ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
  • 1
    Publikationsdatum: 2014-11-26
    Beschreibung: Receptor-interacting protein kinase 3 (RIPK3)-mediated necroptosis is thought to be the pathophysiologically predominant pathway that leads to regulated necrosis of parenchymal cells in ischemia–reperfusion injury (IRI), and loss of either Fas-associated protein with death domain (FADD) or caspase-8 is known to sensitize tissues to undergo spontaneous necroptosis. Here, we demonstrate...
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 2
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-08-28
    Beschreibung: A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins. The different signals that converge on mitochondria to trigger or inhibit these events and their downstream effects delineate several major pathways in physiological cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, D R -- Reed, J C -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1309-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9721092" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Apoptosis ; Cysteine Endopeptidases/metabolism ; Cytochrome c Group/metabolism ; Electron Transport ; Humans ; Intracellular Membranes/metabolism ; Ion Channels/metabolism ; Membrane Potentials ; Mitochondria/*metabolism ; Oxidation-Reduction ; Permeability ; Proto-Oncogene Proteins c-bcl-2/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 3
    Publikationsdatum: 1997-02-21
    Beschreibung: In a cell-free apoptosis system, mitochondria spontaneously released cytochrome c, which activated DEVD-specific caspases, leading to fodrin cleavage and apoptotic nuclear morphology. Bcl-2 acted in situ on mitochondria to prevent the release of cytochrome c and thus caspase activation. During apoptosis in intact cells, cytochrome c translocation was similarly blocked by Bcl-2 but not by a caspase inhibitor, zVAD-fmk. In vitro, exogenous cytochrome c bypassed the inhibitory effect of Bcl-2. Cytochrome c release was unaccompanied by changes in mitochondrial membrane potential. Thus, Bcl-2 acts to inhibit cytochrome c translocation, thereby blocking caspase activation and the apoptotic process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kluck, R M -- Bossy-Wetzel, E -- Green, D R -- Newmeyer, D D -- CA69381/CA/NCI NIH HHS/ -- GM50284/GM/NIGMS NIH HHS/ -- GM52735/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1132-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027315" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; *Apoptosis ; Carrier Proteins/metabolism ; Cell Extracts ; Cell-Free System ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytochrome c Group/*metabolism ; Cytosol/metabolism ; Membrane Potentials ; Microfilament Proteins/metabolism ; Mitochondria/*metabolism ; Ovum ; Proto-Oncogene Proteins c-bcl-2/*metabolism/pharmacology ; Recombinant Proteins ; Xenopus
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 4
    facet.materialart.
    Unbekannt
    Nature Publishing Group (NPG)
    Publikationsdatum: 2010-05-28
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, Douglas R -- England -- Nature. 2010 May 27;465(7297):433. doi: 10.1038/465433a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20505719" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD95/deficiency/genetics/*metabolism ; Apoptosis ; Autocrine Communication ; Cell Proliferation ; Enzyme Activation ; Fas Ligand Protein/deficiency/metabolism ; Humans ; Inflammation/metabolism ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism ; Mice ; Neoplasms/*metabolism/*pathology ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 5
    facet.materialart.
    Unbekannt
    Nature Publishing Group (NPG)
    Publikationsdatum: 2008-10-25
    Beschreibung: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3242476/" 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/PMC3242476/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, Douglas R -- Chipuk, Jerry E -- F32 CA101444/CA/NCI NIH HHS/ -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI040646-14/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1047-9. doi: 10.1038/4551047a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948940" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/*metabolism ; BH3 Interacting Domain Death Agonist Protein/metabolism ; Membrane Proteins/*metabolism ; Mitochondrial Membranes/*metabolism ; Models, Molecular ; Permeability ; Protein Binding ; Proto-Oncogene Proteins/*metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 6
    Publikationsdatum: 2008-11-21
    Beschreibung: The Ca(2+)-dependent cysteine proteases, calpains, regulate cell migration, cell death, insulin secretion, synaptic function and muscle homeostasis. Their endogenous inhibitor, calpastatin, consists of four inhibitory repeats, each of which neutralizes an activated calpain with exquisite specificity and potency. Despite the physiological importance of this interaction, the structural basis of calpain inhibition by calpastatin is unknown. Here we report the 3.0 A structure of Ca(2+)-bound m-calpain in complex with the first calpastatin repeat, both from rat, revealing the mechanism of exclusive specificity. The structure highlights the complexity of calpain activation by Ca(2+), illustrating key residues in a peripheral domain that serve to stabilize the protease core on Ca(2+) binding. Fully activated calpain binds ten Ca(2+) atoms, resulting in several conformational changes allowing recognition by calpastatin. Calpain inhibition is mediated by the intimate contact with three critical regions of calpastatin. Two regions target the penta-EF-hand domains of calpain and the third occupies the substrate-binding cleft, projecting a loop around the active site thiol to evade proteolysis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847431/" 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/PMC2847431/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moldoveanu, Tudor -- Gehring, Kalle -- Green, Douglas R -- P01 CA069381/CA/NCI NIH HHS/ -- P01 CA069381-140010/CA/NCI NIH HHS/ -- P30 EB009998/EB/NIBIB NIH HHS/ -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI040646-14/AI/NIAID NIH HHS/ -- R01 AI044828/AI/NIAID NIH HHS/ -- R01 AI044828-12/AI/NIAID NIH HHS/ -- R01 AI047891/AI/NIAID NIH HHS/ -- R01 AI047891-12/AI/NIAID NIH HHS/ -- R37 GM052735/GM/NIGMS NIH HHS/ -- R37 GM052735-19/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Nov 20;456(7220):404-8. doi: 10.1038/nature07353.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, 332 N Lauderdale, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19020622" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biocatalysis ; Calcium/metabolism ; Calcium-Binding Proteins/*chemistry/genetics/*metabolism ; Calpain/antagonists & inhibitors/*chemistry/*metabolism ; *Catalytic Domain ; Crystallography, X-Ray ; EF Hand Motifs ; Enzyme Activation ; Protein Binding ; Protein Multimerization ; Protein Processing, Post-Translational ; Rats ; Structure-Activity Relationship ; Substrate Specificity
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 7
    Publikationsdatum: 2009-05-02
    Beschreibung: The principal tumour-suppressor protein, p53, accumulates in cells in response to DNA damage, oncogene activation and other stresses. It acts as a nuclear transcription factor that transactivates genes involved in apoptosis, cell cycle regulation and numerous other processes. An emerging area of research unravels additional activities of p53 in the cytoplasm, where it triggers apoptosis and inhibits autophagy. These previously unknown functions contribute to the mission of p53 as a tumour suppressor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2814168/" 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/PMC2814168/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, Douglas R -- Kroemer, Guido -- P01 CA069381/CA/NCI NIH HHS/ -- P01 CA069381-140010/CA/NCI NIH HHS/ -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI040646-14/AI/NIAID NIH HHS/ -- R01 AI044828/AI/NIAID NIH HHS/ -- R01 AI044828-12/AI/NIAID NIH HHS/ -- R01 AI047891/AI/NIAID NIH HHS/ -- R01 AI047891-11/AI/NIAID NIH HHS/ -- R37 GM052735/GM/NIGMS NIH HHS/ -- R37 GM052735-19/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Apr 30;458(7242):1127-30. doi: 10.1038/nature07986.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. douglas.green@stjude.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407794" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis ; Autophagy ; Cell Nucleus/metabolism ; Cytoplasm/*metabolism ; Humans ; Mitochondria/metabolism ; Neoplasms/metabolism/pathology ; Transcription, Genetic ; Tumor Suppressor Protein p53/genetics/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 8
    Publikationsdatum: 1992-07-10
    Beschreibung: Immature T cells and some T cell hybridomas undergo apoptotic cell death when activated through the T cell receptor complex, a phenomenon that is probably related to antigen induced negative selection of developing T cells. This activation-induced apoptosis depends on active protein and RNA synthesis in the dying cells, although none of the genes required for this process have previously been identified. Antisense oligonucleotides corresponding to c-myc block the constitutive expression of c-Myc protein in T cell hybridomas and interfere with all aspects of activation-induced apoptosis without affecting lymphokine production in these cells. These data indicate that c-myc expression is a necessary component of activation-induced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, Y -- Glynn, J M -- Guilbert, L J -- Cotter, T G -- Bissonnette, R P -- Green, D R -- AI31591/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):212-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Alberta, Edmonton, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1378649" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/physiology ; Base Sequence ; Blotting, Western ; Cell Death/drug effects/genetics ; Flow Cytometry ; Gene Expression/drug effects ; Genes, fos/physiology ; Genes, myc/*physiology ; Hybridomas ; Lymphocyte Activation/drug effects/*physiology ; Molecular Sequence Data ; Oligonucleotides, Antisense/genetics/pharmacology ; Proto-Oncogene Proteins c-myc/biosynthesis ; RNA/biosynthesis ; Receptors, Antigen, T-Cell/physiology ; T-Lymphocytes/*physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 9
    Publikationsdatum: 2008-04-19
    Beschreibung: Ocean acidification in response to rising atmospheric CO2 partial pressures is widely expected to reduce calcification by marine organisms. From the mid-Mesozoic, coccolithophores have been major calcium carbonate producers in the world's oceans, today accounting for about a third of the total marine CaCO3 production. Here, we present laboratory evidence that calcification and net primary production in the coccolithophore species Emiliania huxleyi are significantly increased by high CO2 partial pressures. Field evidence from the deep ocean is consistent with these laboratory conclusions, indicating that over the past 220 years there has been a 40% increase in average coccolith mass. Our findings show that coccolithophores are already responding and will probably continue to respond to rising atmospheric CO2 partial pressures, which has important implications for biogeochemical modeling of future oceans and climate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iglesias-Rodriguez, M Debora -- Halloran, Paul R -- Rickaby, Rosalind E M -- Hall, Ian R -- Colmenero-Hidalgo, Elena -- Gittins, John R -- Green, Darryl R H -- Tyrrell, Toby -- Gibbs, Samantha J -- von Dassow, Peter -- Rehm, Eric -- Armbrust, E Virginia -- Boessenkool, Karin P -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):336-40. doi: 10.1126/science.1154122.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Oceanography Centre, Southampton, University of Southampton Waterfront Campus, European Way, Southampton SO14 3ZH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18420926" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Atmosphere ; *Calcification, Physiologic ; Calcium Carbonate/analysis ; *Carbon Dioxide ; Eukaryota/growth & development/*physiology ; Geologic Sediments/chemistry ; Hydrogen-Ion Concentration ; Oceans and Seas ; Photosynthesis ; Phytoplankton/growth & development/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 10
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-12-31
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, D R -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1246-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA. dgreen5240@aol.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411752" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/*metabolism ; *Apoptosis ; Carrier Proteins/metabolism ; Caspase 1 ; Cysteine Endopeptidases/metabolism ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Genes, Tumor Suppressor ; Genes, myc ; Genes, p53 ; Membrane Glycoproteins/genetics/*metabolism ; Ornithine Decarboxylase/metabolism ; Proto-Oncogene Proteins c-myc/*metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...