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  • 1
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    Novel mutant-selective EGFR kinase inhibitors against EGFR T790M (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-25
    Beschreibung: The clinical efficacy of epidermal growth factor receptor (EGFR) kinase inhibitors in EGFR-mutant non-small-cell lung cancer (NSCLC) is limited by the development of drug-resistance mutations, including the gatekeeper T790M mutation. Strategies targeting EGFR T790M with irreversible inhibitors have had limited success and are associated with toxicity due to concurrent inhibition of wild-type EGFR. All current EGFR inhibitors possess a structurally related quinazoline-based core scaffold and were identified as ATP-competitive inhibitors of wild-type EGFR. Here we identify a covalent pyrimidine EGFR inhibitor by screening an irreversible kinase inhibitor library specifically against EGFR T790M. These agents are 30- to 100-fold more potent against EGFR T790M, and up to 100-fold less potent against wild-type EGFR, than quinazoline-based EGFR inhibitors in vitro. They are also effective in murine models of lung cancer driven by EGFR T790M. Co-crystallization studies reveal a structural basis for the increased potency and mutant selectivity of these agents. These mutant-selective irreversible EGFR kinase inhibitors may be clinically more effective and better tolerated than quinazoline-based inhibitors. Our findings demonstrate that functional pharmacological screens against clinically important mutant kinases represent a powerful strategy to identify new classes of mutant-selective kinase inhibitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879581/" 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/PMC2879581/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Wenjun -- Ercan, Dalia -- Chen, Liang -- Yun, Cai-Hong -- Li, Danan -- Capelletti, Marzia -- Cortot, Alexis B -- Chirieac, Lucian -- Iacob, Roxana E -- Padera, Robert -- Engen, John R -- Wong, Kwok-Kin -- Eck, Michael J -- Gray, Nathanael S -- Janne, Pasi A -- P50CA090578/CA/NCI NIH HHS/ -- R01 CA122794/CA/NCI NIH HHS/ -- R01 CA130876/CA/NCI NIH HHS/ -- R01 CA130876-02/CA/NCI NIH HHS/ -- R01 CA135257/CA/NCI NIH HHS/ -- R01AG2400401/AG/NIA NIH HHS/ -- R01CA080942/CA/NCI NIH HHS/ -- R01CA11446/CA/NCI NIH HHS/ -- R01CA116020/CA/NCI NIH HHS/ -- R01CA130876-02/CA/NCI NIH HHS/ -- R01CA135257/CA/NCI NIH HHS/ -- R01GM070590/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1070-4. doi: 10.1038/nature08622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033049" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antineoplastic Agents/chemistry/*pharmacology/toxicity ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Drug Evaluation, Preclinical ; Drug Resistance, Neoplasm/genetics ; Lung/drug effects ; Mice ; Models, Chemical ; Models, Molecular ; Mutation/*genetics ; NIH 3T3 Cells ; Phosphorylation/drug effects ; Protein Kinase Inhibitors/chemistry/*pharmacology/toxicity ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/*genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 2
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    Rewilding can cause rather than solve ecological problems (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-25
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caro, Tim -- Sherman, Paul -- England -- Nature. 2009 Dec 24;462(7276):985. doi: 10.1038/462985b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033023" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Wild ; *Conservation of Natural Resources/methods ; *Ecosystem
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 3
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    Ageing: Diet and longevity in the balance (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-25
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flatt, Thomas -- England -- Nature. 2009 Dec 24;462(7276):989-90. doi: 10.1038/462989a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033028" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging/*physiology ; Amino Acids/metabolism ; Animals ; Caloric Restriction ; *Diet ; Drosophila melanogaster/metabolism/*physiology ; Fertility/physiology ; Longevity/*physiology ; Signal Transduction/physiology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 4
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    The velocity of climate change (2009)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2009-12-25
    Beschreibung: The ranges of plants and animals are moving in response to recent changes in climate. As temperatures rise, ecosystems with 'nowhere to go', such as mountains, are considered to be more threatened. However, species survival may depend as much on keeping pace with moving climates as the climate's ultimate persistence. Here we present a new index of the velocity of temperature change (km yr(-1)), derived from spatial gradients ( degrees C km(-1)) and multimodel ensemble forecasts of rates of temperature increase ( degrees C yr(-1)) in the twenty-first century. This index represents the instantaneous local velocity along Earth's surface needed to maintain constant temperatures, and has a global mean of 0.42 km yr(-1) (A1B emission scenario). Owing to topographic effects, the velocity of temperature change is lowest in mountainous biomes such as tropical and subtropical coniferous forests (0.08 km yr(-1)), temperate coniferous forest, and montane grasslands. Velocities are highest in flooded grasslands (1.26 km yr(-1)), mangroves and deserts. High velocities suggest that the climates of only 8% of global protected areas have residence times exceeding 100 years. Small protected areas exacerbate the problem in Mediterranean-type and temperate coniferous forest biomes. Large protected areas may mitigate the problem in desert biomes. These results indicate management strategies for minimizing biodiversity loss from climate change. Montane landscapes may effectively shelter many species into the next century. Elsewhere, reduced emissions, a much expanded network of protected areas, or efforts to increase species movement may be necessary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loarie, Scott R -- Duffy, Philip B -- Hamilton, Healy -- Asner, Gregory P -- Field, Christopher B -- Ackerly, David D -- England -- Nature. 2009 Dec 24;462(7276):1052-5. doi: 10.1038/nature08649.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Carnegie Institution for Science, Department of Global Ecology, Stanford, California 94305, USA. loarie@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033047" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biodiversity ; Conservation of Natural Resources ; Ecosystem ; *Global Warming ; *Models, Biological ; Time Factors
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 5
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    The chromatin remodeller ACF acts as a dimeric motor to space nucleosomes (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-25
    Beschreibung: Evenly spaced nucleosomes directly correlate with condensed chromatin and gene silencing. The ATP-dependent chromatin assembly factor (ACF) forms such structures in vitro and is required for silencing in vivo. ACF generates and maintains nucleosome spacing by constantly moving a nucleosome towards the longer flanking DNA faster than the shorter flanking DNA. How the enzyme rapidly moves back and forth between both sides of a nucleosome to accomplish bidirectional movement is unknown. Here we show that nucleosome movement depends cooperatively on two ACF molecules, indicating that ACF functions as a dimer of ATPases. Further, the nucleotide state determines whether the dimer closely engages one or both sides of the nucleosome. Three-dimensional reconstruction by single-particle electron microscopy of the ATPase-nucleosome complex in an activated ATP state reveals a dimer architecture in which the two ATPases face each other. Our results indicate a model in which the two ATPases work in a coordinated manner, taking turns to engage either side of a nucleosome, thereby allowing processive bidirectional movement. This novel dimeric motor mechanism differs from that of dimeric motors such as kinesin and dimeric helicases that processively translocate unidirectionally and reflects the unique challenges faced by motors that move nucleosomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869534/" 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/PMC2869534/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Racki, Lisa R -- Yang, Janet G -- Naber, Nariman -- Partensky, Peretz D -- Acevedo, Ashley -- Purcell, Thomas J -- Cooke, Roger -- Cheng, Yifan -- Narlikar, Geeta J -- R01 GM073767/GM/NIGMS NIH HHS/ -- R01 GM073767-01/GM/NIGMS NIH HHS/ -- R01 GM073767-02/GM/NIGMS NIH HHS/ -- R01 GM073767-03/GM/NIGMS NIH HHS/ -- R01 GM073767-03S1/GM/NIGMS NIH HHS/ -- R01 GM073767-04/GM/NIGMS NIH HHS/ -- R01 GM073767-05/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1016-21. doi: 10.1038/nature08621.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033039" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Cell Line ; Chromatin Assembly and Disassembly/*physiology ; Dimerization ; Gene Silencing/physiology ; Histones/metabolism ; Humans ; Microscopy, Electron, Transmission ; *Models, Molecular ; Multiprotein Complexes/*metabolism ; Nucleosomes/chemistry/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Transcription Factors/chemistry/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 6
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    The transcriptional network for mesenchymal transformation of brain tumours (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-25
    Beschreibung: The inference of transcriptional networks that regulate transitions into physiological or pathological cellular states remains a central challenge in systems biology. A mesenchymal phenotype is the hallmark of tumour aggressiveness in human malignant glioma, but the regulatory programs responsible for implementing the associated molecular signature are largely unknown. Here we show that reverse-engineering and an unbiased interrogation of a glioma-specific regulatory network reveal the transcriptional module that activates expression of mesenchymal genes in malignant glioma. Two transcription factors (C/EBPbeta and STAT3) emerge as synergistic initiators and master regulators of mesenchymal transformation. Ectopic co-expression of C/EBPbeta and STAT3 reprograms neural stem cells along the aberrant mesenchymal lineage, whereas elimination of the two factors in glioma cells leads to collapse of the mesenchymal signature and reduces tumour aggressiveness. In human glioma, expression of C/EBPbeta and STAT3 correlates with mesenchymal differentiation and predicts poor clinical outcome. These results show that the activation of a small regulatory module is necessary and sufficient to initiate and maintain an aberrant phenotypic state in cancer cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4011561/" 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/PMC4011561/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carro, Maria Stella -- Lim, Wei Keat -- Alvarez, Mariano Javier -- Bollo, Robert J -- Zhao, Xudong -- Snyder, Evan Y -- Sulman, Erik P -- Anne, Sandrine L -- Doetsch, Fiona -- Colman, Howard -- Lasorella, Anna -- Aldape, Ken -- Califano, Andrea -- Iavarone, Antonio -- 1RC2CA148308-01/CA/NCI NIH HHS/ -- P20 GM075059/GM/NIGMS NIH HHS/ -- P20GM075059/GM/NIGMS NIH HHS/ -- R01 CA085628/CA/NCI NIH HHS/ -- R01 CA101644/CA/NCI NIH HHS/ -- R01 CA109755/CA/NCI NIH HHS/ -- R01 CA127643/CA/NCI NIH HHS/ -- R01 NS061776/NS/NINDS NIH HHS/ -- R01 NS061776-01A2/NS/NINDS NIH HHS/ -- R01 NS061776-02/NS/NINDS NIH HHS/ -- R01CA085628/CA/NCI NIH HHS/ -- R01CA101644/CA/NCI NIH HHS/ -- R01CA109755/CA/NCI NIH HHS/ -- R01NS061776/NS/NINDS NIH HHS/ -- RC2 CA148308/CA/NCI NIH HHS/ -- U01 CA168426/CA/NCI NIH HHS/ -- U54 CA121852/CA/NCI NIH HHS/ -- U54CA121852/CA/NCI NIH HHS/ -- England -- Nature. 2010 Jan 21;463(7279):318-25. doi: 10.1038/nature08712. Epub 2009 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20032975" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain Neoplasms/diagnosis/*genetics/*pathology ; CCAAT-Enhancer-Binding Protein-beta/genetics/metabolism ; Cell Differentiation/genetics ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/metabolism/pathology ; Cellular Reprogramming/genetics ; Computational Biology ; *Gene Expression Regulation, Neoplastic ; *Gene Regulatory Networks ; Glioma/diagnosis/genetics/pathology ; Humans ; Mesenchymal Stromal Cells/metabolism/pathology ; Mesoderm/*metabolism/*pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Invasiveness/genetics/pathology ; Neurons/metabolism/pathology ; Prognosis ; Reproducibility of Results ; STAT3 Transcription Factor/genetics/metabolism ; *Transcription, Genetic
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 7
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    Reprogramming towards pluripotency requires AID-dependent DNA demethylation (2009)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2009-12-23
    Beschreibung: Reprogramming of somatic cell nuclei to yield induced pluripotent stem (iPS) cells makes possible derivation of patient-specific stem cells for regenerative medicine. However, iPS cell generation is asynchronous and slow (2-3 weeks), the frequency is low (〈0.1%), and DNA demethylation constitutes a bottleneck. To determine regulatory mechanisms involved in reprogramming, we generated interspecies heterokaryons (fused mouse embryonic stem (ES) cells and human fibroblasts) that induce reprogramming synchronously, frequently and fast. Here we show that reprogramming towards pluripotency in single heterokaryons is initiated without cell division or DNA replication, rapidly (1 day) and efficiently (70%). Short interfering RNA (siRNA)-mediated knockdown showed that activation-induced cytidine deaminase (AID, also known as AICDA) is required for promoter demethylation and induction of OCT4 (also known as POU5F1) and NANOG gene expression. AID protein bound silent methylated OCT4 and NANOG promoters in fibroblasts, but not active demethylated promoters in ES cells. These data provide new evidence that mammalian AID is required for active DNA demethylation and initiation of nuclear reprogramming towards pluripotency in human somatic cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906123/" 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/PMC2906123/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhutani, Nidhi -- Brady, Jennifer J -- Damian, Mara -- Sacco, Alessandra -- Corbel, Stephane Y -- Blau, Helen M -- AG009521/AG/NIA NIH HHS/ -- AG024987/AG/NIA NIH HHS/ -- AI007328/AI/NIAID NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG024987/AG/NIA NIH HHS/ -- R01 AG024987-05/AG/NIA NIH HHS/ -- T32 AI007328/AI/NIAID NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Feb 25;463(7284):1042-7. doi: 10.1038/nature08752.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Institute for Stem Cell Biology and Regenerative Medicine, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5175, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20027182" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Division ; Cell Fusion ; Cell Line ; Cells, Cultured ; Cellular Reprogramming/genetics/*physiology ; Chromatin Immunoprecipitation ; Cytidine Deaminase/deficiency/genetics/*metabolism ; DNA/chemistry/genetics/metabolism ; *DNA Methylation ; DNA Replication ; Embryonic Stem Cells/cytology/metabolism ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; Gene Knockdown Techniques ; Homeodomain Proteins/genetics ; Humans ; Induced Pluripotent Stem Cells/*cytology/enzymology/*metabolism ; Lung/cytology/embryology ; Mice ; Models, Biological ; Octamer Transcription Factor-3/genetics ; Promoter Regions, Genetic/genetics ; Time Factors
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 8
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    Human host factors required for influenza virus replication (2009)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2009-12-23
    Beschreibung: Influenza A virus is an RNA virus that encodes up to 11 proteins and this small coding capacity demands that the virus use the host cellular machinery for many aspects of its life cycle. Knowledge of these host cell requirements not only informs us of the molecular pathways exploited by the virus but also provides further targets that could be pursued for antiviral drug development. Here we use an integrative systems approach, based on genome-wide RNA interference screening, to identify 295 cellular cofactors required for early-stage influenza virus replication. Within this group, those involved in kinase-regulated signalling, ubiquitination and phosphatase activity are the most highly enriched, and 181 factors assemble into a highly significant host-pathogen interaction network. Moreover, 219 of the 295 factors were confirmed to be required for efficient wild-type influenza virus growth, and further analysis of a subset of genes showed 23 factors necessary for viral entry, including members of the vacuolar ATPase (vATPase) and COPI-protein families, fibroblast growth factor receptor (FGFR) proteins, and glycogen synthase kinase 3 (GSK3)-beta. Furthermore, 10 proteins were confirmed to be involved in post-entry steps of influenza virus replication. These include nuclear import components, proteases, and the calcium/calmodulin-dependent protein kinase (CaM kinase) IIbeta (CAMK2B). Notably, growth of swine-origin H1N1 influenza virus is also dependent on the identified host factors, and we show that small molecule inhibitors of several factors, including vATPase and CAMK2B, antagonize influenza virus replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862546/" 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/PMC2862546/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Konig, Renate -- Stertz, Silke -- Zhou, Yingyao -- Inoue, Atsushi -- Hoffmann, H-Heinrich -- Bhattacharyya, Suchita -- Alamares, Judith G -- Tscherne, Donna M -- Ortigoza, Mila B -- Liang, Yuhong -- Gao, Qinshan -- Andrews, Shane E -- Bandyopadhyay, Sourav -- De Jesus, Paul -- Tu, Buu P -- Pache, Lars -- Shih, Crystal -- Orth, Anthony -- Bonamy, Ghislain -- Miraglia, Loren -- Ideker, Trey -- Garcia-Sastre, Adolfo -- Young, John A T -- Palese, Peter -- Shaw, Megan L -- Chanda, Sumit K -- 1 P01 AI058113/AI/NIAID NIH HHS/ -- 1 S10 RR0 9145-01/RR/NCRR NIH HHS/ -- 1 T32 AI07647/AI/NIAID NIH HHS/ -- 1F32AI081428/AI/NIAID NIH HHS/ -- 1R21AI083673/AI/NIAID NIH HHS/ -- 5R24 CA095823-04/CA/NCI NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- HHSN272200900032C/PHS HHS/ -- P01 AI058113/AI/NIAID NIH HHS/ -- P01 AI058113-010004/AI/NIAID NIH HHS/ -- P01 AI058113-020004/AI/NIAID NIH HHS/ -- P01 AI058113-030004/AI/NIAID NIH HHS/ -- P01 AI058113-040004/AI/NIAID NIH HHS/ -- P01 AI058113-050004/AI/NIAID NIH HHS/ -- T32 AI007647/AI/NIAID NIH HHS/ -- T32 AI007647-01/AI/NIAID NIH HHS/ -- T32 AI007647-02/AI/NIAID NIH HHS/ -- T32 AI007647-03/AI/NIAID NIH HHS/ -- T32 AI007647-04/AI/NIAID NIH HHS/ -- T32 AI007647-05/AI/NIAID NIH HHS/ -- T32 AI007647-06/AI/NIAID NIH HHS/ -- T32 AI007647-07/AI/NIAID NIH HHS/ -- T32 AI007647-08/AI/NIAID NIH HHS/ -- T32 AI007647-09/AI/NIAID NIH HHS/ -- T32 AI007647-10/AI/NIAID NIH HHS/ -- T32 GM007280/GM/NIGMS NIH HHS/ -- U01 AI074539/AI/NIAID NIH HHS/ -- U01 AI074539-01/AI/NIAID NIH HHS/ -- U01 AI074539-02/AI/NIAID NIH HHS/ -- U01 AI074539-03/AI/NIAID NIH HHS/ -- U01 AI1074539/AI/NIAID NIH HHS/ -- U54 AI057158/AI/NIAID NIH HHS/ -- U54 AI057158-065713/AI/NIAID NIH HHS/ -- U54 AI057159/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Feb 11;463(7282):813-7. doi: 10.1038/nature08699.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Infectious and Inflammatory Disease Center, Burnham Institute for Medical Research.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20027183" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Factors/*genetics/*physiology ; Cell Line ; Cercopithecus aethiops ; Gene Library ; Genome, Human/genetics ; Host-Pathogen Interactions/genetics/*physiology ; Humans ; Influenza A Virus, H1N1 Subtype/classification/growth & development ; Influenza A virus/classification/*growth & development ; Influenza, Human/*genetics/*virology ; RNA Interference ; Vero Cells ; Virus Internalization ; Virus Replication/*physiology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 9
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    Deubiquitinase USP9X stabilizes MCL1 and promotes tumour cell survival (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-22
    Beschreibung: MCL1 is essential for the survival of stem and progenitor cells of multiple lineages, and is unique among pro-survival BCL2 family members in that it is rapidly turned over through the action of ubiquitin ligases. B- and mantle-cell lymphomas, chronic myeloid leukaemia, and multiple myeloma, however, express abnormally high levels of MCL1, contributing to chemoresistance and disease relapse. The mechanism of MCL1 overexpression in cancer is not well understood. Here we show that the deubiquitinase USP9X stabilizes MCL1 and thereby promotes cell survival. USP9X binds MCL1 and removes the Lys 48-linked polyubiquitin chains that normally mark MCL1 for proteasomal degradation. Increased USP9X expression correlates with increased MCL1 protein in human follicular lymphomas and diffuse large B-cell lymphomas. Moreover, patients with multiple myeloma overexpressing USP9X have a poor prognosis. Knockdown of USP9X increases MCL1 polyubiquitination, which enhances MCL1 turnover and cell killing by the BH3 mimetic ABT-737. These results identify USP9X as a prognostic and therapeutic target, and they show that deubiquitinases may stabilize labile oncoproteins in human malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwickart, Martin -- Huang, Xiaodong -- Lill, Jennie R -- Liu, Jinfeng -- Ferrando, Ronald -- French, Dorothy M -- Maecker, Heather -- O'Rourke, Karen -- Bazan, Fernando -- Eastham-Anderson, Jeffrey -- Yue, Peng -- Dornan, David -- Huang, David C S -- Dixit, Vishva M -- England -- Nature. 2010 Jan 7;463(7277):103-7. doi: 10.1038/nature08646. Epub 2009 Dec 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20023629" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis/drug effects ; Biphenyl Compounds/pharmacology ; Cell Line ; Cell Line, Tumor ; Cell Survival ; DNA Damage ; Etoposide/pharmacology ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Half-Life ; Humans ; Lysine/metabolism ; Mice ; Mice, SCID ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasms/diagnosis/*metabolism/*pathology ; Nitrophenols/pharmacology ; Phosphorylation/radiation effects ; Piperazines/pharmacology ; Polyubiquitin/*metabolism ; Prognosis ; Protein Binding/radiation effects ; Protein Stability ; Proto-Oncogene Proteins c-bcl-2/genetics/*metabolism ; RNA Interference ; Sulfonamides/pharmacology ; Taxoids/pharmacology ; Ubiquitin Thiolesterase/deficiency/genetics/*metabolism ; Ubiquitination ; Ultraviolet Rays ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Innate production of T(H)2 cytokines by adipose tissue-associated c-Kit(+)Sca-1(+) lymphoid cells (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-22
    Beschreibung: Innate immune responses are important in combating various microbes during the early phases of infection. Natural killer (NK) cells are innate lymphocytes that, unlike T and B lymphocytes, do not express antigen receptors but rapidly exhibit cytotoxic activities against virus-infected cells and produce various cytokines. Here we report a new type of innate lymphocyte present in a novel lymphoid structure associated with adipose tissues in the peritoneal cavity. These cells do not express lineage (Lin) markers but do express c-Kit, Sca-1 (also known as Ly6a), IL7R and IL33R. Similar lymphoid clusters were found in both human and mouse mesentery and we term this tissue 'FALC' (fat-associated lymphoid cluster). FALC Lin(-)c-Kit(+)Sca-1(+) cells are distinct from lymphoid progenitors and lymphoid tissue inducer cells. These cells proliferate in response to IL2 and produce large amounts of T(H)2 cytokines such as IL5, IL6 and IL13. IL5 and IL6 regulate B-cell antibody production and self-renewal of B1 cells. Indeed, FALC Lin(-)c-Kit(+)Sca-1(+) cells support the self-renewal of B1 cells and enhance IgA production. IL5 and IL13 mediate allergic inflammation and protection against helminth infection. After helminth infection and in response to IL33, FALC Lin(-)c-Kit(+)Sca-1(+) cells produce large amounts of IL13, which leads to goblet cell hyperplasia-a critical step for helminth expulsion. In mice devoid of FALC Lin(-)c-Kit(+)Sca-1(+) cells, such goblet cell hyperplasia was not induced. Thus, FALC Lin(-)c-Kit(+)Sca-1(+) cells are T(H)2-type innate lymphocytes, and we propose that these cells be called 'natural helper cells'.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moro, Kazuyo -- Yamada, Taketo -- Tanabe, Masanobu -- Takeuchi, Tsutomu -- Ikawa, Tomokatsu -- Kawamoto, Hiroshi -- Furusawa, Jun-Ichi -- Ohtani, Masashi -- Fujii, Hideki -- Koyasu, Shigeo -- England -- Nature. 2010 Jan 28;463(7280):540-4. doi: 10.1038/nature08636. Epub 2009 Dec 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20023630" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipose Tissue/*cytology/*immunology ; Animals ; Antigens, Ly/genetics/*immunology/metabolism ; B-Lymphocytes/cytology/immunology ; Cell Proliferation ; Cytokines/*immunology ; *Gene Expression Regulation ; Humans ; Lymphocytes/*immunology ; Membrane Proteins/genetics/*immunology ; Mesentery/immunology ; Mice ; Mice, Inbred C57BL ; Nematoda/physiology ; Nematode Infections/immunology ; Proto-Oncogene Proteins c-kit/genetics/*immunology ; Th2 Cells/immunology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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