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  • 1
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    Annexin-1 regulated by HAUSP is essential for UV-induced damage response (2015)
    Springer Nature
    Details
    Publication Date: 2015-02-20
    Description: Annexin-1 regulated by HAUSP is essential for UV-induced damage response Cell Death and Disease 6, e1654 (February 2015). doi:10.1038/cddis.2015.32 Authors: J-J Park, K-H Lim & K-H Baek
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 2
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    Structural features of influenza A virus panhandle RNA enabling the activation of RIG-I independently of 5'-triphosphate (2016)
    Oxford University Press
    Details
    Publication Date: 2016-10-08
    Description: Retinoic acid-inducible gene I (RIG-I) recognizes specific molecular patterns of viral RNAs for inducing type I interferon. The C-terminal domain (CTD) of RIG-I binds to double-stranded RNA (dsRNA) with the 5'-triphosphate (5'-PPP), which induces a conformational change in RIG-I to an active form. It has been suggested that RIG-I detects infection of influenza A virus by recognizing the 5'-triphosphorylated panhandle structure of the viral RNA genome. Influenza panhandle RNA has a unique structure with a sharp helical bending. In spite of extensive studies of how viral RNAs activate RIG-I, whether the structural elements of the influenza panhandle RNA confer the ability to activate RIG-I signaling has been poorly explored. Here, we investigated the dynamics of the influenza panhandle RNA in complex with RIG-I CTD using NMR spectroscopy and showed that the bending structure of the panhandle RNA negates the requirement of a 5'-PPP moiety for RIG-I activation.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 3
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    Tumour maintenance is mediated by eNOS (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-03-18
    Description: Tumour cells become addicted to the expression of initiating oncogenes like Ras, such that loss of oncogene expression in established tumours leads to tumour regression. HRas, NRas or KRas are mutated to remain in the active GTP-bound oncogenic state in many cancers. Although Ras activates several proteins to initiate human tumour growth, only PI3K, through activation of protein kinase B (PKB; also known as AKT), must remain activated by oncogenic Ras to maintain this growth. Here we show that blocking phosphorylation of the AKT substrate, endothelial nitric oxide synthase (eNOS or NOS3), inhibits tumour initiation and maintenance. Moreover, eNOS enhances the nitrosylation and activation of endogenous wild-type Ras proteins, which are required throughout tumorigenesis. We suggest that activation of the PI3K-AKT-eNOS-(wild-type) Ras pathway by oncogenic Ras in cancer cells is required to initiate and maintain tumour growth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688829/" 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/PMC2688829/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, Kian-Huat -- Ancrile, Brooke B -- Kashatus, David F -- Counter, Christopher M -- R01 CA094184/CA/NCI NIH HHS/ -- R01 CA094184-01/CA/NCI NIH HHS/ -- R01 CA094184-02/CA/NCI NIH HHS/ -- R01 CA094184-03/CA/NCI NIH HHS/ -- R01 CA094184-04/CA/NCI NIH HHS/ -- R01 CA094184-05/CA/NCI NIH HHS/ -- R01 CA123031/CA/NCI NIH HHS/ -- R01 CA123031-01A2/CA/NCI NIH HHS/ -- England -- Nature. 2008 Apr 3;452(7187):646-9. doi: 10.1038/nature06778. Epub 2008 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18344980" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Cell Line, Transformed ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Humans ; Mice ; Neoplasms/drug therapy/*enzymology/*pathology ; Nitric Oxide Synthase Type III/deficiency/genetics/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; 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)
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  • 4
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    Oncogenically active MYD88 mutations in human lymphoma (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-24
    Description: The activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL) remains the least curable form of this malignancy despite recent advances in therapy. Constitutive nuclear factor (NF)-kappaB and JAK kinase signalling promotes malignant cell survival in these lymphomas, but the genetic basis for this signalling is incompletely understood. Here we describe the dependence of ABC DLBCLs on MYD88, an adaptor protein that mediates toll and interleukin (IL)-1 receptor signalling, and the discovery of highly recurrent oncogenic mutations affecting MYD88 in ABC DLBCL tumours. RNA interference screening revealed that MYD88 and the associated kinases IRAK1 and IRAK4 are essential for ABC DLBCL survival. High-throughput RNA resequencing uncovered MYD88 mutations in ABC DLBCL lines. Notably, 29% of ABC DLBCL tumours harboured the same amino acid substitution, L265P, in the MYD88 Toll/IL-1 receptor (TIR) domain at an evolutionarily invariant residue in its hydrophobic core. This mutation was rare or absent in other DLBCL subtypes and Burkitt's lymphoma, but was observed in 9% of mucosa-associated lymphoid tissue lymphomas. At a lower frequency, additional mutations were observed in the MYD88 TIR domain, occurring in both the ABC and germinal centre B-cell-like (GCB) DLBCL subtypes. Survival of ABC DLBCL cells bearing the L265P mutation was sustained by the mutant but not the wild-type MYD88 isoform, demonstrating that L265P is a gain-of-function driver mutation. The L265P mutant promoted cell survival by spontaneously assembling a protein complex containing IRAK1 and IRAK4, leading to IRAK4 kinase activity, IRAK1 phosphorylation, NF-kappaB signalling, JAK kinase activation of STAT3, and secretion of IL-6, IL-10 and interferon-beta. Hence, the MYD88 signalling pathway is integral to the pathogenesis of ABC DLBCL, supporting the development of inhibitors of IRAK4 kinase and other components of this pathway for the treatment of tumours bearing oncogenic MYD88 mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ngo, Vu N -- Young, Ryan M -- Schmitz, Roland -- Jhavar, Sameer -- Xiao, Wenming -- Lim, Kian-Huat -- Kohlhammer, Holger -- Xu, Weihong -- Yang, Yandan -- Zhao, Hong -- Shaffer, Arthur L -- Romesser, Paul -- Wright, George -- Powell, John -- Rosenwald, Andreas -- Muller-Hermelink, Hans Konrad -- Ott, German -- Gascoyne, Randy D -- Connors, Joseph M -- Rimsza, Lisa M -- Campo, Elias -- Jaffe, Elaine S -- Delabie, Jan -- Smeland, Erlend B -- Fisher, Richard I -- Braziel, Rita M -- Tubbs, Raymond R -- Cook, J R -- Weisenburger, Denny D -- Chan, Wing C -- Staudt, Louis M -- U01-CA 114778/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2011 Feb 3;470(7332):115-9. doi: 10.1038/nature09671. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179087" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Burkitt Lymphoma/genetics ; Cell Line, Tumor ; Cell Survival ; Cytokines/metabolism/secretion ; High-Throughput Nucleotide Sequencing ; Humans ; Hydrophobic and Hydrophilic Interactions ; Interleukin-1 Receptor-Associated Kinases/biosynthesis/genetics/metabolism ; Janus Kinases/metabolism ; Lymphoma, B-Cell, Marginal Zone/genetics ; Lymphoma, Large B-Cell, Diffuse/classification/*genetics/*pathology ; Molecular Sequence Data ; Mutant Proteins/chemistry/genetics/metabolism ; Mutation/*genetics ; Myeloid Differentiation Factor 88/chemistry/*genetics/*metabolism ; NF-kappa B/metabolism ; Oncogenes/*genetics ; Phosphorylation ; Protein Structure, Tertiary ; RNA Interference ; Receptors, Interleukin-1/metabolism ; STAT3 Transcription Factor/metabolism ; Sequence Analysis, RNA ; Signal Transduction ; Toll-Like Receptors/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)
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  • 5
    Electronic Resource
    Electronic Resource
    Gemeinsame Einwirkung von elementarem Schwefel und Äthylenimin auf Ketone, 3. Mitt.: Über die gemeinsame Einwirkung von elementarem Schwefel und gasförmigem Ammoniak auf Ketone, 74. Mitt. (1971)
    Springer
    Monatshefte für Chemie 102 (1971), S. 321-332 
    Details
    ISSN: 1434-4475
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Abstract The reaction of ethylenimine and sulfur with methyl ethyl ketone, methyl isopropyl ketone and ethyl isopropyl ketone, resp., yields the structurally isomeric 5.6-dihydro-1.4-thiazines (1–6) and as by-products the thiazolidines (7–9) derived from the corresponding ketones. The 5.6-dihydro-1.4-thiazines are converted with formic acid to the N-formyl thiomorpholines10–15, which are easily hydrolyzed with dilute hydrochloric acid to the corresponding thiomorpholines (16–21). The ratio of the pairs of structurally isomeric thiomorpholines is determined by quantitative gas chromatography.
    Notes: Zusammenfassung Bei der Einwirkung von Äthylenimin und Schwefel auf Methyläthylketon, Methylisopropylketon und Äthylisopropylketon entstehen strukturisomere 5,6-Dihydro-1,4-thiazine (1–6) und als Nebenprodukte die dem jeweiligen Keton entsprechenden Thiazolidine (7–9). Die 5,6-Dihydro-1,4-thiazine werden mit Ameisensäure in N-Formylthiomorpholine (10–15) übergeführt, die mit verd. HCl glatt zu den entsprechenden Thiomorpholinen (16–21) hydrolysiert werden. Das Verhältnis der Thiomorpholin-Isomerenpaare wird gaschromatographisch quantitativ bestimmt.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00909244
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  • 6
    Electronic Resource
    Electronic Resource
    Gemeinsame Einwirkung von elementarem Schwefel und Äthylenimin auf Ketone, 2. Mitt. (1970)
    Springer
    Monatshefte für Chemie 101 (1970), S. 1281-1294 
    Details
    ISSN: 1434-4475
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Abstract The interaction of sulfur and ethylenimine with 4-heptanone, cyclopentanone, cyclohexanone, and cyclooctanone leads to 5.6-dihydro-4H-1.4-thiazines (3–6) in good yields. As byproducts of3, 4 and5 2.2-dialkylated thiazolidines (7–9, resp.) are isolated. When this reaction is carried out with phenyl isopropyl ketone, however, the main product is 2-isopropyl-2-phenylthiazolidine (12), the corresponding 5.6-dihydro-2H-1.4-thiazine (11) is but formed in a small quantity. The mechanisms of the formation of 5.6-dihydro-1.4-thiazines, as well as the formation of the thiazolidines are discussed. Reaction of 5.6-dihydro-1.4-thiazines (1, 3–5, 11) with excess formic acid leads to N-formylthiomorpholines (13–17) which can be easily saponified with dil. HCl to the corresponding thiomorpholines (18–22).
    Notes: Zusammenfassung Bei der gemeinsamen Einwirkung von Schwefel und Äthylenimin auf 4-Heptanon, Cyclopentanon, Cyclohexanon und Cyclooctanon bilden sich in glatter Reaktion 5,6-Dihydro-4H-1,4-thiazine (3–6). Als Nebenprodukte von3, 4 und5 fallen die dem jeweiligen Keton zugrunde liegenden 2,2-dialkylierten Thiazolidine (7–9) an. Bei Einsatz von Phenylisopropylketon in diese Reaktion wird dagegen das 2-Isopropyl-2-phenylthiazolidin (12) zum Hauptprodukt, während das entsprechende 5,6-Dihydro-2H-1,4-thiazin (11) nur in untergeordnetem Maße entsteht. Die Reaktionsmechanismen sowohl der 5,6-Dihydro-1,4-thiazin-als auch der Thiazolidin-Bildung werden diskutiert. Die Umsetzung der 5,6-Dihydro-1,4-thiazine (1, 3–5, 11) mit überschüss. Ameisensäure führt zu N-Formylthiomorpholinen (13–17), die sich mit verd. HCl glatt zu den entsprechenden Thiomorpholinen (18–22) verseifen lassen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00911394
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  • 7
    Electronic Resource
    Electronic Resource
    Thermal degradation of transition metal carbonyl complexes. Part II (1988)
    Springer
    Journal of thermal analysis and calorimetry 34 (1988), S. 121-133 
    Details
    ISSN: 1572-8943
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Zusammenfassung Der thermische Abbau von drei monosubstituierten Hexacarbonylkomplexen der allgemeinen Formel M(CO)5py (mit M=Cr, Mo und W; py=Pyridin) wurden mittels TG und DSC untersucht. Von jeder der drei Komplexe wird die Ausgangssubstanz M(CO)6 erhalten, die sofort unverändert mit oder ohne gleichzeitigem Verlust an Carbonyl (CO)-Liganden sublimiert und die erste große Gewichtsverluststufe ergibt. Diesem Schritt folgt gleich die Verflüchtigung des Pyridinliganden und bei höheren Temperaturen die Abgabe weiterer CO-Liganden. Die mit den genannten Schritten einhergehenden Enthalpieveränderungen werden mitgeteilt. Die Umwandlung von M(CO)5py zu M(CO)6 und anderen Produkten wurden durch Analyse des Rückstandes nach der Pyrolyse in einem Röhrenofen unter ähnlichen Bedingungen wie in den TG-Versuchen bestätigt.
    Abstract: Резюме Методами ТГ и ДСК изуч ено термическое разложение трех моно замещенных гексакарбонильных к омплексов М(СО)5ру, где M=хром, молибден и вольфрам, а ру=пиридин. Найдено, что разложен ие комплексов протек ает с образованием исходн ого гексакарбонила, который сразу же субл имируется неизменны м или же с сопутствующей потер ей карбонильных лигандов, давая тем са мым первию стадию с бо льшой потерей веса. Близко к этой стадии происходило выделен ие пиридиновых лиган дов, а при более высоких темпер атурах происходило дальнейшее выделени е карбонильных лиган дов. Приведены изменения энтальпии для вышеупомянутых стад ий. Образование гекса карбонилов металлов и других про дуктов разложения было подтверждено ан ализом конечных прод уктов пиролиза в трубчатой печи в условиях подобных таковым, как и в методе ТГ.
    Notes: Abstract The thermal degradation of three monosubstituted hexacarbonyl complexes, M(CO)5py (where M=Cr, Mo, and W; py=pyridine) has been studied by thermogravimetry (TG) and differential scanning calorimetry (DSC) and their results reported. It was found that for each of the three complexes studied, the starting material M(CO)6 was formed which immediately sublimed unchanged with or without concomitant loss of carbonyl (CO) ligands to give the first large weight loss step. This was closely followed by the volatilisation of the pyridine ligands and at higher temperatures the loss of further CO ligands. The enthalpy changes associated with the above-mentioned steps are reported. The conversion of M(CO)5py to M(CO)6 and other products was confirmed by the analysis of residue after pyrolysis in a tube furnace under conditions similar to those observed in TG experiments.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01913379
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  • 8
    Electronic Resource
    Electronic Resource
    Analysis of coatings which inhibit epoxy bleeding in electronic packaging (1997)
    Springer
    Journal of materials science 8 (1997), S. 73-77 
    Details
    ISSN: 1573-482X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Electrical Engineering, Measurement and Control Technology , Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Abstract The bleeding of epoxy resin around surfaces, undergoing bonding in electronic packaging assembly, has for long caused sporadic yield-loss. This loss is more severe in advanced and dense packages. Previously it has been supposed that the loss results from surface contaminants which are reduced by vacuum bakeout. In fact, that procedure generates coatings of hydrocarbons as we show by surface analysis. The coatings very strongly affect the wettabilities and measured surface energies of substrates. In particular, the comparatively low surface energy of hydrocarbon films on gold surfaces shows how the surfaces can be engineered, with coatings of “appropriate cleanliness”, to systematically inhibit epoxy bleeding.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018561106025
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  • 9
    Electronic Resource
    Electronic Resource
    Gemeinsame Einwirkung von elementarem Schwefel und Äthylenimin auf Diäthylketon (1968)
    Springer
    Monatshefte für Chemie 99 (1968), S. 2090-2094 
    Details
    ISSN: 1434-4475
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Abstract 2-Methyl-3-ethyl-5.6-dihydro-4H-1.4-thiazine (1) may be synthesised in 75% yield by the concomitant action of sulphur and ethylene imine upon diethyl ketone.
    Notes: Zusammenfassung 2-Methyl-3-äthyl-5,6-dihydro-4H-1,4-thiazin (1) läßt sich in 75proz. Ausb. durch die gemeinsame Einwirkung von Schwefel und Äthylenimin auf Diäthylketon darstellen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00904344
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  • 10
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    Confocal light absorption and scattering spectroscopic microscopy monitors organelles in live cells with no exogenous labels (2007)
    National Academy of Sciences
    Details
    Publication Date: 2007-10-23
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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