ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Articles  (51)
  • Chemistry  (45)
  • Cell Line, Tumor  (6)
Collection
  • Articles  (51)
Source
Keywords
Publisher
Years
Journal
Topic
  • 1
    facet.materialart.
    Unknown
    PDK1 nucleates T cell receptor-induced signaling complex for NF-kappaB activation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-02
    Description: Activation of the transcription factor NF-kappaB after engagement of the T cell receptor (TCR) is important for T cell proliferation and activation during the adaptive immune response. Recent reports have elucidated a signaling pathway that involves the protein kinase C (PKC), the scaffold protein CARD11 (also called CARMA-1), the caspase recruitment domain (CARD)-containing protein Bcl10, and the paracaspase (protease related to caspases) MALT1 as critical intermediates linking the TCR to the IkappaB kinase (IKK) complex. However, the events proximal to the TCR that initiate the activation of this signaling pathway remain poorly defined. We demonstrate that 3-phosphoinositide-dependent kinase 1 (PDK1) has an essential role in this pathway by regulating the activation of PKC and through signal-dependent recruiting of both PKC and CARD11 to lipid rafts. PDK1-associated PKC recruits the IKK complex, whereas PDK1-associated CARD11 recruits the Bcl10-MALT1 complex, thereby allowing activation of the IKK complex through Bcl10-MALT1-dependent ubiquitination of the IKK complex subunit known as NEMO (NF-kappaB essential modifier). Hence, PDK1 plays a critical role by nucleating the TCR-induced NF-kappaB activation pathway in T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Ki-Young -- D'Acquisto, Fulvio -- Hayden, Matthew S -- Shim, Jae-Hyuck -- Ghosh, Sankar -- R37 AI033443/AI/NIAID NIH HHS/ -- R37-AI33443/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):114-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Department of Molecular Biophysics and Biochemistry, 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/15802604" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Adaptor Proteins, Signal Transducing/metabolism ; Apoptosis Regulatory Proteins ; CARD Signaling Adaptor Proteins ; Carrier Proteins/metabolism ; Caspases ; Cell Line ; Cell Line, Tumor ; Enzyme Activation ; Guanylate Cyclase/metabolism ; Humans ; I-kappa B Kinase ; Isoenzymes/genetics/*metabolism ; Jurkat Cells ; Lymphocyte Activation ; Lymphoma, B-Cell, Marginal Zone/metabolism ; Membrane Microdomains/metabolism ; Membrane Proteins/metabolism ; Models, Biological ; NF-kappa B/*metabolism ; Neoplasm Proteins/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein Kinase C/genetics/*metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; RNA Interference ; Receptors, Antigen, T-Cell/immunology/*metabolism ; *Signal Transduction ; T-Lymphocytes/enzymology/immunology/*metabolism ; Transfection
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    RAS-MAPK-MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1 (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-05-31
    Description: Many neurodegenerative disorders, such as Alzheimer's, Parkinson's and polyglutamine diseases, share a common pathogenic mechanism: the abnormal accumulation of disease-causing proteins, due to either the mutant protein's resistance to degradation or overexpression of the wild-type protein. We have developed a strategy to identify therapeutic entry points for such neurodegenerative disorders by screening for genetic networks that influence the levels of disease-driving proteins. We applied this approach, which integrates parallel cell-based and Drosophila genetic screens, to spinocerebellar ataxia type 1 (SCA1), a disease caused by expansion of a polyglutamine tract in ataxin 1 (ATXN1). Our approach revealed that downregulation of several components of the RAS-MAPK-MSK1 pathway decreases ATXN1 levels and suppresses neurodegeneration in Drosophila and mice. Importantly, pharmacological inhibitors of components of this pathway also decrease ATXN1 levels, suggesting that these components represent new therapeutic targets in mitigating SCA1. Collectively, these data reveal new therapeutic entry points for SCA1 and provide a proof-of-principle for tackling other classes of intractable neurodegenerative diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4020154/" 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/PMC4020154/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Jeehye -- Al-Ramahi, Ismael -- Tan, Qiumin -- Mollema, Nissa -- Diaz-Garcia, Javier R -- Gallego-Flores, Tatiana -- Lu, Hsiang-Chih -- Lagalwar, Sarita -- Duvick, Lisa -- Kang, Hyojin -- Lee, Yoontae -- Jafar-Nejad, Paymaan -- Sayegh, Layal S -- Richman, Ronald -- Liu, Xiuyun -- Gao, Yan -- Shaw, Chad A -- Arthur, J Simon C -- Orr, Harry T -- Westbrook, Thomas F -- Botas, Juan -- Zoghbi, Huda Y -- HD024064/HD/NICHD NIH HHS/ -- MC_U127081014/Medical Research Council/United Kingdom -- NS42179/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- R01 NS027699/NS/NINDS NIH HHS/ -- R01 NS042179/NS/NINDS NIH HHS/ -- T32 GM007526/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jun 20;498(7454):325-31. doi: 10.1038/nature12204. Epub 2013 May 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23719381" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Ataxin-1 ; Ataxins ; Cell Line, Tumor ; Disease Models, Animal ; Down-Regulation/drug effects ; Drosophila melanogaster/genetics/*metabolism ; Female ; Humans ; MAP Kinase Signaling System/drug effects ; Male ; Mice ; Mitogen-Activated Protein Kinases/*metabolism ; Molecular Sequence Data ; Molecular Targeted Therapy ; Nerve Tissue Proteins/chemistry/genetics/*metabolism/*toxicity ; Nuclear Proteins/chemistry/genetics/*metabolism/*toxicity ; Phosphorylation ; Protein Stability/drug effects ; Ribosomal Protein S6 Kinases, 90-kDa/deficiency/genetics/*metabolism ; Spinocerebellar Ataxias/*metabolism/*pathology ; Transgenes ; ras Proteins/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Cyclin D1-Cdk4 controls glucose metabolism independently of cell cycle progression (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-05-30
    Description: Insulin constitutes a principal evolutionarily conserved hormonal axis for maintaining glucose homeostasis; dysregulation of this axis causes diabetes. PGC-1alpha (peroxisome-proliferator-activated receptor-gamma coactivator-1alpha) links insulin signalling to the expression of glucose and lipid metabolic genes. The histone acetyltransferase GCN5 (general control non-repressed protein 5) acetylates PGC-1alpha and suppresses its transcriptional activity, whereas sirtuin 1 deacetylates and activates PGC-1alpha. Although insulin is a mitogenic signal in proliferative cells, whether components of the cell cycle machinery contribute to its metabolic action is poorly understood. Here we report that in mice insulin activates cyclin D1-cyclin-dependent kinase 4 (Cdk4), which, in turn, increases GCN5 acetyltransferase activity and suppresses hepatic glucose production independently of cell cycle progression. Through a cell-based high-throughput chemical screen, we identify a Cdk4 inhibitor that potently decreases PGC-1alpha acetylation. Insulin/GSK-3beta (glycogen synthase kinase 3-beta) signalling induces cyclin D1 protein stability by sequestering cyclin D1 in the nucleus. In parallel, dietary amino acids increase hepatic cyclin D1 messenger RNA transcripts. Activated cyclin D1-Cdk4 kinase phosphorylates and activates GCN5, which then acetylates and inhibits PGC-1alpha activity on gluconeogenic genes. Loss of hepatic cyclin D1 results in increased gluconeogenesis and hyperglycaemia. In diabetic models, cyclin D1-Cdk4 is chronically elevated and refractory to fasting/feeding transitions; nevertheless further activation of this kinase normalizes glycaemia. Our findings show that insulin uses components of the cell cycle machinery in post-mitotic cells to control glucose homeostasis independently of cell division.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076706/" 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/PMC4076706/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Yoonjin -- Dominy, John E -- Choi, Yoon Jong -- Jurczak, Michael -- Tolliday, Nicola -- Camporez, Joao Paulo -- Chim, Helen -- Lim, Ji-Hong -- Ruan, Hai-Bin -- Yang, Xiaoyong -- Vazquez, Francisca -- Sicinski, Piotr -- Shulman, Gerald I -- Puigserver, Pere -- DK059635/DK/NIDDK NIH HHS/ -- F32 DK083871/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- R01 CA083688/CA/NCI NIH HHS/ -- R01 CA108420/CA/NCI NIH HHS/ -- R01 DK069966/DK/NIDDK NIH HHS/ -- R01 DK089098/DK/NIDDK NIH HHS/ -- R01069966/PHS HHS/ -- R03 DA032468/DA/NIDA NIH HHS/ -- R03 MH092174/MH/NIMH NIH HHS/ -- R24 DK080261/DK/NIDDK NIH HHS/ -- R24DK080261-06/DK/NIDDK NIH HHS/ -- U24 DK059635/DK/NIDDK NIH HHS/ -- England -- Nature. 2014 Jun 26;510(7506):547-51. doi: 10.1038/nature13267. Epub 2014 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Department of Chemistry and Chemical Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Yale's Mouse Metabolic Phenotyping Center and Departments of Internal Medicine and Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA. ; Chemical Biology Platform, Broad Institute of Harvard and MIT, 7 Cambridge Center, Cambridge, Massachusetts 02141, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24870244" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acids/pharmacology ; Animals ; *Cell Cycle ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclin D1/deficiency/genetics/*metabolism ; Cyclin-Dependent Kinase 4/antagonists & inhibitors/*metabolism ; Diabetes Mellitus/metabolism ; Enzyme Activation ; Fasting ; Gene Deletion ; Gluconeogenesis/genetics ; Glucose/*metabolism ; Glycogen Synthase Kinase 3/metabolism ; Hepatocytes/cytology/drug effects/metabolism ; Histone Acetyltransferases/metabolism ; Homeostasis ; Humans ; Hyperglycemia/metabolism ; Hyperinsulinism/metabolism ; Insulin/*metabolism ; Male ; Mice ; Phosphorylation ; RNA, Messenger/analysis/genetics ; *Signal Transduction ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Mapping the cellular response to small molecules using chemogenomic fitness signatures (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-04-12
    Description: Genome-wide characterization of the in vivo cellular response to perturbation is fundamental to understanding how cells survive stress. Identifying the proteins and pathways perturbed by small molecules affects biology and medicine by revealing the mechanisms of drug action. We used a yeast chemogenomics platform that quantifies the requirement for each gene for resistance to a compound in vivo to profile 3250 small molecules in a systematic and unbiased manner. We identified 317 compounds that specifically perturb the function of 121 genes and characterized the mechanism of specific compounds. Global analysis revealed that the cellular response to small molecules is limited and described by a network of 45 major chemogenomic signatures. Our results provide a resource for the discovery of functional interactions among genes, chemicals, and biological processes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4254748/" 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/PMC4254748/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Anna Y -- St Onge, Robert P -- Proctor, Michael J -- Wallace, Iain M -- Nile, Aaron H -- Spagnuolo, Paul A -- Jitkova, Yulia -- Gronda, Marcela -- Wu, Yan -- Kim, Moshe K -- Cheung-Ong, Kahlin -- Torres, Nikko P -- Spear, Eric D -- Han, Mitchell K L -- Schlecht, Ulrich -- Suresh, Sundari -- Duby, Geoffrey -- Heisler, Lawrence E -- Surendra, Anuradha -- Fung, Eula -- Urbanus, Malene L -- Gebbia, Marinella -- Lissina, Elena -- Miranda, Molly -- Chiang, Jennifer H -- Aparicio, Ana Maria -- Zeghouf, Mahel -- Davis, Ronald W -- Cherfils, Jacqueline -- Boutry, Marc -- Kaiser, Chris A -- Cummins, Carolyn L -- Trimble, William S -- Brown, Grant W -- Schimmer, Aaron D -- Bankaitis, Vytas A -- Nislow, Corey -- Bader, Gary D -- Giaever, Guri -- GM103504/GM/NIGMS NIH HHS/ -- GM44530/GM/NIGMS NIH HHS/ -- MOP-700724/Canadian Institutes of Health Research/Canada -- MOP-79368/Canadian Institutes of Health Research/Canada -- MOP-81340/Canadian Institutes of Health Research/Canada -- P01 HG000205/HG/NHGRI NIH HHS/ -- P41 GM103504/GM/NIGMS NIH HHS/ -- R01 003317-07/PHS HHS/ -- R01 CA157456/CA/NCI NIH HHS/ -- R01 GM044530/GM/NIGMS NIH HHS/ -- R01 HG003317/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 11;344(6180):208-11. doi: 10.1126/science.1250217.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24723613" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cells/*drug effects ; Drug Evaluation, Preclinical/*methods ; Drug Resistance/*genetics ; *Gene Regulatory Networks ; Genome-Wide Association Study/*methods ; Haploinsufficiency ; Humans ; Pharmacogenetics ; Saccharomyces cerevisiae/drug effects/genetics ; Small Molecule Libraries/*pharmacology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Prevention of Brca1-mediated mammary tumorigenesis in mice by a progesterone antagonist (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-02
    Description: Women with mutations in the breast cancer susceptibility gene BRCA1 are predisposed to breast and ovarian cancers. Why the BRCA1 protein suppresses tumor development specifically in ovarian hormone-sensitive tissues remains unclear. We demonstrate that mammary glands of nulliparous Brca1/p53-deficient mice accumulate lateral branches and undergo extensive alveologenesis, a phenotype that occurs only during pregnancy in wild-type mice. Progesterone receptors, but not estrogen receptors, are overexpressed in the mutant mammary epithelial cells because of a defect in their degradation by the proteasome pathway. Treatment of Brca1/p53-deficient mice with the progesterone antagonist mifepristone (RU 486) prevented mammary tumorigenesis. These findings reveal a tissue-specific function for the BRCA1 protein and raise the possibility that antiprogesterone treatment may be useful for breast cancer prevention in individuals with BRCA1 mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poole, Aleksandra Jovanovic -- Li, Ying -- Kim, Yoon -- Lin, Suh-Chin J -- Lee, Wen-Hwa -- Lee, Eva Y-H P -- CA049649/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1467-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of California, Irvine, CA 92697-4037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17138902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Epithelial Cells/cytology/metabolism ; Estradiol/pharmacology ; Estrous Cycle ; Female ; *Genes, BRCA1 ; Genes, p53 ; Hormone Antagonists/*pharmacology/therapeutic use ; Humans ; Mammary Glands, Animal/cytology/metabolism ; Mammary Neoplasms, Animal/genetics/*prevention & control ; Mice ; Mifepristone/*pharmacology/therapeutic use ; Mutation ; Phosphorylation ; Progesterone/*antagonists & inhibitors/pharmacology ; Proteasome Endopeptidase Complex/metabolism ; RNA, Small Interfering ; Receptors, Estrogen/metabolism ; Receptors, Progesterone/genetics/*metabolism ; Ubiquitin/metabolism
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    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
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    Electronic Resource
    Electronic Resource
    Model filled polymers. I. Synthesis of crosslinked monodisperse polystyrene beads (1990)
    Bognor Regis [u.a.] : Wiley-Blackwell
    Journal of Polymer Science Part A: Polymer Chemistry 28 (1990), S. 1909-1921 
    Details
    ISSN: 0887-624X
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Monodisperse crosslinked polystyrene beads of varied size and crosslink density are prepared by emulsion copolymerization of styrene and divinylbenzene in the absence of emulsifier. Tumbling and internally stirred reactors were used for synthesis, with minimal agglomeration at at least 0.22 wt % potassium persulfate and up to 10% by weight of styrene in aqueous emulsion in the absence of oxygen. Particle sizes decreased from 800 to 200 nm on raising the polymerization temperature from 60 to 95°C. The glass transition temperature of the beads increased from 104.4 to 133°C by the inclusion of up to 10% by weight of divinylbenzene. The thermal stability of the beads was higher for peroxide than for persulfate initiation. The crosslink density estimated from the degree of swelling was about one third that expected from stoichiometry. The polystyrene beads are used as filler particles in polymer composites.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/pola.1990.080280722
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Design and characterization of thermosetting polyimide structural adhesive and composite matrix systems (1997)
    Bognor Regis [u.a.] : Wiley-Blackwell
    Journal of Polymer Science Part A: Polymer Chemistry 35 (1997), S. 2943-2954 
    Details
    ISSN: 0887-624X
    Keywords: phenyl ethynyl ether imides ; amorphous or semicrystalline morphology ; volatile free thermosetting matrix ; structural adhesives ; composites ; Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Fully cyclized, organo soluble, phenylethynyl-terminated, ether-imide oligomers of 2-10,000 g/mol (Mn) were prepared by the reaction of 2,2′-bis[4-(3,4-dicarboxyphenoxy)phenyl]-propane dianhydride (bisphenol-A dianhydride, BPADA) with a stoichiometric excess of either para, meta, or isomeric mixtures of phenylene diamine and phenylethynylphthalic anhydride (4-PEPA) endcapper. High para-containing oligomers produced semicrystalline powders, but the all meta isomer was completely amorphous. The lower molecular weight oligomers displayed an attractive low viscosity melt and were cured to very high gel content networks at 350-380°C for 30-90 min. The cured 3000 g/mol oligomers showed a (DSC) glass transition temperature (Tg) of 267°C and produced tough, solvent-resistant films. Excellent adhesion to surface-treated titanium alloys was achieved, as judged by single-lap shear measurements. Resin infusion molding was conducted, which permitted low-void, graphite-fabric composite panels to be prepared. © 1997 John Wiley & Sons, Inc. J Polym Sci A: Polym Chem 35: 2943-2954, 1997
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 9
    Electronic Resource
    Electronic Resource
    Inulin hydrolysis to fructose by a novel catalyst (1995)
    Weinheim : Wiley-Blackwell
    Chemical Engineering & Technology - CET 18 (1995), S. 440-444 
    Details
    ISSN: 0930-7516
    Keywords: Chemistry ; Industrial Chemistry and Chemical Engineering
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Acidic zeolite LZ-M-8 was used to catalyse the hydrolysis reaction of inulin into fructose. Fructose contents of 96% and 75% were obtained when commercial inulin and Jerusalem artichoke extract were used respectively as substrates. Zeolite LZ-M-8 was found to be extremely selective towards inulin hydrolysis as compared to fructose decomposition. Formation of hydroxymethyl furfural (HmF) was not detected and it was confirmed that zeolite LZ-M-8 does not adsorb HMF. The catalytic activity of the zeolite remained intact upon repeated use of the catalyst. The superiority of the zeolite over other catalysts used in inulin hydrolysis was demonstrated experimentally.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ceat.270180612
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    The forming properties of high molecular weight polyethylene (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Applied Polymer Science 43 (1991), S. 29-37 
    Details
    ISSN: 0021-8995
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: The formabilities of cold-rolled high molecular weight polyethylene (HMWPE) sheets have been studied by measuring their plastic anisotropy ratio (R value), strain-hardening exponent (n value), strain distribution, and the forming limit diagram (FLD). The deep drawability of the polymer is improved by rolling. After 40% or more reduction in thickness by cold rolling, the HMWPE sheet could be deep-drawn into a cylindrical cup. The results of R value measurement indicate that the R value is responsible for improved drawability. Cold rolling also increases the n value but decreases the strain gradient. Stretch forming tests have also been carried out, and the results show that cold working could also improve the stretchability of this polymer. The results of the FLD are in agreement with the other properties studied. The mechanical properties, environmental stress cracking resistance, and shape, size, and property stability of the deep-drawn HMWPE cups have also been investigated.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/app.1991.070430105
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...