated exocytosis of insulin-containing granules from the readily releasable pool. Exogenously applied IP7 dose-dependently enhanced exocytosis at physiological concentrations. We determined that IP6K1 and IP6K2 were present in beta cells. RNA silencing of IP6K1, but not IP6K2, inhibited exocytosis, which suggests that IP6K1 is the critical endogenous kinase. Maintenance of high concentrations of IP7 in the pancreatic beta cell may enhance the immediate exocytotic capacity and consequently allow rapid adjustment of insulin secretion in response to increased demand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Illies, Christopher -- Gromada, Jesper -- Fiume, Roberta -- Leibiger, Barbara -- Yu, Jia -- Juhl, Kirstine -- Yang, Shao-Nian -- Barma, Deb K -- Falck, John R -- Saiardi, Adolfo -- Barker, Christopher J -- Berggren, Per-Olof -- GM31278/GM/NIGMS NIH HHS/ -- MC_U122680443/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1299-302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033884" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; Electric Capacitance ; *Exocytosis ; Inositol Phosphates/*metabolism ; Insulin/*secretion ; Insulin-Secreting Cells/*metabolism/secretion ; Islets of Langerhans/metabolism ; Mice ; Patch-Clamp Techniques ; Phosphotransferases (Phosphate Group Acceptor)/genetics/metabolism ; Phytic Acid/metabolism ; RNA Interference ; Rats ; Secretory Vesicles/*metabolism ; Transfection
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    Free-range eggs? (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLaren, Anne -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):339.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Embryo Research ; Embryonic Stem Cells/*cytology/physiology ; Female ; Humans ; Male ; Mice ; Nuclear Transfer Techniques ; *Oocyte Donation/ethics ; Ovum/*cytology/physiology ; Spermatozoa/cytology/physiology
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    Rheb activates mTOR by antagonizing its endogenous inhibitor, FKBP38 (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-10
    Description: The mammalian target of rapamycin, mTOR, is a central regulator of cell growth. Its activity is regulated by Rheb, a Ras-like small guanosine triphosphatase (GTPase), in response to growth factor stimulation and nutrient availability. We show that Rheb regulates mTOR through FKBP38, a member of the FK506-binding protein (FKBP) family that is structurally related to FKBP12. FKBP38 binds to mTOR and inhibits its activity in a manner similar to that of the FKBP12-rapamycin complex. Rheb interacts directly with FKBP38 and prevents its association with mTOR in a guanosine 5'-triphosphate (GTP)-dependent manner. Our findings suggest that FKBP38 is an endogenous inhibitor of mTOR, whose inhibitory activity is antagonized by Rheb in response to growth factor stimulation and nutrient availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bai, Xiaochun -- Ma, Dongzhu -- Liu, Anling -- Shen, Xiaoyun -- Wang, Qiming J -- Liu, Yongjian -- Jiang, Yu -- GM068832/GM/NIGMS NIH HHS/ -- R01 CA129821/CA/NCI NIH HHS/ -- R01 GM068832/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):977-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Pittsburgh School of Medicine, E1357 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991864" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Cell Line ; Culture Media ; Guanosine Triphosphate/metabolism ; Humans ; Insulin/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Monomeric GTP-Binding Proteins/*metabolism ; Multiprotein Complexes ; Mutant Proteins/metabolism ; Neuropeptides/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/chemistry/*metabolism ; Protein Structure, Tertiary ; Proteins ; Recombinant Proteins/metabolism ; Serum ; Signal Transduction ; Sirolimus/metabolism/pharmacology ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins/antagonists & inhibitors/*metabolism ; Transcription Factors/metabolism
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    Quantitative morphological signatures define local signaling networks regulating cell morphology (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-06-26
    Description: Although classical genetic and biochemical approaches have identified hundreds of proteins that function in the dynamic remodeling of cell shape in response to upstream signals, there is currently little systems-level understanding of the organization and composition of signaling networks that regulate cell morphology. We have developed quantitative morphological profiling methods to systematically investigate the role of individual genes in the regulation of cell morphology in a fast, robust, and cost-efficient manner. We analyzed a compendium of quantitative morphological signatures and described the existence of local signaling networks that act to regulate cell protrusion, adhesion, and tension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakal, Chris -- Aach, John -- Church, George -- Perrimon, Norbert -- New York, N.Y. -- Science. 2007 Jun 22;316(5832):1753-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17588932" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Movement/genetics/physiology ; Cell Shape/*genetics/physiology ; Drosophila ; Green Fluorescent Proteins ; Metabolic Networks and Pathways/*genetics ; Phenotype ; RNA Interference ; Signal Transduction/*genetics
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    Regulation of gammadelta versus alphabeta T lymphocyte differentiation by the transcription factor SOX13 (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-01-16
    Description: alphabeta and gammadelta T cells originate from a common, multipotential precursor population in the thymus, but the molecular mechanisms regulating this lineage-fate decision are unknown. We have identified Sox13 as a gammadelta-specific gene in the immune system. Using Sox13 transgenic mice, we showed that this transcription factor promotes gammadelta T cell development while opposing alphabeta T cell differentiation. Conversely, mice deficient in Sox13 expression exhibited impaired development of gammadelta T cells but not alphabeta T cells. One mechanism of SOX13 function is the inhibition of signaling by the developmentally important Wnt/T cell factor (TCF) pathway. Our data thus reveal a dominant pathway regulating the developmental fate of these two lineages of T lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Melichar, Heather J -- Narayan, Kavitha -- Der, Sandy D -- Hiraoka, Yoshiki -- Gardiol, Noemie -- Jeannet, Gregoire -- Held, Werner -- Chambers, Cynthia A -- Kang, Joonsoo -- R01CA100382/92614/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 12;315(5809):230-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Graduate Program in Immunology and Virology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17218525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics ; Autoantigens/genetics/*metabolism ; Cell Line ; Cell Lineage ; Cell Proliferation ; Embryonic Development ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Rearrangement, T-Lymphocyte ; High Mobility Group Proteins/genetics/*metabolism ; Humans ; *Lymphopoiesis ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*analysis ; Receptors, Antigen, T-Cell, gamma-delta/*analysis/genetics ; Signal Transduction ; T Cell Transcription Factor 1/physiology ; T-Lymphocyte Subsets/*cytology/immunology/metabolism ; Wnt Proteins/metabolism
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    ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damage (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: Cellular responses to DNA damage are mediated by a number of protein kinases, including ATM (ataxia telangiectasia mutated) and ATR (ATM and Rad3-related). The outlines of the signal transduction portion of this pathway are known, but little is known about the physiological scope of the DNA damage response (DDR). We performed a large-scale proteomic analysis of proteins phosphorylated in response to DNA damage on consensus sites recognized by ATM and ATR and identified more than 900 regulated phosphorylation sites encompassing over 700 proteins. Functional analysis of a subset of this data set indicated that this list is highly enriched for proteins involved in the DDR. This set of proteins is highly interconnected, and we identified a large number of protein modules and networks not previously linked to the DDR. This database paints a much broader landscape for the DDR than was previously appreciated and opens new avenues of investigation into the responses to DNA damage in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuoka, Shuhei -- Ballif, Bryan A -- Smogorzewska, Agata -- McDonald, E Robert 3rd -- Hurov, Kristen E -- Luo, Ji -- Bakalarski, Corey E -- Zhao, Zhenming -- Solimini, Nicole -- Lerenthal, Yaniv -- Shiloh, Yosef -- Gygi, Steven P -- Elledge, Stephen J -- 1U19A1067751/PHS HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1160-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and 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/17525332" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; Binding Sites ; Cell Cycle/physiology ; Cell Cycle Proteins/*physiology ; Cell Line ; Computational Biology ; Consensus Sequence ; *DNA Damage ; *DNA Repair ; DNA Replication/physiology ; DNA-Binding Proteins/*physiology ; Humans ; Immunoprecipitation ; Isotope Labeling ; Mice ; NIH 3T3 Cells ; Phosphorylation ; Protein-Serine-Threonine Kinases/*physiology ; Proteome/isolation & purification/physiology ; RNA, Small Interfering ; Signal Transduction ; Substrate Specificity ; Tumor Suppressor Proteins/*physiology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    TARP auxiliary subunits switch AMPA receptor antagonists into partial agonists (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-03
    Description: Quinoxalinedione compounds such as 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) are the most commonly used alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonists. However, we find that in the presence of transmembrane AMPA receptor regulatory proteins (TARPs), which are AMPA receptor auxiliary subunits, CNQX acts as a partial agonist. CNQX induced small depolarizing currents in neurons of the central nervous system, and reconstitution of this agonist activity required coexpression of TARPs. A crystal structure of CNQX bound to the TARP-less AMPA receptor ligand-binding domain showed that, although CNQX induces partial domain closure, this movement is not transduced into linker separation, suggesting that TARPs may increase agonist efficacy by strengthening the coupling between domain closure and channel opening. Our results demonstrate that the presence of an auxiliary subunit can determine whether a compound functions as an agonist or antagonist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Menuz, Karen -- Stroud, Robert M -- Nicoll, Roger A -- Hays, Franklin A -- GM078754/GM/NIGMS NIH HHS/ -- P50 GM73210/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):815-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California at San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975069" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione/chemistry/*pharmacology ; Animals ; Benzodiazepines/pharmacology ; Binding, Competitive ; Cell Line ; Cerebellum/cytology ; Crystallography, X-Ray ; *Drug Partial Agonism ; Hippocampus/cytology ; Humans ; In Vitro Techniques ; Interneurons/drug effects ; Mice ; Models, Molecular ; Patch-Clamp Techniques ; Protein Conformation ; Protein Subunits/*physiology ; Pyramidal Cells/drug effects/metabolism ; Quinoxalines/pharmacology ; Receptors, AMPA/*agonists/*antagonists & inhibitors ; Structure-Activity Relationship ; Synaptic Transmission/drug effects ; Trichlormethiazide/pharmacology
    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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    Immunization by avian H5 influenza hemagglutinin mutants with altered receptor binding specificity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-11
    Description: Influenza virus entry is mediated by the receptor binding domain (RBD) of its spike, the hemagglutinin (HA). Adaptation of avian viruses to humans is associated with HA specificity for alpha2,6- rather than alpha2,3-linked sialic acid (SA) receptors. Here, we define mutations in influenza A subtype H5N1 (avian) HA that alter its specificity for SA either by decreasing alpha2,3- or increasing alpha2,6-SA recognition. RBD mutants were used to develop vaccines and monoclonal antibodies that neutralized new variants. Structure-based modification of HA specificity can guide the development of preemptive vaccines and therapeutic monoclonal antibodies that can be evaluated before the emergence of human-adapted H5N1 strains.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367145/" 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/PMC2367145/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Zhi-Yong -- Wei, Chih-Jen -- Kong, Wing-Pui -- Wu, Lan -- Xu, Ling -- Smith, David F -- Nabel, Gary J -- Z99 AI999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 10;317(5839):825-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine Research Center, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Building 40, Room 4502, Mailstop Code MSC-3005, 40 Convent Drive, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17690300" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Viral/immunology ; Carbohydrate Conformation ; Cell Line ; Female ; Genes, Viral ; Hemagglutination Inhibition Tests ; Hemagglutinin Glycoproteins, Influenza Virus/*genetics/*immunology/metabolism ; Humans ; Influenza A Virus, H5N1 Subtype/*genetics/*immunology/metabolism ; Influenza Vaccines/immunology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; *Mutation ; Neutralization Tests ; Receptors, Virus/*metabolism ; Sialic Acids/*metabolism ; Vaccination
    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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    Rev-erbalpha, a heme sensor that coordinates metabolic and circadian pathways (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-17
    Description: The circadian clock temporally coordinates metabolic homeostasis in mammals. Central to this is heme, an iron-containing porphyrin that serves as prosthetic group for enzymes involved in oxidative metabolism as well as transcription factors that regulate circadian rhythmicity. The circadian factor that integrates this dual function of heme is not known. We show that heme binds reversibly to the orphan nuclear receptor Rev-erbalpha, a critical negative component of the circadian core clock, and regulates its interaction with a nuclear receptor corepressor complex. Furthermore, heme suppresses hepatic gluconeogenic gene expression and glucose output through Rev-erbalpha-mediated gene repression. Thus, Rev-erbalpha serves as a heme sensor that coordinates the cellular clock, glucose homeostasis, and energy metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, Lei -- Wu, Nan -- Curtin, Joshua C -- Qatanani, Mohammed -- Szwergold, Nava R -- Reid, Robert A -- Waitt, Gregory M -- Parks, Derek J -- Pearce, Kenneth H -- Wisely, G Bruce -- Lazar, Mitchell A -- R01 DK45586/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Dec 14;318(5857):1786-9. Epub 2007 Nov 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006707" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks ; Cell Line ; Cell Line, Tumor ; *Circadian Rhythm/genetics ; DNA-Binding Proteins/*metabolism ; Energy Metabolism ; *Gene Expression Regulation ; Gluconeogenesis/genetics ; Glucose/*metabolism ; Glucose-6-Phosphatase/genetics/metabolism ; Heme/*metabolism ; Hemin/pharmacology ; Histone Deacetylases/metabolism ; Homeostasis ; Humans ; Male ; *Metabolic Networks and Pathways ; Mice ; Nuclear Proteins/metabolism ; Nuclear Receptor Co-Repressor 1 ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Repressor Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    TLR3 deficiency in patients with herpes simplex encephalitis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-18
    Description: Some Toll and Toll-like receptors (TLRs) provide immunity to experimental infections in animal models, but their contribution to host defense in natural ecosystems is unknown. We report a dominant-negative TLR3 allele in otherwise healthy children with herpes simplex virus 1 (HSV-1) encephalitis. TLR3 is expressed in the central nervous system (CNS), where it is required to control HSV-1, which spreads from the epithelium to the CNS via cranial nerves. TLR3 is also expressed in epithelial and dendritic cells, which apparently use TLR3-independent pathways to prevent further dissemination of HSV-1 and to provide resistance to other pathogens in TLR3-deficient patients. Human TLR3 appears to be redundant in host defense to most microbes but is vital for natural immunity to HSV-1 in the CNS, which suggests that neurotropic viruses have contributed to the evolutionary maintenance of TLR3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Shen-Ying -- Jouanguy, Emmanuelle -- Ugolini, Sophie -- Smahi, Asma -- Elain, Gaelle -- Romero, Pedro -- Segal, David -- Sancho-Shimizu, Vanessa -- Lorenzo, Lazaro -- Puel, Anne -- Picard, Capucine -- Chapgier, Ariane -- Plancoulaine, Sabine -- Titeux, Matthias -- Cognet, Celine -- von Bernuth, Horst -- Ku, Cheng-Lung -- Casrouge, Armanda -- Zhang, Xin-Xin -- Barreiro, Luis -- Leonard, Joshua -- Hamilton, Claire -- Lebon, Pierre -- Heron, Benedicte -- Vallee, Louis -- Quintana-Murci, Lluis -- Hovnanian, Alain -- Rozenberg, Flore -- Vivier, Eric -- Geissmann, Frederic -- Tardieu, Marc -- Abel, Laurent -- Casanova, Jean-Laurent -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 14;317(5844):1522-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, Institut National de la Sante et de la Recherche Medicale (INSERM), U550, Faculty Necker, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872438" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; CD8-Positive T-Lymphocytes/immunology ; Cell Line ; Child, Preschool ; Dendritic Cells/immunology ; Encephalitis, Herpes Simplex/*genetics/*immunology ; Female ; Fibroblasts/immunology/metabolism/virology ; Genes, Dominant ; *Herpesvirus 1, Human/physiology ; Heterozygote ; Humans ; Immunity, Innate ; Infant ; Interferons/biosynthesis ; Keratinocytes/immunology ; Killer Cells, Natural/immunology ; Leukocytes, Mononuclear/immunology ; Mutation ; Poly I-C/pharmacology ; Toll-Like Receptor 3/chemistry/*deficiency/*genetics/physiology
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    Mussel-inspired surface chemistry for multifunctional coatings (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-20
    Description: We report a method to form multifunctional polymer coatings through simple dip-coating of objects in an aqueous solution of dopamine. Inspired by the composition of adhesive proteins in mussels, we used dopamine self-polymerization to form thin, surface-adherent polydopamine films onto a wide range of inorganic and organic materials, including noble metals, oxides, polymers, semiconductors, and ceramics. Secondary reactions can be used to create a variety of ad-layers, including self-assembled monolayers through deposition of long-chain molecular building blocks, metal films by electroless metallization, and bioinert and bioactive surfaces via grafting of macromolecules.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2601629/" 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/PMC2601629/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Haeshin -- Dellatore, Shara M -- Miller, William M -- Messersmith, Phillip B -- DE 14193/DE/NIDCR NIH HHS/ -- HL 74151/HL/NHLBI NIH HHS/ -- R01 DE014193/DE/NIDCR NIH HHS/ -- R01 DE014193-03/DE/NIDCR NIH HHS/ -- R01 HL074151/HL/NHLBI NIH HHS/ -- R01 HL074151-04/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):426-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biomedical Engineering, Northwestern University, 2145 Sheridan Road, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947576" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesiveness ; Animals ; Biopolymers/chemistry ; Cell Adhesion ; Cell Adhesion Molecules/chemistry ; Cell Line ; Ceramics/chemistry ; Dihydroxyphenylalanine/chemistry ; Dopamine/*chemistry ; Fibroblasts/physiology ; Humans ; Hyaluronic Acid/chemistry ; Hydrogen-Ion Concentration ; Metals/chemistry ; Mytilus edulis/chemistry/physiology ; Oxidation-Reduction ; Oxides/chemistry ; Polymers/*chemistry ; Proteins/chemistry ; Semiconductors ; Surface Properties
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    Complex I binding by a virally encoded RNA regulates mitochondria-induced cell death (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-06-02
    Description: Human cytomegalovirus infection perturbs multiple cellular processes that could promote the release of proapoptotic stimuli. Consequently, it encodes mechanisms to prevent cell death during infection. Using rotenone, a potent inhibitor of the mitochondrial enzyme complex I (reduced nicotinamide adenine dinucleotide-ubiquinone oxido-reductase), we found that human cytomegalovirus infection protected cells from rotenone-induced apoptosis, a protection mediated by a 2.7-kilobase virally encoded RNA (beta2.7). During infection, beta2.7 RNA interacted with complex I and prevented the relocalization of the essential subunit genes associated with retinoid/interferon-induced mortality-19, in response to apoptotic stimuli. This interaction, which is important for stabilizing the mitochondrial membrane potential, resulted in continued adenosine triphosphate production, which is critical for the successful completion of the virus' life cycle. Complex I targeting by a viral RNA represents a refined strategy to modulate the metabolic viability of the infected host cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reeves, Matthew B -- Davies, Andrew A -- McSharry, Brian P -- Wilkinson, Gavin W -- Sinclair, John H -- G0700142/Medical Research Council/United Kingdom -- G9202171/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1345-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540903" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; *Apoptosis ; Apoptosis Regulatory Proteins/genetics/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytomegalovirus/genetics/growth & development/*physiology ; Electron Transport Complex I/antagonists & inhibitors/*metabolism ; Enzyme Inhibitors/pharmacology ; Fibroblasts/metabolism/virology ; Humans ; Membrane Potential, Mitochondrial ; Mitochondria/*metabolism ; NADH, NADPH Oxidoreductases/genetics/metabolism ; Neurons/*cytology/*virology ; Oxidative Stress ; RNA, Untranslated/genetics/metabolism ; RNA, Viral/genetics/*metabolism ; Rotenone/pharmacology
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    Restriction of an extinct retrovirus by the human TRIM5alpha antiviral protein (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-26
    Description: Primate genomes contain a large number of endogenous retroviruses and encode evolutionarily dynamic proteins that provide intrinsic immunity to retroviral infections. We report here the resurrection of the core protein of a 4-million-year-old endogenous virus from the chimpanzee genome and show that the human variant of the intrinsic immune protein TRIM5alpha can actively prevent infection by this virus. However, we suggest that selective changes that have occurred in the human lineage during the acquisition of resistance to this virus, and perhaps similar viruses, may have left our species more susceptible to infection by human immunodeficiency virus type 1 (HIV-1).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Shari M -- Malik, Harmit S -- Emerman, Michael -- New York, N.Y. -- Science. 2007 Jun 22;316(5832):1756-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17588933" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Biological Evolution ; Carrier Proteins/genetics/*physiology ; Cats ; Cell Line ; Dna ; Disease Susceptibility ; Endogenous Retroviruses/genetics/*physiology ; Evolution, Molecular ; Gorilla gorilla ; HIV Infections/genetics/immunology ; Hiv-1 ; Humans ; Immunity, Innate/genetics ; Macaca mulatta ; Molecular Sequence Data ; Pan troglodytes/genetics/virology ; Retroviridae Infections/genetics/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Wnt induces LRP6 signalosomes and promotes dishevelled-dependent LRP6 phosphorylation (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-16
    Description: Multiple signaling pathways, including Wnt signaling, participate in animal development, stem cell biology, and human cancer. Although many components of the Wnt pathway have been identified, unresolved questions remain as to the mechanism by which Wnt binding to its receptors Frizzled and Low-density lipoprotein receptor-related protein 6 (LRP6) triggers downstream signaling events. With live imaging of vertebrate cells, we show that Wnt treatment quickly induces plasma membrane-associated LRP6 aggregates. LRP6 aggregates are phosphorylated and can be detergent-solubilized as ribosome-sized multiprotein complexes. Phospho-LRP6 aggregates contain Wnt-pathway components but no common vesicular traffic markers except caveolin. The scaffold protein Dishevelled (Dvl) is required for LRP6 phosphorylation and aggregation. We propose that Wnts induce coclustering of receptors and Dvl in LRP6-signalosomes, which in turn triggers LRP6 phosphorylation to promote Axin recruitment and beta-catenin stabilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bilic, Josipa -- Huang, Ya-Lin -- Davidson, Gary -- Zimmermann, Timo -- Cruciat, Cristina-Maria -- Bienz, Mariann -- Niehrs, Christof -- MC_U105192713/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1619-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Embryology, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569865" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*metabolism ; Animals ; Axin Protein ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Centrifugation, Density Gradient ; Cytoplasm/metabolism ; Drosophila ; Glycogen Synthase Kinase 3/analysis/metabolism ; HeLa Cells ; Humans ; LDL-Receptor Related Proteins/analysis/genetics/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphoproteins/*metabolism ; Phosphorylation ; Repressor Proteins/analysis/metabolism ; *Signal Transduction ; Transfection ; Wnt Proteins/*metabolism ; Wnt3 Protein ; beta Catenin/metabolism
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    Genes required for mitotic spindle assembly in Drosophila S2 cells (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-07
    Description: The formation of a metaphase spindle, a bipolar microtubule array with centrally aligned chromosomes, is a prerequisite for the faithful segregation of a cell's genetic material. Using a full-genome RNA interference screen of Drosophila S2 cells, we identified about 200 genes that contribute to spindle assembly, more than half of which were unexpected. The screen, in combination with a variety of secondary assays, led to new insights into how spindle microtubules are generated; how centrosomes are positioned; and how centrioles, centrosomes, and kinetochores are assembled.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2837481/" 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/PMC2837481/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goshima, Gohta -- Wollman, Roy -- Goodwin, Sarah S -- Zhang, Nan -- Scholey, Jonathan M -- Vale, Ronald D -- Stuurman, Nico -- R37 GM038499/GM/NIGMS NIH HHS/ -- R37 GM038499-21/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):417-21. Epub 2007 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and the Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16th Street, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Centrosome/metabolism/ultrastructure ; Chromosomes/physiology/ultrastructure ; Drosophila Proteins/*genetics/*physiology ; Drosophila melanogaster ; *Genes, Insect ; Image Processing, Computer-Assisted ; Kinetochores/metabolism ; Metaphase ; Microtubules/metabolism ; Mitosis ; Phenotype ; RNA Interference ; Spindle Apparatus/*genetics/*metabolism/ultrastructure ; Tubulin/metabolism
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    An X chromosome gene, WTX, is commonly inactivated in Wilms tumor (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-06
    Description: Wilms tumor is a pediatric kidney cancer associated with inactivation of the WT1 tumor-suppressor gene in 5 to 10% of cases. Using a high-resolution screen for DNA copy-number alterations in Wilms tumor, we identified somatic deletions targeting a previously uncharacterized gene on the X chromosome. This gene, which we call WTX, is inactivated in approximately one-third of Wilms tumors (15 of 51 tumors). Tumors with mutations in WTX lack WT1 mutations, and both genes share a restricted temporal and spatial expression pattern in normal renal precursors. In contrast to biallelic inactivation of autosomal tumor-suppressor genes, WTX is inactivated by a monoallelic "single-hit" event targeting the single X chromosome in tumors from males and the active X chromosome in tumors from females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rivera, Miguel N -- Kim, Woo Jae -- Wells, Julie -- Driscoll, David R -- Brannigan, Brian W -- Han, Moonjoo -- Kim, James C -- Feinberg, Andrew P -- Gerald, William L -- Vargas, Sara O -- Chin, Lynda -- Iafrate, A John -- Bell, Daphne W -- Haber, Daniel A -- P01-CA101942/CA/NCI NIH HHS/ -- R37 CA054358/CA/NCI NIH HHS/ -- R37 CA054358-17/CA/NCI NIH HHS/ -- R37-CA058596/CA/NCI NIH HHS/ -- T32-CA009216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):642-5. Epub 2007 Jan 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Harvard Medical Center, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204608" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Alleles ; Amino Acid Sequence ; Animals ; Cell Line ; Chromosome Deletion ; Chromosomes, Human, X/*genetics ; Female ; Gene Expression ; *Gene Silencing ; *Genes, Wilms Tumor ; Heterozygote ; Humans ; In Situ Hybridization, Fluorescence ; Kidney/embryology/metabolism ; Kidney Neoplasms/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Point Mutation ; Tumor Suppressor Proteins/chemistry/*genetics/physiology ; Wilms Tumor/*genetics ; beta Catenin/genetics
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    UHRF1 plays a role in maintaining DNA methylation in mammalian cells (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-04
    Description: Epigenetic inheritance in mammals relies in part on robust propagation of DNA methylation patterns throughout development. We show that the protein UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1), also known as NP95 in mouse and ICBP90 in human, is required for maintaining DNA methylation. UHRF1 colocalizes with the maintenance DNA methyltransferase protein DNMT1 throughout S phase. UHRF1 appears to tether DNMT1 to chromatin through its direct interaction with DNMT1. Furthermore UHRF1 contains a methyl DNA binding domain, the SRA (SET and RING associated) domain, that shows strong preferential binding to hemimethylated CG sites, the physiological substrate for DNMT1. These data suggest that UHRF1 may help recruit DNMT1 to hemimethylated DNA to facilitate faithful maintenance of DNA methylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bostick, Magnolia -- Kim, Jong Kyong -- Esteve, Pierre-Olivier -- Clark, Amander -- Pradhan, Sriharsa -- Jacobsen, Steven E -- GM060398/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1760-4. Epub 2007 Aug 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CCAAT-Enhancer-Binding Proteins/*metabolism ; COS Cells ; Cell Line ; Cercopithecus aethiops ; Chromatin/metabolism ; DNA (Cytosine-5-)-Methyltransferase/*metabolism ; *DNA Methylation ; HeLa Cells ; Humans ; Mice ; Nuclear Proteins/*metabolism ; Protein Binding ; Protein Structure, Tertiary
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  • 168
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    The phosphothreonine lyase activity of a bacterial type III effector family (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-17
    Description: Pathogenic bacteria use the type III secretion system to deliver effector proteins into host cells to modulate the host signaling pathways. In this study, the Shigella type III effector OspF was shown to inactivate mitogen-activated protein kinases (MAPKs) [extracellular signal-regulated kinases 1 and 2 (Erk1/2), c-Jun N-terminal kinase, and p38]. OspF irreversibly removed phosphate groups from the phosphothreonine but not from the phosphotyrosine residue in the activation loop of MAPKs. Mass spectrometry revealed a mass loss of 98 daltons in p-Erk2, due to the abstraction of the alpha proton concomitant with cleavage of the C-OP bond in the phosphothreonine residue. This unexpected enzymatic activity, termed phosphothreonine lyase, appeared specific for MAPKs and was shared by other OspF family members.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Hongtao -- Xu, Hao -- Zhou, Yan -- Zhang, Jie -- Long, Chengzu -- Li, Shuqin -- Chen, She -- Zhou, Jian-Min -- Shao, Feng -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):1000-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Biological Sciences, Beijing, 102206, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17303758" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacterial Proteins/genetics/*metabolism ; Cell Line ; HeLa Cells ; Humans ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinase 3/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism ; Molecular Sequence Data ; Mutagenesis ; NF-kappa B/metabolism ; Phosphoprotein Phosphatases/*metabolism ; Phosphorylation ; Salmonella typhimurium ; Shigella flexneri/*metabolism/physiology ; Tyrosine/metabolism ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism
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    Relative impact of nucleotide and copy number variation on gene expression phenotypes (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-10
    Description: Extensive studies are currently being performed to associate disease susceptibility with one form of genetic variation, namely, single-nucleotide polymorphisms (SNPs). In recent years, another type of common genetic variation has been characterized, namely, structural variation, including copy number variants (CNVs). To determine the overall contribution of CNVs to complex phenotypes, we have performed association analyses of expression levels of 14,925 transcripts with SNPs and CNVs in individuals who are part of the International HapMap project. SNPs and CNVs captured 83.6% and 17.7% of the total detected genetic variation in gene expression, respectively, but the signals from the two types of variation had little overlap. Interrogation of the genome for both types of variants may be an effective way to elucidate the causes of complex phenotypes and disease in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665772/" 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/PMC2665772/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stranger, Barbara E -- Forrest, Matthew S -- Dunning, Mark -- Ingle, Catherine E -- Beazley, Claude -- Thorne, Natalie -- Redon, Richard -- Bird, Christine P -- de Grassi, Anna -- Lee, Charles -- Tyler-Smith, Chris -- Carter, Nigel -- Scherer, Stephen W -- Tavare, Simon -- Deloukas, Panagiotis -- Hurles, Matthew E -- Dermitzakis, Emmanouil T -- 065535/Wellcome Trust/United Kingdom -- 076113/Wellcome Trust/United Kingdom -- 077009/Wellcome Trust/United Kingdom -- 077014/Wellcome Trust/United Kingdom -- 077046/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):848-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289997" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Female ; Gene Deletion ; *Gene Dosage ; Gene Duplication ; *Gene Expression Regulation ; *Genetic Variation ; Genetics, Population ; *Genome, Human ; Genomics/methods ; Haplotypes ; Humans ; Linkage Disequilibrium ; Male ; Mutation ; Nucleic Acid Hybridization ; Phenotype ; *Polymorphism, Single Nucleotide ; Regression Analysis
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    Ethics. The ISSCR guidelines for human embryonic stem cell research (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daley, George Q -- Ahrlund Richter, Lars -- Auerbach, Jonathan M -- Benvenisty, Nissim -- Charo, R Alta -- Chen, Grace -- Deng, Hong-Kui -- Goldstein, Lawrence S -- Hudson, Kathy L -- Hyun, Insoo -- Junn, Sung Chull -- Love, Jane -- Lee, Eng Hin -- McLaren, Anne -- Mummery, Christine L -- Nakatsuji, Norio -- Racowsky, Catherine -- Rooke, Heather -- Rossant, Janet -- Scholer, Hans R -- Solbakk, Jan Helge -- Taylor, Patrick -- Trounson, Alan O -- Weissman, Irving L -- Wilmut, Ian -- Yu, John -- Zoloth, Laurie -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):603-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital, Boston, Massachusetts, USA. george.daley@childrens.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272706" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chimera ; *Embryo Research/ethics/legislation & jurisprudence ; Embryonic Development ; *Embryonic Stem Cells ; *Guidelines as Topic ; Humans ; Informed Consent ; International Cooperation ; Oocyte Donation/economics/ethics ; Pluripotent Stem Cells ; Societies, Scientific ; Tissue Donors/ethics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    IRE1 signaling affects cell fate during the unfolded protein response (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-10
    Description: Endoplasmic reticulum (ER) stress activates a set of signaling pathways, collectively termed the unfolded protein response (UPR). The three UPR branches (IRE1, PERK, and ATF6) promote cell survival by reducing misfolded protein levels. UPR signaling also promotes apoptotic cell death if ER stress is not alleviated. How the UPR integrates its cytoprotective and proapoptotic outputs to select between life or death cell fates is unknown. We found that IRE1 and ATF6 activities were attenuated by persistent ER stress in human cells. By contrast, PERK signaling, including translational inhibition and proapoptotic transcription regulator Chop induction, was maintained. When IRE1 activity was sustained artificially, cell survival was enhanced, suggesting a causal link between the duration of UPR branch signaling and life or death cell fate after ER stress. Key findings from our studies in cell culture were recapitulated in photoreceptors expressing mutant rhodopsin in animal models of retinitis pigmentosa.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670588/" 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/PMC3670588/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Jonathan H -- Li, Han -- Yasumura, Douglas -- Cohen, Hannah R -- Zhang, Chao -- Panning, Barbara -- Shokat, Kevan M -- Lavail, Matthew M -- Walter, Peter -- K08 EY018313/EY/NEI NIH HHS/ -- K08 EY018313-01/EY/NEI NIH HHS/ -- R01 EY020846/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):944-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA. Jonathan.Lin@ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991856" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 6/metabolism ; Animals ; Animals, Genetically Modified ; *Apoptosis ; Cell Line ; *Cell Survival ; Disease Models, Animal ; Endoplasmic Reticulum/*metabolism ; Endoribonucleases/genetics/*metabolism ; Humans ; Kinetics ; Membrane Proteins/genetics/*metabolism ; Mice ; Mutation ; *Protein Folding ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Proteins/chemistry/*metabolism ; Rats ; Retina/metabolism ; Retinitis Pigmentosa/metabolism ; Rhodopsin/chemistry/metabolism ; *Signal Transduction ; eIF-2 Kinase/metabolism
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    NOV (CCN3) functions as a regulator of human hematopoietic stem or progenitor cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: Clinically successful hematopoietic cell transplantation is dependent on hematopoietic stem and progenitor cells. Here we identify the matricellular protein Nephroblastoma Overexpressed (Nov, CCN3) as being essential for their functional integrity. Nov expression is restricted to the primitive (CD34) compartments of umbilical vein cord blood, and its knockdown in these cells by lentivirus-mediated RNA interference abrogates their function in vitro and in vivo. Conversely, forced expression of Nov and addition of recombinant Nov protein both enhance primitive stem and/or progenitor activity. Taken together, our results identify Nov (CCN3) as a regulator of human hematopoietic stem or progenitor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gupta, Rajeev -- Hong, Dengli -- Iborra, Francisco -- Sarno, Samantha -- Enver, Tariq -- MC_U137961143/Medical Research Council/United Kingdom -- MC_U137973816/Medical Research Council/United Kingdom -- MC_U137973817/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Apr 27;316(5824):590-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Headington, OX3 9DS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Cell Line ; Cells, Cultured ; Colony-Forming Units Assay ; Connective Tissue Growth Factor ; Genetic Vectors ; Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology/*physiology ; Humans ; Immediate-Early Proteins/genetics/*physiology ; Intercellular Signaling Peptides and Proteins/genetics/*physiology ; Lentivirus/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Nephroblastoma Overexpressed Protein ; RNA Interference ; Recombinant Proteins/metabolism ; Transfection ; Transplantation, Heterologous
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    Augmented Wnt signaling in a mammalian model of accelerated aging (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-11
    Description: The contribution of stem and progenitor cell dysfunction and depletion in normal aging remains incompletely understood. We explored this concept in the Klotho mouse model of accelerated aging. Analysis of various tissues and organs from young Klotho mice revealed a decrease in stem cell number and an increase in progenitor cell senescence. Because klotho is a secreted protein, we postulated that klotho might interact with other soluble mediators of stem cells. We found that klotho bound to various Wnt family members. In a cell culture model, the Wnt-klotho interaction resulted in the suppression of Wnt biological activity. Tissues and organs from klotho-deficient animals showed evidence of increased Wnt signaling, and ectopic expression of klotho antagonized the activity of endogenous and exogenous Wnt. Both in vitro and in vivo, continuous Wnt exposure triggered accelerated cellular senescence. Thus, klotho appears to be a secreted Wnt antagonist and Wnt proteins have an unexpected role in mammalian aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Hongjun -- Fergusson, Maria M -- Castilho, Rogerio M -- Liu, Jie -- Cao, Liu -- Chen, Jichun -- Malide, Daniela -- Rovira, Ilsa I -- Schimel, Daniel -- Kuo, Calvin J -- Gutkind, J Silvio -- Hwang, Paul M -- Finkel, Toren -- 1 R01 DK069989-01/DK/NIDDK NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 10;317(5839):803-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17690294" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Apoptosis ; Bone Density ; Bone and Bones/metabolism ; Cell Aging/*physiology ; Cell Count ; Cell Line ; Cell Shape ; Glucuronidase/chemistry/genetics/*metabolism ; Humans ; Mice ; Mice, Transgenic ; Protein Structure, Tertiary ; *Signal Transduction ; Stem Cells/cytology/*physiology ; Wnt Proteins/antagonists & inhibitors/*metabolism ; Wnt1 Protein/metabolism ; Wnt3 Protein
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    GPCR engineering yields high-resolution structural insights into beta2-adrenergic receptor function (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-27
    Description: The beta2-adrenergic receptor (beta2AR) is a well-studied prototype for heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors (GPCRs) that respond to diffusible hormones and neurotransmitters. To overcome the structural flexibility of the beta2AR and to facilitate its crystallization, we engineered a beta2AR fusion protein in which T4 lysozyme (T4L) replaces most of the third intracellular loop of the GPCR ("beta2AR-T4L") and showed that this protein retains near-native pharmacologic properties. Analysis of adrenergic receptor ligand-binding mutants within the context of the reported high-resolution structure of beta2AR-T4L provides insights into inverse-agonist binding and the structural changes required to accommodate catecholamine agonists. Amino acids known to regulate receptor function are linked through packing interactions and a network of hydrogen bonds, suggesting a conformational pathway from the ligand-binding pocket to regions that interact with G proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenbaum, Daniel M -- Cherezov, Vadim -- Hanson, Michael A -- Rasmussen, Soren G F -- Thian, Foon Sun -- Kobilka, Tong Sun -- Choi, Hee-Jung -- Yao, Xiao-Jie -- Weis, William I -- Stevens, Raymond C -- Kobilka, Brian K -- F32 GM082028/GM/NIGMS NIH HHS/ -- NS028471/NS/NINDS NIH HHS/ -- P50 GM073197/GM/NIGMS NIH HHS/ -- P50 GM62411/GM/NIGMS NIH HHS/ -- R01 GM056169/GM/NIGMS NIH HHS/ -- R21 GM075811/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1266-73. Epub 2007 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17962519" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/chemistry/metabolism ; Adrenergic beta-Antagonists/chemistry/metabolism ; Amino Acid Sequence ; Bacteriophage T4/enzymology ; Binding Sites ; Cell Line ; Cell Membrane/chemistry/metabolism ; Crystallization ; Crystallography, X-Ray ; Drug Inverse Agonism ; Humans ; Immunoglobulin Fab Fragments/chemistry/metabolism ; Ligands ; Models, Molecular ; Molecular Sequence Data ; Muramidase/chemistry/metabolism ; Propanolamines/chemistry/metabolism ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Adrenergic, beta-2/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism
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    Structure of Galphaq-p63RhoGEF-RhoA complex reveals a pathway for the activation of RhoA by GPCRs (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-12-22
    Description: The guanine nucleotide exchange factor p63RhoGEF is an effector of the heterotrimeric guanine nucleotide-binding protein (G protein) Galphaq and thereby links Galphaq-coupled receptors (GPCRs) to the activation of the small-molecular-weight G protein RhoA. We determined the crystal structure of the Galphaq-p63RhoGEF-RhoA complex, detailing the interactions of Galphaq with the Dbl and pleckstrin homology (DH and PH) domains of p63RhoGEF. These interactions involve the effector-binding site and the C-terminal region of Galphaq and appear to relieve autoinhibition of the catalytic DH domain by the PH domain. Trio, Duet, and p63RhoGEF are shown to constitute a family of Galphaq effectors that appear to activate RhoA both in vitro and in intact cells. We propose that this structure represents the crux of an ancient signal transduction pathway that is expected to be important in an array of physiological processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lutz, Susanne -- Shankaranarayanan, Aruna -- Coco, Cassandra -- Ridilla, Marc -- Nance, Mark R -- Vettel, Christiane -- Baltus, Doris -- Evelyn, Chris R -- Neubig, Richard R -- Wieland, Thomas -- Tesmer, John J G -- HL071818/HL/NHLBI NIH HHS/ -- HL086865/HL/NHLBI NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1923-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental and Clinical Pharmacology and Toxicology, Medical Faculty Mannheim, University of Heidelberg, Maybachstrasse 14, D-68169 Mannheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18096806" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Cell Line ; Crystallography, X-Ray ; GTP-Binding Protein alpha Subunits, Gq-G11/*chemistry/metabolism ; Guanine Nucleotide Exchange Factors/*chemistry/metabolism ; Humans ; Models, Molecular ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rho Guanine Nucleotide Exchange Factors ; Signal Transduction ; rhoA GTP-Binding Protein/*chemistry/metabolism
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    Blue-light-activated histidine kinases: two-component sensors in bacteria (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-25
    Description: Histidine kinases, used for environmental sensing by bacterial two-component systems, are involved in regulation of bacterial gene expression, chemotaxis, phototaxis, and virulence. Flavin-containing domains function as light-sensory modules in plant and algal phototropins and in fungal blue-light receptors. We have discovered that the prokaryotes Brucella melitensis, Brucella abortus, Erythrobacter litoralis, and Pseudomonas syringae contain light-activated histidine kinases that bind a flavin chromophore and undergo photochemistry indicative of cysteinyl-flavin adduct formation. Infection of macrophages by B. abortus was stimulated by light in the wild type but was limited in photochemically inactive and null mutants, indicating that the flavin-containing histidine kinase functions as a photoreceptor regulating B. abortus virulence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swartz, Trevor E -- Tseng, Tong-Seung -- Frederickson, Marcus A -- Paris, Gaston -- Comerci, Diego J -- Rajashekara, Gireesh -- Kim, Jung-Gun -- Mudgett, Mary Beth -- Splitter, Gary A -- Ugalde, Rodolfo A -- Goldbaum, Fernando A -- Briggs, Winslow R -- Bogomolni, Roberto A -- 1.U54-AI-057153/AI/NIAID NIH HHS/ -- R01 GM068886/GM/NIGMS NIH HHS/ -- R01-GM068886/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1090-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, Santa Cruz, Santa Cruz, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717187" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Brucella abortus/*enzymology/growth & development/pathogenicity ; Brucella melitensis/*enzymology ; Cell Line ; Cloning, Molecular ; Enzyme Activation ; Flavin Mononucleotide/metabolism ; *Light ; Macrophages/*microbiology ; Mice ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Photochemistry ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Structure, Tertiary ; Pseudomonas syringae/*enzymology ; Signal Transduction ; Sphingomonadaceae/*enzymology ; Virulence
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Targeting of diacylglycerol degradation to M1 muscarinic receptors by beta-arrestins (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: Seven-transmembrane receptor (7TMR) signaling is transduced by second messengers such as diacylglycerol (DAG) generated in response to the heterotrimeric guanine nucleotide-binding protein Gq and is terminated by receptor desensitization and degradation of the second messengers. We show that beta-arrestins coordinate both processes for the Gq-coupled M1 muscarinic receptor. beta-Arrestins physically interact with diacylglycerol kinases (DGKs), enzymes that degrade DAG. Moreover, beta-arrestins are essential for conversion of DAG to phosphatidic acid after agonist stimulation, and this activity requires recruitment of the beta-arrestin-DGK complex to activated 7TMRs. The dual function of beta-arrestins, limiting production of diacylglycerol (by receptor desensitization) while enhancing its rate of degradation, is analogous to their ability to recruit adenosine 3',5'-monophosphate phosphodiesterases to Gs-coupled beta2-adrenergic receptors. Thus, beta-arrestins can serve similar regulatory functions for disparate classes of 7TMRs through structurally dissimilar enzymes that degrade chemically distinct second messengers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Christopher D -- Perry, Stephen J -- Regier, Debra S -- Prescott, Stephen M -- Topham, Matthew K -- Lefkowitz, Robert J -- CA95463/CA/NCI NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- HL70631/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):663-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, 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/17272726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/*metabolism ; COS Cells ; Carbachol/pharmacology ; Cell Line ; Cercopithecus aethiops ; Diacylglycerol Kinase/genetics/*metabolism ; Diglycerides/*metabolism ; Humans ; Mutation ; Phosphatidic Acids/metabolism ; Protein Binding ; RNA, Small Interfering ; Receptor, Muscarinic M1/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; *Signal Transduction ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Suppression of microRNA-silencing pathway by HIV-1 during virus replication (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-27
    Description: MicroRNAs (miRNAs) are single-stranded noncoding RNAs of 19 to 25 nucleotides that function as gene regulators and as a host cell defense against both RNA and DNA viruses. We provide evidence for a physiological role of the miRNA-silencing machinery in controlling HIV-1 replication. Type III RNAses Dicer and Drosha, responsible for miRNA processing, inhibited virus replication both in peripheral blood mononuclear cells from HIV-1-infected donors and in latently infected cells. In turn, HIV-1 actively suppressed the expression of the polycistronic miRNA cluster miR-17/92. This suppression was found to be required for efficient viral replication and was dependent on the histone acetyltransferase Tat cofactor PCAF. Our results highlight the involvement of the miRNA-silencing pathway in HIV-1 replication and latency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Triboulet, Robinson -- Mari, Bernard -- Lin, Yea-Lih -- Chable-Bessia, Christine -- Bennasser, Yamina -- Lebrigand, Kevin -- Cardinaud, Bruno -- Maurin, Thomas -- Barbry, Pascal -- Baillat, Vincent -- Reynes, Jacques -- Corbeau, Pierre -- Jeang, Kuan-Teh -- Benkirane, Monsef -- New York, N.Y. -- Science. 2007 Mar 16;315(5818):1579-82. Epub 2007 Feb 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Virologie Moleculaire, Institut de Genetique Humaine, Montpellier, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17322031" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Cell Cycle Proteins/genetics/metabolism ; Cell Line ; Gene Expression Regulation ; Gene Products, tat/metabolism ; HIV-1/genetics/*physiology ; HeLa Cells ; Histone Acetyltransferases/genetics/metabolism ; Humans ; Jurkat Cells ; Leukocytes, Mononuclear/enzymology/*virology ; MicroRNAs/*genetics ; Oligonucleotide Array Sequence Analysis ; *RNA Interference ; RNA, Small Interfering/genetics ; Ribonuclease III/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transfection ; Virus Latency ; *Virus Replication ; p300-CBP Transcription Factors ; tat Gene Products, Human Immunodeficiency Virus
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    A -defensin mutation causes black coat color in domestic dogs (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-20
    Description: Genetic analysis of mammalian color variation has provided fundamental insight into human biology and disease. In most vertebrates, two key genes, Agouti and Melanocortin 1 receptor (Mc1r), encode a ligand-receptor system that controls pigment type-switching, but in domestic dogs, a third gene is implicated, the K locus, whose genetic characteristics predict a previously unrecognized component of the melanocortin pathway. We identify the K locus as beta-defensin 103 (CBD103) and show that its protein product binds with high affinity to the Mc1r and has a simple and strong effect on pigment type-switching in domestic dogs and transgenic mice. These results expand the functional role of beta-defensins, a protein family previously implicated in innate immunity, and identify an additional class of ligands for signaling through melanocortin receptors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906624/" 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/PMC2906624/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Candille, Sophie I -- Kaelin, Christopher B -- Cattanach, Bruce M -- Yu, Bin -- Thompson, Darren A -- Nix, Matthew A -- Kerns, Julie A -- Schmutz, Sheila M -- Millhauser, Glenn L -- Barsh, Gregory S -- R01 DK064265/DK/NIDDK NIH HHS/ -- R01 DK064265-08/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1418-23. Epub 2007 Oct 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Genetics and Pediatrics, Stanford University, Stanford, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947548" target="_blank"〉PubMed〈/a〉
    Keywords: Agouti Signaling Protein/genetics/metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Chromosome Mapping ; Dogs/*genetics/metabolism ; Female ; Hair Color/*genetics ; Haplotypes ; Humans ; Keratinocytes/metabolism ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Polymorphism, Genetic ; Receptor, Melanocortin, Type 1/*metabolism ; Sequence Analysis, DNA ; Sequence Deletion ; Signal Transduction ; Skin/metabolism ; beta-Defensins/chemistry/*genetics/*metabolism
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    Left-right dynein motor implicated in selective chromatid segregation in mouse cells (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-01-06
    Description: During cell division, copies of mouse chromosome 7 are segregated selectively or randomly to daughter cells depending on the cell type. The mechanism for differential segregation is unknown. Because mouse left-right dynein (LRD) gene mutations result in randomization of visceral organs' laterality, we hypothesized that LRD may also function in selective chromatid segregation. Indeed, upon knock-down by RNA interference methods, LRD depletion disrupts biased segregation. LRD messenger RNA presence or absence correlates with the observed segregation patterns. This work supports the claim that LRD functions in a mechanism for selective chromatid segregation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Armakolas, Athanasios -- Klar, Amar J S -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):100-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Regulation and Chromosome Biology Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Post Office Box B, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonemal Dyneins ; Body Patterning ; Cell Line ; Cell Lineage ; Chromatids/*physiology ; *Chromosome Segregation ; DNA Replication ; Dyneins/*genetics/*physiology ; Ectoderm/*cytology ; Embryonic Stem Cells/*cytology ; Endoderm/*cytology ; Interphase ; Mice ; Mitosis ; Mutation ; RNA Interference ; Recombination, Genetic
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    Serine-7 of the RNA polymerase II CTD is specifically required for snRNA gene expression (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-15
    Description: RNA polymerase II (Pol II) transcribes genes that encode proteins and noncoding small nuclear RNAs (snRNAs). The carboxyl-terminal repeat domain (CTD) of the largest subunit of mammalian RNA Pol II, comprising tandem repeats of the heptapeptide consensus Tyr1-Ser2-Pro3-Thr4-Ser5-Pro6-Ser7, is required for expression of both gene types. We show that mutation of serine-7 to alanine causes a specific defect in snRNA gene expression. We also present evidence that phosphorylation of serine-7 facilitates interaction with the snRNA gene-specific Integrator complex. These findings assign a biological function to this amino acid and highlight a gene type-specific requirement for a residue within the CTD heptapeptide, supporting the existence of a CTD code.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2263945/" 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/PMC2263945/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egloff, Sylvain -- O'Reilly, Dawn -- Chapman, Rob D -- Taylor, Alice -- Tanzhaus, Katrin -- Pitts, Laura -- Eick, Dirk -- Murphy, Shona -- 072107/Wellcome Trust/United Kingdom -- 081312/Wellcome Trust/United Kingdom -- G0400653/Medical Research Council/United Kingdom -- G0400653(71330)/Medical Research Council/United Kingdom -- G9826944/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Dec 14;318(5857):1777-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18079403" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine ; Amino Acid Sequence ; Cell Line ; Consensus Sequence ; *Gene Expression Regulation ; Heterogeneous-Nuclear Ribonucleoproteins/genetics ; Humans ; Mutation ; Oligopeptides/chemistry/metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein Subunits/genetics/metabolism ; RNA Polymerase II/chemistry/genetics/*metabolism ; RNA Processing, Post-Transcriptional ; RNA, Messenger/genetics/metabolism ; RNA, Small Nuclear/*genetics ; Serine/*metabolism ; Templates, Genetic ; *Transcription, Genetic
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    A two-amino acid change in the hemagglutinin of the 1918 influenza virus abolishes transmission (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-03
    Description: The 1918 influenza pandemic was a catastrophic series of virus outbreaks that spread across the globe. Here, we show that only a modest change in the 1918 influenza hemagglutinin receptor binding site alters the transmissibility of this pandemic virus. Two amino acid mutations that cause a switch in receptor binding preference from the human alpha-2,6 to the avian alpha-2,3 sialic acid resulted in a virus incapable of respiratory droplet transmission between ferrets but that maintained its lethality and replication efficiency in the upper respiratory tract. Furthermore, poor transmission of a 1918 virus with dual alpha-2,6 and alpha-2,3 specificity suggests that a predominant human alpha-2,6 sialic acid binding preference is essential for optimal transmission of this pandemic virus. These findings confirm an essential role of hemagglutinin receptor specificity for the transmission of influenza viruses among mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tumpey, Terrence M -- Maines, Taronna R -- Van Hoeven, Neal -- Glaser, Laurel -- Solorzano, Alicia -- Pappas, Claudia -- Cox, Nancy J -- Swayne, David E -- Palese, Peter -- Katz, Jacqueline M -- Garcia-Sastre, Adolfo -- P01 AI058113/AI/NIAID NIH HHS/ -- U19 AI62623/AI/NIAID NIH HHS/ -- U54 AIO57158/PHS HHS/ -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):655-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Influenza Branch, Mailstop G-16, Division of Viral and Ricksettial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road NE, Atlanta, GA 30333, USA. tft9@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272724" target="_blank"〉PubMed〈/a〉
    Keywords: *Amino Acid Substitution ; Animals ; Cell Line ; Disease Models, Animal ; Dogs ; Ferrets ; Galactose/metabolism ; Glycoconjugates/metabolism ; Hemagglutinin Glycoproteins, Influenza Virus/*genetics/metabolism ; Humans ; Influenza A Virus, H1N1 Subtype/*genetics/pathogenicity/physiology ; Influenza, Human/pathology/*transmission/*virology ; Lung/pathology/virology ; Male ; *Mutation ; Nose/virology ; Receptors, Virus/metabolism ; Respiratory System/virology ; Sialic Acids/metabolism ; Virulence ; Virus Replication ; Virus Shedding
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    Wilms tumor suppressor WTX negatively regulates WNT/beta-catenin signaling (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-05-19
    Description: Aberrant WNT signal transduction is involved in many diseases. In colorectal cancer and melanoma, mutational disruption of proteins involved in the degradation of beta-catenin, the key effector of the WNT signaling pathway, results in stabilization of beta-catenin and, in turn, activation of transcription. We have used tandem-affinity protein purification and mass spectrometry to define the protein interaction network of the beta-catenin destruction complex. This assay revealed that WTX, a protein encoded by a gene mutated in Wilms tumors, forms a complex with beta-catenin, AXIN1, beta-TrCP2 (beta-transducin repeat-containing protein 2), and APC (adenomatous polyposis coli). Functional analyses in cultured cells, Xenopus, and zebrafish demonstrate that WTX promotes beta-catenin ubiquitination and degradation, which antagonize WNT/beta-catenin signaling. These data provide a possible mechanistic explanation for the tumor suppressor activity of WTX.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Major, Michael B -- Camp, Nathan D -- Berndt, Jason D -- Yi, Xianhua -- Goldenberg, Seth J -- Hubbert, Charlotte -- Biechele, Travis L -- Gingras, Anne-Claude -- Zheng, Ning -- Maccoss, Michael J -- Angers, Stephane -- Moon, Randall T -- New York, N.Y. -- Science. 2007 May 18;316(5827):1043-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Washington School of Medicine, Box 357370, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510365" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adenomatous Polyposis Coli Protein/metabolism ; Animals ; Axin Protein ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Genes, Wilms Tumor ; Humans ; Kidney Neoplasms/genetics ; Protein Binding ; Protein Interaction Mapping ; Proteomics ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; Transduction, Genetic ; Tumor Suppressor Proteins/chemistry/genetics/*metabolism ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Wilms Tumor/genetics ; Wnt Proteins/*metabolism ; Xenopus Proteins ; Zebrafish ; beta Catenin/*metabolism ; beta-Transducin Repeat-Containing Proteins/metabolism
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    Embryonic stem cells. Stem cell science advances as politics stall (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2007 Jun 29;316(5833):1825.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17600188" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Organism ; Embryo Implantation ; Embryo Research/ethics/legislation & jurisprudence ; Embryo, Mammalian ; Embryonic Development ; *Embryonic Stem Cells/cytology/physiology ; Humans ; Mice ; *Pluripotent Stem Cells/cytology ; Politics ; Rats
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    Stem cells. Reprogramming, take two (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2007 Jun 8;316(5830):1404.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17556554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cellular Reprogramming ; Cloning, Organism ; *Embryonic Stem Cells ; Mice ; *Nuclear Transfer Techniques ; *Zygote
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    Sensing X chromosome pairs before X inactivation via a novel X-pairing region of the Xic (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-12-08
    Description: Mammalian dosage compensation involves silencing of one of the two X chromosomes in females and is controlled by the X-inactivation center (Xic). The Xic, which includes Xist and its antisense transcription unit Tsix/Xite, somehow senses the number of X chromosomes and triggers Xist up-regulation from one of the two X chromosomes in females. We found that a segment of the mouse Xic lying several hundred kilobases upstream of Xist brings the two Xics together before the onset of X inactivation. This region can autonomously drive Xic trans-interactions even as an ectopic single-copy transgene. Its introduction into male embryonic stem cells is strongly selected against, consistent with a possible role in trans-activating Xist. We propose that homologous associations driven by this novel X-pairing region (Xpr) of the Xic enable a cell to sense that more than one X chromosome is present and coordinate reciprocal Xist/Tsix expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Augui, S -- Filion, G J -- Huart, S -- Nora, E -- Guggiari, M -- Maresca, M -- Stewart, A F -- Heard, E -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1632-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR218, Curie Institute, 26 rue d'Ulm, Paris 75005, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063799" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Differentiation ; Cell Line ; *Chromosome Pairing ; Chromosomes, Artificial, Bacterial ; Down-Regulation ; Embryonic Stem Cells ; Female ; Mice ; Mice, Transgenic ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; S Phase ; Transfection ; Transgenes ; Up-Regulation ; X Chromosome/*genetics/physiology ; *X Chromosome Inactivation
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    Neuroscience. Astrocytes secrete substance that kills motor neurons in ALS (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):353.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446359" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/genetics/metabolism/*pathology ; Animals ; Astrocytes/*metabolism ; Cell Death ; Cell Line ; Cells, Cultured ; Embryonic Stem Cells/cytology ; Glutamic Acid/metabolism ; Humans ; Mice ; Motor Neurons/*pathology ; Mutation ; Superoxide Dismutase/*genetics/metabolism
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    Stem cells. Versatile stem cells without the ethical baggage? (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2007 Jan 12;315(5809):170.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17218496" target="_blank"〉PubMed〈/a〉
    Keywords: Amniotic Fluid/*cytology ; Bioethical Issues ; Cell Differentiation ; Cell Line ; Cell Separation ; Embryonic Stem Cells/cytology ; Humans ; *Pluripotent Stem Cells/cytology
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    Molecular linkage between the kinase ATM and NF-kappaB signaling in response to genotoxic stimuli (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-25
    Description: The transcription factor NF-kappaB modulates apoptotic responses induced by genotoxic stress. We show that NF-kappaB essential modulator (NEMO), the regulatory subunit of IkappaB kinase (IKK) (which phosphorylates the NF-kappaB inhibitor IkappaB), associates with activated ataxia telangiectasia mutated (ATM) after the induction of DNA double-strand breaks. ATM phosphorylates serine-85 of NEMO to promote its ubiquitin-dependent nuclear export. ATM is also exported in a NEMO-dependent manner to the cytoplasm, where it associates with and causes the activation of IKK in a manner dependent on another IKK regulator, a protein rich in glutamate, leucine, lysine, and serine (ELKS). Thus, regulated nuclear shuttling of NEMO links two signaling kinases, ATM and IKK, to activate NF-kappaB by genotoxic signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Zhao-Hui -- Shi, Yuling -- Tibbetts, Randal S -- Miyamoto, Shigeki -- R01-CA77474/CA/NCI NIH HHS/ -- R01-CA81065/CA/NCI NIH HHS/ -- R01-GM067868/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1141-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Wisconsin-Madison, 301 SMI, 1300 University Avenue, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497931" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Adaptor Proteins, Signal Transducing/genetics/metabolism ; Amino Acid Motifs ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/*metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; *DNA Damage ; DNA-Binding Proteins/*metabolism ; Humans ; I-kappa B Kinase/*metabolism ; I-kappa B Proteins/genetics/metabolism ; NF-kappa B/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/metabolism ; *Signal Transduction ; Tumor Suppressor Proteins/*metabolism ; Ubiquitin/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 190
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    Oligonucleotide-modified gold nanoparticles for intracellular gene regulation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-20
    Description: We describe the use of gold nanoparticle-oligonucleotide complexes as intracellular gene regulation agents for the control of protein expression in cells. These oligonucleotide-modified nanoparticles have affinity constants for complementary nucleic acids that are higher than their unmodified oligonucleotide counterparts, are less susceptible to degradation by nuclease activity, exhibit greater than 99% cellular uptake, can introduce oligonucleotides at a higher effective concentration than conventional transfection agents, and are nontoxic to the cells under the conditions studied. By chemically tailoring the density of DNA bound to the surface of gold nanoparticles, we demonstrated a tunable gene knockdown.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosi, Nathaniel L -- Giljohann, David A -- Thaxton, C Shad -- Lytton-Jean, Abigail K R -- Han, Min Su -- Mirkin, Chad A -- New York, N.Y. -- Science. 2006 May 19;312(5776):1027-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and International Institute for Nanotechnology, Northwestern University, 2145 Sheridan Road, Evanston, IL 60208-3113 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16709779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Deoxyribonucleases/metabolism ; *Gene Expression Regulation ; Glutathione/metabolism ; *Gold ; Green Fluorescent Proteins/genetics ; HeLa Cells ; Humans ; Mice ; *Nanostructures ; *Oligodeoxyribonucleotides, Antisense/metabolism ; RNA, Messenger
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  • 191
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    An essential role for LEDGF/p75 in HIV integration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-09
    Description: Chromosomal integration enables human immunodeficiency virus (HIV) to establish a permanent reservoir that can be therapeutically suppressed but not eradicated. Participation of cellular proteins in this obligate replication step is poorly understood. We used intensified RNA interference and dominant-negative protein approaches to show that the cellular transcriptional coactivator lens epithelium-derived growth factor (LEDGF)/p75 (p75) is an essential HIV integration cofactor. The mechanism requires both linkages of a molecular tether that p75 forms between integrase and chromatin. Fractionally minute levels of endogenous p75 are sufficient to enable integration, showing that cellular factors that engage HIV after entry may elude identification in less intensive knockdowns. Perturbing the p75-integrase interaction may have therapeutic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Llano, Manuel -- Saenz, Dyana T -- Meehan, Anne -- Wongthida, Phonphimon -- Peretz, Mary -- Walker, William H -- Teo, Wulin -- Poeschla, Eric M -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):461-4. Epub 2006 Sep 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Medicine Program, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16959972" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/chemistry/genetics/metabolism/*physiology ; CD4-Positive T-Lymphocytes/metabolism/*virology ; Cell Line ; Chromatin/*metabolism ; HIV Integrase/*metabolism ; HIV-1/*physiology ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/metabolism/*physiology ; *Virus Integration ; Virus Replication
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  • 192
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    Receptor activation alters inner surface potential during phagocytosis (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-07-22
    Description: The surface potential of biological membranes varies according to their lipid composition. We devised genetically encoded probes to assess surface potential in intact cells. These probes revealed marked, localized alterations in the charge of the inner surface of the plasma membrane of macrophages during the course of phagocytosis. Hydrolysis of phosphoinositides and displacement of phosphatidylserine accounted for the change in surface potential at the phagosomal cup. Signaling molecules such as K-Ras, Rac1, and c-Src that are targeted to the membrane by electrostatic interactions were rapidly released from membrane subdomains where the surface charge was altered by lipid remodeling during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Tony -- Terebiznik, Mauricio -- Yu, Liming -- Silvius, John -- Abidi, Wasif M -- Philips, Mark -- Levine, Tim -- Kapus, Andras -- Grinstein, Sergio -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):347-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Hepatology, and Nutrition Department, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Line ; Cell Membrane/*physiology ; Fluorescent Dyes/metabolism ; Hydrophobic and Hydrophilic Interactions ; Immunoglobulin G/immunology ; Ionomycin/pharmacology ; Lipid Bilayers/metabolism ; Liposomes/metabolism ; Macrophages/*physiology ; Membrane Potentials ; Mice ; Molecular Probes/metabolism ; Neuropeptides/metabolism ; Opsonin Proteins ; Peptides/metabolism ; *Phagocytosis ; Phagosomes/physiology ; Phospholipids/analysis/metabolism ; Receptors, Fc/immunology/metabolism ; Static Electricity ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein ; ras Proteins/metabolism
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  • 193
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    Lamin A-dependent nuclear defects in human aging (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-04-29
    Description: Mutations in the nuclear structural protein lamin A cause the premature aging syndrome Hutchinson-Gilford progeria (HGPS). Whether lamin A plays any role in normal aging is unknown. We show that the same molecular mechanism responsible for HGPS is active in healthy cells. Cell nuclei from old individuals acquire defects similar to those of HGPS patient cells, including changes in histone modifications and increased DNA damage. Age-related nuclear defects are caused by sporadic use, in healthy individuals, of the same cryptic splice site in lamin A whose constitutive activation causes HGPS. Inhibition of this splice site reverses the nuclear defects associated with aging. These observations implicate lamin A in physiological aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1855250/" 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/PMC1855250/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scaffidi, Paola -- Misteli, Tom -- Z01 BC010309-07/BC/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 May 19;312(5776):1059-63. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645051" target="_blank"〉PubMed〈/a〉
    Keywords: Aged, 80 and over ; Aging/*physiology ; Cell Line ; Cell Nucleus/pathology ; DNA Damage ; Exons ; Histones/metabolism ; Humans ; Lamin Type A/genetics/*physiology ; Progeria/genetics/pathology ; RNA Splicing/genetics ; Signal Transduction ; Tumor Suppressor Protein p53/genetics/metabolism
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  • 194
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    ATM engages autodegradation of the E3 ubiquitin ligase COP1 after DNA damage (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-08-26
    Description: The ataxia telangiectasia mutated (ATM) protein kinase is a critical component of a DNA-damage response network configured to maintain genomic integrity. The abundance of an essential downstream effecter of this pathway, the tumor suppressor protein p53, is tightly regulated by controlled degradation through COP1 and other E3 ubiquitin ligases, such as MDM2 and Pirh2; however, the signal transduction pathway that regulates the COP1-p53 axis following DNA damage remains enigmatic. We observed that in response to DNA damage, ATM phosphorylated COP1 on Ser(387) and stimulated a rapid autodegradation mechanism. Ionizing radiation triggered an ATM-dependent movement of COP1 from the nucleus to the cytoplasm, and ATM-dependent phosphorylation of COP1 on Ser(387) was both necessary and sufficient to disrupt the COP1-p53 complex and subsequently to abrogate the ubiquitination and degradation of p53. Furthermore, phosphorylation of COP1 on Ser(387) was required to permit p53 to become stabilized and to exert its tumor suppressor properties in response to DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dornan, David -- Shimizu, Harumi -- Mah, Angie -- Dudhela, Tanay -- Eby, Michael -- O'rourke, Karen -- Seshagiri, Somasekar -- Dixit, Vishva M -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1122-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931761" target="_blank"〉PubMed〈/a〉
    Keywords: Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; *DNA Damage ; DNA-Binding Proteins/genetics/*metabolism ; Escherichia coli/genetics/metabolism ; Etoposide/pharmacology ; Humans ; Mutation ; Nuclear Proteins/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; RNA, Small Interfering ; Radiation, Ionizing ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics/metabolism ; Tumor Suppressor Proteins/genetics/*metabolism ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism
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  • 195
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    S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-10-21
    Description: The tumor suppressor programmed cell death protein 4 (PDCD4) inhibits the translation initiation factor eIF4A, an RNA helicase that catalyzes the unwinding of secondary structure at the 5' untranslated region (5'UTR) of messenger RNAs (mRNAs). In response to mitogens, PDCD4 was rapidly phosphorylated on Ser67 by the protein kinase S6K1 and subsequently degraded via the ubiquitin ligase SCF(betaTRCP). Expression in cultured cells of a stable PDCD4 mutant that is unable to bind betaTRCP inhibited translation of an mRNA with a structured 5'UTR, resulted in smaller cell size, and slowed down cell cycle progression. We propose that regulated degradation of PDCD4 in response to mitogens allows efficient protein synthesis and consequently cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorrello, N Valerio -- Peschiaroli, Angelo -- Guardavaccaro, Daniele -- Colburn, Nancy H -- Sherman, Nicholas E -- Pagano, Michele -- R01-CA76584/CA/NCI NIH HHS/ -- R01-GM57587/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):467-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053147" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions ; Amino Acid Motifs ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; Binding Sites ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cell Size ; Eukaryotic Initiation Factor-4A/antagonists & inhibitors/metabolism ; Eukaryotic Initiation Factor-4F/metabolism ; Eukaryotic Initiation Factor-4G/metabolism ; Eukaryotic Initiation Factors/metabolism ; Humans ; Mitogens/pharmacology ; Phosphorylation ; *Protein Biosynthesis ; RNA, Small Interfering ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Ribosomal Protein S6 Kinases/metabolism ; SKP Cullin F-Box Protein Ligases/*metabolism ; Serine/metabolism ; Serum ; Signal Transduction ; beta-Transducin Repeat-Containing Proteins/genetics/*metabolism
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  • 196
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    Escherichia coli induces DNA double-strand breaks in eukaryotic cells (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-08-12
    Description: Transient infection of eukaryotic cells with commensal and extraintestinal pathogenic Escherichia coli of phylogenetic group B2 blocks mitosis and induces megalocytosis. This trait is linked to a widely spread genomic island that encodes giant modular nonribosomal peptide and polyketide synthases. Contact with E. coli expressing this gene cluster causes DNA double-strand breaks and activation of the DNA damage checkpoint pathway, leading to cell cycle arrest and eventually to cell death. Discovery of hybrid peptide-polyketide genotoxins in E. coli will change our view on pathogenesis and commensalism and open new biotechnological applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nougayrede, Jean-Philippe -- Homburg, Stefan -- Taieb, Frederic -- Boury, Michele -- Brzuszkiewicz, Elzbieta -- Gottschalk, Gerhard -- Buchrieser, Carmen -- Hacker, Jorg -- Dobrindt, Ulrich -- Oswald, Eric -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INRA, UMR1225, Ecole Nationale Veterinaire de Toulouse, Toulouse F-31076, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Death ; Cell Line ; Cell Nucleus/chemistry ; Cytotoxins/*metabolism ; DNA/analysis ; *DNA Damage ; DNA-Binding Proteins/metabolism ; Escherichia coli/genetics/*pathogenicity/*physiology ; G2 Phase ; *Genomic Islands ; HeLa Cells ; Histones/metabolism ; Humans ; Intestinal Mucosa/cytology/microbiology ; Molecular Sequence Data ; Mutagenesis ; Mutagens/*metabolism ; Peptides/*metabolism ; Phosphorylation ; Polyketide Synthases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Signal Transduction ; Tumor Suppressor Proteins/metabolism
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  • 197
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    Research conduct. Lessons of the stem cell scandal (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Mildred K -- McGee, Glenn -- Magnus, David -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):614-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford Center for Biomedical Ethics, Department of Pediatrics; Palo Alto, CA 94304, USA. micho@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16456065" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes/ethics/*standards ; Authorship ; Biomedical Research/*ethics/*standards ; Cell Line ; *Ethics, Research ; Female ; Humans ; Korea ; Oocyte Donation/adverse effects ; Research Personnel/*ethics/standards ; Research Support as Topic ; Scientific Misconduct ; Stem Cells ; United States
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    Stem cell research. Scientists object to Massachusetts rules (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1372.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16959980" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cloning, Organism/legislation & jurisprudence ; Embryo Research/ethics/*legislation & jurisprudence ; Embryo, Mammalian/cytology ; Humans ; Massachusetts ; Research Embryo Creation/ethics/legislation & jurisprudence ; *Stem Cells
    Print ISSN: 0036-8075
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  • 199
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    Protrudin induces neurite formation by directional membrane trafficking (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-04
    Description: Guanosine triphosphatases of the Rab family are key regulators of membrane trafficking, with Rab11 playing a specific role in membrane recycling. We identified a mammalian protein, protrudin, that promoted neurite formation through interaction with the guanosine diphosphate (GDP)-bound form of Rab11. Phosphorylation of protrudin by extracellular signal-regulated kinase (ERK) in response to nerve growth factor promoted protrudin association with Rab11-GDP. Down-regulation of protrudin by RNA interference induced membrane extension in all directions and inhibited neurite formation. Thus, protrudin regulates Rab11-dependent membrane recycling to promote the directional membrane trafficking required for neurite formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirane, Michiko -- Nakayama, Keiichi I -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082457" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Guanosine Diphosphate/metabolism ; HeLa Cells ; Humans ; MAP Kinase Kinase 1/metabolism ; Membrane Proteins ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Growth Factor/pharmacology/physiology ; Neurites/*physiology ; PC12 Cells ; Phosphorylation ; RNA Interference ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Vesicular Transport Proteins ; rab GTP-Binding Proteins/metabolism
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  • 200
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    Antibody class switching mediated by yeast endonuclease-generated DNA breaks (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-12-16
    Description: Antibody class switching in activated B cells uses class switch recombination (CSR), which joins activation-induced cytidine deaminase (AID)-dependent double-strand breaks (DSBs) within two large immunoglobulin heavy chain (IgH) locus switch (S) regions that lie up to 200 kilobases apart. To test postulated roles of S regions and AID in CSR, we generated mutant B cells in which donor Smu and accepter Sgamma1 regions were replaced with yeast I-SceI endonuclease sites. We found that site-specific I-SceI DSBs mediate recombinational IgH locus class switching from IgM to IgG1 without S regions or AID. We propose that CSR evolved to exploit a general DNA repair process that promotes joining of widely separated DSBs within a chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zarrin, Ali A -- Del Vecchio, Catherine -- Tseng, Eva -- Gleason, Megan -- Zarin, Payam -- Tian, Ming -- Alt, Frederick W -- 2P01AI031541-15/AI/NIAID NIH HHS/ -- P01CA092625-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 19;315(5810):377-81. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Children's Hospital, CBR Institute for Biomedical Research, and Department of Genetics, Harvard University Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Cell Line ; Cytidine Deaminase/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair ; Deoxyribonucleases, Type II Site-Specific/genetics/*metabolism ; Embryonic Stem Cells ; Gene Targeting ; Genes, Immunoglobulin Heavy Chain ; Hybridomas ; *Immunoglobulin Class Switching ; Immunoglobulin G/biosynthesis/genetics ; Immunoglobulin M/biosynthesis/genetics ; *Immunoglobulin Switch Region ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Recombination, Genetic ; Saccharomyces cerevisiae/enzymology ; Saccharomyces cerevisiae Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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