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  • Mice  (9)
  • Cell Line, Tumor  (4)
  • American Association for the Advancement of Science (AAAS)  (10)
  • Elsevier
  • 2015-2019  (2)
  • 2005-2009  (8)
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  • 1
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    Structural insight into pre-B cell receptor function (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-14
    Description: The pre-B cell receptor (pre-BCR) serves as a checkpoint in B cell development. In the 2.7 angstrom structure of a human pre-BCR Fab-like fragment, consisting of an antibody heavy chain (HC) paired with the surrogate light chain, the "unique regions" of VpreB and lambda5 replace the complementarity-determining region 3 (CDR3) loop of an antibody light chain and appear to "probe" the HC CDR3, potentially influencing the selection of the antibody repertoire. Biochemical analysis indicates that the pre-BCR is impaired in its ability to recognize antigen, which, together with electron microscopic visualization of a pre-BCR dimer, suggests ligand-independent oligomerization as the likely signaling mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bankovich, Alexander J -- Raunser, Stefan -- Juo, Z Sean -- Walz, Thomas -- Davis, Mark M -- Garcia, K Christopher -- T32 AI007290/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 13;316(5822):291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Immunology, 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/17431183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Complementarity Determining Regions/chemistry/physiology ; Crystallography, X-Ray ; Humans ; Immunoglobulin Heavy Chains/chemistry/physiology ; Immunoglobulin Light Chains/chemistry/physiology ; Immunoglobulin Light Chains, Surrogate ; Membrane Glycoproteins/*chemistry/physiology/ultrastructure ; Mice ; Models, Molecular ; Pre-B Cell Receptors ; Protein Conformation ; Receptors, Antigen, B-Cell/*chemistry/physiology/ultrastructure ; Recombinant Proteins ; Structure-Activity Relationship
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    A stress signaling pathway in adipose tissue regulates hepatic insulin resistance (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: A high-fat diet causes activation of the regulatory protein c-Jun NH2-terminal kinase 1 (JNK1) and triggers development of insulin resistance. JNK1 is therefore a potential target for therapeutic treatment of metabolic syndrome. We explored the mechanism of JNK1 signaling by engineering mice in which the Jnk1 gene was ablated selectively in adipose tissue. JNK1 deficiency in adipose tissue suppressed high-fat diet-induced insulin resistance in the liver. JNK1-dependent secretion of the inflammatory cytokine interleukin-6 by adipose tissue caused increased expression of liver SOCS3, a protein that induces hepatic insulin resistance. Thus, JNK1 activation in adipose tissue can cause insulin resistance in the liver.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643026/" 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/PMC2643026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabio, Guadalupe -- Das, Madhumita -- Mora, Alfonso -- Zhang, Zhiyou -- Jun, John Y -- Ko, Hwi Jin -- Barrett, Tamera -- Kim, Jason K -- Davis, Roger J -- DK52530/DK/NIDDK NIH HHS/ -- R01 CA065861/CA/NCI NIH HHS/ -- R01 CA065861-14/CA/NCI NIH HHS/ -- R01 DK080756/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1539-43. doi: 10.1126/science.1160794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/19056984" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/enzymology/*metabolism ; Adipose Tissue/enzymology/metabolism ; Animals ; Dietary Fats/administration & dosage ; Enzyme Activation ; Glucose/metabolism ; Insulin/metabolism ; Insulin Receptor Substrate Proteins/metabolism ; *Insulin Resistance ; Interleukin-6/administration & dosage/metabolism ; Liver/*metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 8/deficiency/genetics/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; *Signal Transduction ; *Stress, Physiological ; Suppressor of Cytokine Signaling 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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  • 3
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    Oncogenic CARD11 mutations in human diffuse large B cell lymphoma (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-08
    Description: Diffuse large B cell lymphoma (DLBCL) is the most common form of non-Hodgkin's lymphoma. In the least curable (ABC) subtype of DLBCL, survival of the malignant cells is dependent on constitutive activation of the nuclear factor-kappaB (NF-kappaB) signaling pathway. In normal B cells, antigen receptor-induced NF-kappaB activation requires CARD11, a cytoplasmic scaffolding protein. To determine whether CARD11 contributes to tumorigenesis, we sequenced the CARD11 gene in human DLBCL tumors. We detected missense mutations in 7 of 73 ABC DLBCL biopsies (9.6%), all within exons encoding the coiled-coil domain. Experimental introduction of CARD11 coiled-coil domain mutants into lymphoma cell lines resulted in constitutive NF-kappaB activation and enhanced NF-kappaB activity upon antigen receptor stimulation. These results demonstrate that CARD11 is a bona fide oncogenein DLBCL, providing a genetic rationale for the development of pharmacological inhibitors of the CARD11 pathway for DLBCL therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lenz, Georg -- Davis, R Eric -- Ngo, Vu N -- Lam, Lloyd -- George, Thaddeus C -- Wright, George W -- Dave, Sandeep S -- Zhao, Hong -- Xu, Weihong -- Rosenwald, Andreas -- Ott, German -- Muller-Hermelink, Hans Konrad -- Gascoyne, Randy D -- Connors, Joseph M -- Rimsza, Lisa M -- Campo, Elias -- Jaffe, Elaine S -- Delabie, Jan -- Smeland, Erlend B -- Fisher, Richard I -- Chan, Wing C -- Staudt, Louis M -- UO1-CA84967/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 21;319(5870):1676-9. doi: 10.1126/science.1153629. Epub 2008 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, Division of Cancer Treatment and Diagnosis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323416" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Apoptosis Regulatory Proteins/chemistry/*genetics/metabolism ; CARD Signaling Adaptor Proteins/chemistry/*genetics/metabolism ; Cell Line, Tumor ; Cytoplasm/metabolism ; Guanylate Cyclase/chemistry/*genetics/metabolism ; Humans ; I-kappa B Kinase/metabolism ; Jurkat Cells ; Lymphoma, Large B-Cell, Diffuse/*genetics ; Molecular Sequence Data ; *Mutation, Missense ; NF-kappa B ; *Oncogenes ; Protein Structure, Tertiary ; Receptors, Antigen, B-Cell/physiology ; Sequence Analysis, DNA
    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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  • 4
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    Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-03
    Description: Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder. Ten percent of cases are inherited; most involve unidentified genes. We report here 13 mutations in the fused in sarcoma/translated in liposarcoma (FUS/TLS) gene on chromosome 16 that were specific for familial ALS. The FUS/TLS protein binds to RNA, functions in diverse processes, and is normally located predominantly in the nucleus. In contrast, the mutant forms of FUS/TLS accumulated in the cytoplasm of neurons, a pathology that is similar to that of the gene TAR DNA-binding protein 43 (TDP43), whose mutations also cause ALS. Neuronal cytoplasmic protein aggregation and defective RNA metabolism thus appear to be common pathogenic mechanisms involved in ALS and possibly in other neurodegenerative disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwiatkowski, T J Jr -- Bosco, D A -- Leclerc, A L -- Tamrazian, E -- Vanderburg, C R -- Russ, C -- Davis, A -- Gilchrist, J -- Kasarskis, E J -- Munsat, T -- Valdmanis, P -- Rouleau, G A -- Hosler, B A -- Cortelli, P -- de Jong, P J -- Yoshinaga, Y -- Haines, J L -- Pericak-Vance, M A -- Yan, J -- Ticozzi, N -- Siddique, T -- McKenna-Yasek, D -- Sapp, P C -- Horvitz, H R -- Landers, J E -- Brown, R H Jr -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1205-8. doi: 10.1126/science.1166066.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA. tkwiatkowski@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251627" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Amino Acid Substitution ; Amyotrophic Lateral Sclerosis/*genetics/metabolism/pathology ; Animals ; Brain/pathology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Chromosomes, Human, Pair 16/*genetics ; Cytoplasm/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Exons ; Female ; Humans ; Male ; Mice ; Motor Neurons/chemistry/metabolism/ultrastructure ; Mutant Proteins/chemistry/genetics/metabolism ; *Mutation, Missense ; Neurons/metabolism/ultrastructure ; RNA/metabolism ; RNA-Binding Protein FUS/chemistry/*genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Analysis, DNA ; Spinal Cord/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Sequence variants in SLITRK1 are associated with Tourette's syndrome (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-15
    Description: Tourette's syndrome (TS) is a genetically influenced developmental neuropsychiatric disorder characterized by chronic vocal and motor tics. We studied Slit and Trk-like 1 (SLITRK1) as a candidate gene on chromosome 13q31.1 because of its proximity to a de novo chromosomal inversion in a child with TS. Among 174 unrelated probands, we identified a frameshift mutation and two independent occurrences of the identical variant in the binding site for microRNA hsa-miR-189. These variants were absent from 3600 control chromosomes. SLITRK1 mRNA and hsa-miR-189 showed an overlapping expression pattern in brain regions previously implicated in TS. Wild-type SLITRK1, but not the frameshift mutant, enhanced dendritic growth in primary neuronal cultures. Collectively, these findings support the association of rare SLITRK1 sequence variants with TS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, Jesse F -- Kwan, Kenneth Y -- O'Roak, Brian J -- Baek, Danielle Y -- Stillman, Althea A -- Morgan, Thomas M -- Mathews, Carol A -- Pauls, David L -- Rasin, Mladen-Roko -- Gunel, Murat -- Davis, Nicole R -- Ercan-Sencicek, A Gulhan -- Guez, Danielle H -- Spertus, John A -- Leckman, James F -- Dure, Leon S 4th -- Kurlan, Roger -- Singer, Harvey S -- Gilbert, Donald L -- Farhi, Anita -- Louvi, Angeliki -- Lifton, Richard P -- Sestan, Nenad -- State, Matthew W -- K23 RR16118/RR/NCRR NIH HHS/ -- R01 NS054273/NS/NINDS NIH HHS/ -- R01 NS43520/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):317-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Child Study Center, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224024" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Adolescent ; Animals ; Attention Deficit Disorder with Hyperactivity/complications/genetics ; Brain/metabolism ; Child ; Child, Preschool ; Chromosome Inversion ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Dna ; DNA Mutational Analysis ; Female ; Frameshift Mutation ; Humans ; In Situ Hybridization, Fluorescence ; Male ; Membrane Proteins/*genetics ; Mice ; *Mutation ; Nerve Tissue Proteins/*genetics ; Pedigree ; Sequence Analysis, DNA ; Tourette Syndrome/complications/*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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  • 6
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    Human IRGM induces autophagy to eliminate intracellular mycobacteria (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-05
    Description: Immunity-related p47 guanosine triphosphatases (IRG) play a role in defense against intracellular pathogens. We found that the murine Irgm1 (LRG-47) guanosine triphosphatase induced autophagy and generated large autolysosomal organelles as a mechanism for the elimination of intracellular Mycobacterium tuberculosis. We also identified a function for a human IRG protein in the control of intracellular pathogens and report that the human Irgm1 ortholog, IRGM, plays a role in autophagy and in the reduction of intracellular bacillary load.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Sudha B -- Davis, Alexander S -- Taylor, Gregory A -- Deretic, Vojo -- AI42999/AI/NIAID NIH HHS/ -- AI45148/AI/NIAID NIH HHS/ -- AI57831/AI/NIAID NIH HHS/ -- R01 AI057831/AI/NIAID NIH HHS/ -- T32 AI007538/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1438-41. Epub 2006 Aug 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16888103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cell Line ; Cytosol/metabolism ; GTP-Binding Proteins/genetics/*physiology ; HeLa Cells ; Humans ; Interferon-gamma/immunology ; Lysosomes/metabolism/microbiology/ultrastructure ; Macrophages/*immunology/*microbiology ; Mice ; Microbial Viability ; Microtubule-Associated Proteins/metabolism ; Mycobacterium bovis/*immunology/physiology ; Phagosomes/metabolism/microbiology/*ultrastructure ; RNA, Small Interfering ; Transfection ; Vacuoles/metabolism/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Phosphorylation by p38 MAPK as an alternative pathway for GSK3beta inactivation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-03
    Description: Glycogen synthase kinase 3beta (GSK3beta) is involved in metabolism, neurodegeneration, and cancer. Inhibition of GSK3beta activity is the primary mechanism that regulates this widely expressed active kinase. Although the protein kinase Akt inhibits GSK3beta by phosphorylation at the N terminus, preventing Akt-mediated phosphorylation does not affect the cell-survival pathway activated through the GSK3beta substrate beta-catenin. Here, we show that p38 mitogen-activated protein kinase (MAPK) also inactivates GSK3beta by direct phosphorylation at its C terminus, and this inactivation can lead to an accumulation of beta-catenin. p38 MAPK-mediated phosphorylation of GSK3beta occurs primarily in the brain and thymocytes. Activation of beta-catenin-mediated signaling through GSK3beta inhibition provides a potential mechanism for p38 MAPK-mediated survival in specific tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597039/" 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/PMC2597039/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thornton, Tina M -- Pedraza-Alva, Gustavo -- Deng, Bin -- Wood, C David -- Aronshtam, Alexander -- Clements, James L -- Sabio, Guadalupe -- Davis, Roger J -- Matthews, Dwight E -- Doble, Bradley -- Rincon, Mercedes -- P20 RR021905/RR/NCRR NIH HHS/ -- P20 RR15557/RR/NCRR NIH HHS/ -- P20 RR16462/RR/NCRR NIH HHS/ -- R01 AI051454/AI/NIAID NIH HHS/ -- R01 AI051454-01A1/AI/NIAID NIH HHS/ -- R01 AI051454-02/AI/NIAID NIH HHS/ -- R01 AI051454-03/AI/NIAID NIH HHS/ -- R01 AI051454-04/AI/NIAID NIH HHS/ -- R01 AI051454-05/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 May 2;320(5876):667-70. doi: 10.1126/science.1156037.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine/Immunobiology Program, University of Vermont, Burlington, VT 05405-0068, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451303" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/enzymology ; Glycogen Synthase Kinase 3/*antagonists & inhibitors/immunology/metabolism ; Humans ; Mice ; Phosphorylation ; Protein Kinase Inhibitors/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Serine/metabolism ; Thymus Gland/cytology/enzymology ; beta Catenin/metabolism ; p38 Mitogen-Activated Protein Kinases/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Apicomplexan parasites co-opt host calpains to facilitate their escape from infected cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: Apicomplexan parasites, including Plasmodium falciparum and Toxoplasma gondii (the causative agents of malaria and toxoplasmosis, respectively), are responsible for considerable morbidity and mortality worldwide. These pathogenic protozoa replicate within an intracellular vacuole inside of infected host cells, from which they must escape to initiate a new lytic cycle. By integrating cell biological, pharmacological, and genetic approaches, we provide evidence that both Plasmodium and Toxoplasma hijack host cell calpain proteases to facilitate parasite egress. Immunodepletion or inhibition of calpain-1 in hypotonically lysed and resealed erythrocytes prevented the escape of P. falciparum parasites, which was restored by adding purified calpain-1. Similarly, efficient egress of T. gondii from mammalian fibroblasts was blocked by either small interfering RNA-mediated suppression or genetic deletion of calpain activity and could be restored by genetic complementation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391539/" 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/PMC3391539/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandramohanadas, Rajesh -- Davis, Paul H -- Beiting, Daniel P -- Harbut, Michael B -- Darling, Claire -- Velmourougane, Geetha -- Lee, Ming Yeh -- Greer, Peter A -- Roos, David S -- Greenbaum, Doron C -- F32 AI075846/AI/NIAID NIH HHS/ -- F32 AI075846-02/AI/NIAID NIH HHS/ -- F32 AI077268/AI/NIAID NIH HHS/ -- F32 AI077268-02/AI/NIAID NIH HHS/ -- R37 AI028724/AI/NIAID NIH HHS/ -- R37 AI028724-17/AI/NIAID NIH HHS/ -- T32 GM008076/GM/NIGMS NIH HHS/ -- T32 GM008076-24/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 8;324(5928):794-7. doi: 10.1126/science.1171085. Epub 2009 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calpain/blood/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Erythrocytes/*parasitology ; Fibroblasts/parasitology ; Humans ; Leucine/analogs & derivatives/pharmacology ; Life Cycle Stages ; Merozoites/physiology ; Mice ; Mice, Knockout ; Plasmodium falciparum/growth & development/metabolism/*pathogenicity/physiology ; RNA, Small Interfering ; Schizonts/physiology ; Toxoplasma/growth & development/metabolism/*pathogenicity/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
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    Cell biology. Reversible centriole depletion with an inhibitor of Polo-like kinase 4 (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-02
    Description: Centrioles are ancient organelles that build centrosomes, the major microtubule-organizing centers of animal cells. Extra centrosomes are a common feature of cancer cells. To investigate the importance of centrosomes in the proliferation of normal and cancer cells, we developed centrinone, a reversible inhibitor of Polo-like kinase 4 (Plk4), a serine-threonine protein kinase that initiates centriole assembly. Centrinone treatment caused centrosome depletion in human and other vertebrate cells. Centrosome loss irreversibly arrested normal cells in a senescence-like G1 state by a p53-dependent mechanism that was independent of DNA damage, stress, Hippo signaling, extended mitotic duration, or segregation errors. In contrast, cancer cell lines with normal or amplified centrosome numbers could proliferate indefinitely after centrosome loss. Upon centrinone washout, each cancer cell line returned to an intrinsic centrosome number "set point." Thus, cells with cancer-associated mutations fundamentally differ from normal cells in their response to centrosome loss.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4764081/" 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/PMC4764081/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, Yao Liang -- Anzola, John V -- Davis, Robert L -- Yoon, Michelle -- Motamedi, Amir -- Kroll, Ashley -- Seo, Chanmee P -- Hsia, Judy E -- Kim, Sun K -- Mitchell, Jennifer W -- Mitchell, Brian J -- Desai, Arshad -- Gahman, Timothy C -- Shiau, Andrew K -- Oegema, Karen -- GM074207/GM/NIGMS NIH HHS/ -- GM089970/GM/NIGMS NIH HHS/ -- GM103403/GM/NIGMS NIH HHS/ -- R01 GM089970/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jun 5;348(6239):1155-60. doi: 10.1126/science.aaa5111. Epub 2015 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Medicine, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA. ; Small Molecule Discovery Program, Ludwig Institute for Cancer Research, La Jolla, CA 92093, USA. ; Department of Cell and Molecular Biology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. ; Small Molecule Discovery Program, Ludwig Institute for Cancer Research, La Jolla, CA 92093, USA. koegema@ucsd.edu ashiau@ucsd.edu. ; Department of Cellular and Molecular Medicine, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA. koegema@ucsd.edu ashiau@ucsd.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25931445" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Proliferation ; Centrioles/*drug effects ; Humans ; Mice ; Piperazines/pharmacology ; Protein Kinase Inhibitors/chemistry/*pharmacology ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors ; Pyrimidines/chemistry/*pharmacology ; Sulfones/chemistry/*pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Transcribed enhancers lead waves of coordinated transcription in transitioning mammalian cells (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-14
    Description: Although it is generally accepted that cellular differentiation requires changes to transcriptional networks, dynamic regulation of promoters and enhancers at specific sets of genes has not been previously studied en masse. Exploiting the fact that active promoters and enhancers are transcribed, we simultaneously measured their activity in 19 human and 14 mouse time courses covering a wide range of cell types and biological stimuli. Enhancer RNAs, then messenger RNAs encoding transcription factors, dominated the earliest responses. Binding sites for key lineage transcription factors were simultaneously overrepresented in enhancers and promoters active in each cellular system. Our data support a highly generalizable model in which enhancer transcription is the earliest event in successive waves of transcriptional change during cellular differentiation or activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681433/" 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/PMC4681433/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arner, Erik -- Daub, Carsten O -- Vitting-Seerup, Kristoffer -- Andersson, Robin -- Lilje, Berit -- Drablos, Finn -- Lennartsson, Andreas -- Ronnerblad, Michelle -- Hrydziuszko, Olga -- Vitezic, Morana -- Freeman, Tom C -- Alhendi, Ahmad M N -- Arner, Peter -- Axton, Richard -- Baillie, J Kenneth -- Beckhouse, Anthony -- Bodega, Beatrice -- Briggs, James -- Brombacher, Frank -- Davis, Margaret -- Detmar, Michael -- Ehrlund, Anna -- Endoh, Mitsuhiro -- Eslami, Afsaneh -- Fagiolini, Michela -- Fairbairn, Lynsey -- Faulkner, Geoffrey J -- Ferrai, Carmelo -- Fisher, Malcolm E -- Forrester, Lesley -- Goldowitz, Daniel -- Guler, Reto -- Ha, Thomas -- Hara, Mitsuko -- Herlyn, Meenhard -- Ikawa, Tomokatsu -- Kai, Chieko -- Kawamoto, Hiroshi -- Khachigian, Levon M -- Klinken, S Peter -- Kojima, Soichi -- Koseki, Haruhiko -- Klein, Sarah -- Mejhert, Niklas -- Miyaguchi, Ken -- Mizuno, Yosuke -- Morimoto, Mitsuru -- Morris, Kelly J -- Mummery, Christine -- Nakachi, Yutaka -- Ogishima, Soichi -- Okada-Hatakeyama, Mariko -- Okazaki, Yasushi -- Orlando, Valerio -- Ovchinnikov, Dmitry -- Passier, Robert -- Patrikakis, Margaret -- Pombo, Ana -- Qin, Xian-Yang -- Roy, Sugata -- Sato, Hiroki -- Savvi, Suzana -- Saxena, Alka -- Schwegmann, Anita -- Sugiyama, Daisuke -- Swoboda, Rolf -- Tanaka, Hiroshi -- Tomoiu, Andru -- Winteringham, Louise N -- Wolvetang, Ernst -- Yanagi-Mizuochi, Chiyo -- Yoneda, Misako -- Zabierowski, Susan -- Zhang, Peter -- Abugessaisa, Imad -- Bertin, Nicolas -- Diehl, Alexander D -- Fukuda, Shiro -- Furuno, Masaaki -- Harshbarger, Jayson -- Hasegawa, Akira -- Hori, Fumi -- Ishikawa-Kato, Sachi -- Ishizu, Yuri -- Itoh, Masayoshi -- Kawashima, Tsugumi -- Kojima, Miki -- Kondo, Naoto -- Lizio, Marina -- Meehan, Terrence F -- Mungall, Christopher J -- Murata, Mitsuyoshi -- Nishiyori-Sueki, Hiromi -- Sahin, Serkan -- Nagao-Sato, Sayaka -- Severin, Jessica -- de Hoon, Michiel J L -- Kawai, Jun -- Kasukawa, Takeya -- Lassmann, Timo -- Suzuki, Harukazu -- Kawaji, Hideya -- Summers, Kim M -- Wells, Christine -- FANTOM Consortium -- Hume, David A -- Forrest, Alistair R R -- Sandelin, Albin -- Carninci, Piero -- Hayashizaki, Yoshihide -- P30 CA010815/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Feb 27;347(6225):1010-4. doi: 10.1126/science.1259418. Epub 2015 Feb 12.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25678556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cattle ; Cell Differentiation/*genetics ; Dogs ; *Enhancer Elements, Genetic ; *Gene Expression Regulation, Developmental ; Mice ; RNA, Messenger/genetics/metabolism ; Rats ; Stem Cells/*cytology/metabolism ; Transcription Factors/*metabolism ; *Transcription, Genetic
    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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