ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
  • 1
    Publication Date: 1997-02-21
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-12-31
    Description: 〈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〉
    Keywords: *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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2008-04-19
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    facet.materialart.
    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2008-10-25
    Description: 〈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〉
    Keywords: 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
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2009-05-02
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2014-02-28
    Description: Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments and regulate many cellular processes(1),(2). Recently Narayan et al., reported that SIRT2 was required for necroptosis based on their findings that SIRT2 inhibition, knock-down or knock-out prevented necroptosis. We sought to confirm and explore the role of SIRT2 in necroptosis and tested four different sources of the SIRT2 inhibitor AGK2, three independent siRNAs against SIRT2, and cells from two independently generated Sirt2-/- mouse strains, however we were unable to show that inhibiting or depleting SIRT2 protected cells from necroptosis. Furthermore, Sirt2-/- mice succumbed to TNF induced Systemic Inflammatory Response Syndrome (SIRS) more rapidly than wild type mice while Ripk3-/- mice were resistant. Our results therefore question the importance of SIRT2 in the necroptosis cell death pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005920/" 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/PMC4005920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newton, Kim -- Hildebrand, Joanne M -- Shen, Zhirong -- Rodriguez, Diego -- Alvarez-Diaz, Silvia -- Petersen, Sean -- Shah, Saumil -- Dugger, Debra L -- Huang, Chunzi -- Auwerx, Johan -- Vandenabeele, Peter -- Green, Douglas R -- Ashkenazi, Avi -- Dixit, Vishva M -- Kaiser, William J -- Strasser, Andreas -- Degterev, Alexei -- Silke, John -- P30 CA021765/CA/NCI NIH HHS/ -- R01 AI044828/AI/NIAID NIH HHS/ -- R01 CA169291/CA/NCI NIH HHS/ -- England -- Nature. 2014 Feb 27;506(7489):E4-6. doi: 10.1038/nature13024.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, Inc., South San Francisco, California 94080, USA. ; 1] The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria 3050, Australia. ; National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China. ; Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Biochemistry, Tufts University, Boston, Massachusetts 02111, USA. ; Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA. ; Laboratory of Integrative and Systems Physiology, EPFL, CH-1015 Lausanne, Switzerland. ; 1] Molecular Signaling and Cell Death Unit, Inflammation Research Center, VIB, 9052 Gent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, 9052 Gent, Belgium [3] Methusalem BOF09/01M00709, Ghent University, 9052 Gent, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24572428" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Humans ; Male ; Necrosis/*enzymology ; Sirtuin 2/*genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 7
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2004-08-03
    Description: In the mitochondrial pathway of apoptosis, caspase activation is closely linked to mitochondrial outer membrane permeabilization (MOMP). Numerous pro-apoptotic signal-transducing molecules and pathological stimuli converge on mitochondria to induce MOMP. The local regulation and execution of MOMP involve proteins from the Bcl-2 family, mitochondrial lipids, proteins that regulate bioenergetic metabolite flux, and putative components of the permeability transition pore. MOMP is lethal because it results in the release of caspase-activating molecules and caspase-independent death effectors, metabolic failure in the mitochondria, or both. Drugs designed to suppress excessive MOMP may avoid pathological cell death, and the therapeutic induction of MOMP may restore apoptosis in cancer cells in which it is disabled. The general rules governing the pathophysiology of MOMP and controversial issues regarding its regulation are discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, Douglas R -- Kroemer, Guido -- New York, N.Y. -- Science. 2004 Jul 30;305(5684):626-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA. doug@liai.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15286356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Disease/*etiology ; Humans ; Intracellular Membranes/*physiology ; Mitochondria/*physiology ; Models, Biological ; Neoplasms/physiopathology ; Permeability ; Proteins/*metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Signal Transduction ; Viral Proteins/metabolism ; Virus Physiological Phenomena
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 2005-09-10
    Description: The Trp53 tumor suppressor gene product (p53) functions in the nucleus to regulate proapoptotic genes, whereas cytoplasmic p53 directly activates proapoptotic Bcl-2 proteins to permeabilize mitochondria and initiate apoptosis. Here, we demonstrate that a tripartite nexus between Bcl-xL, cytoplasmic p53, and PUMA coordinates these distinct p53 functions. After genotoxic stress, Bcl-xL sequestered cytoplasmic p53. Nuclear p53 caused expression of PUMA, which then displaced p53 from Bcl-xL, allowing p53 to induce mitochondrial permeabilization. Mutant Bcl-xL that bound p53, but not PUMA, rendered cells resistant to p53-induced apoptosis irrespective of PUMA expression. Thus, PUMA couples the nuclear and cytoplasmic proapoptotic functions of p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chipuk, Jerry E -- Bouchier-Hayes, Lisa -- Kuwana, Tomomi -- Newmeyer, Donald D -- Green, Douglas R -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular Immunology, 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/16151013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Line, Tumor ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cytoplasm/*metabolism ; DNA Damage ; Gene Expression Regulation ; Humans ; Immunoprecipitation ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Models, Biological ; Permeability ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins/chemistry/*metabolism ; Ultraviolet Rays ; bcl-2-Associated X Protein ; bcl-X Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 9
    Publication Date: 2011-08-27
    Description: Alterations of mitochondrial functions are linked to multiple degenerative or acute diseases. As mitochondria age in our cells, they become progressively inefficient and potentially toxic, and acute damage can trigger the permeabilization of mitochondrial membranes to initiate apoptosis or necrosis. Moreover, mitochondria have an important role in pro-inflammatory signaling. Autophagic turnover of cellular constituents, be it general or specific for mitochondria (mitophagy), eliminates dysfunctional or damaged mitochondria, thus counteracting degeneration, dampening inflammation, and preventing unwarranted cell loss. Decreased expression of genes that regulate autophagy or mitophagy can cause degenerative diseases in which deficient quality control results in inflammation and the death of cell populations. Thus, a combination of mitochondrial dysfunction and insufficient autophagy may contribute to multiple aging-associated pathologies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3405151/" 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/PMC3405151/" 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 -- Galluzzi, Lorenzo -- Kroemer, Guido -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI047891/AI/NIAID NIH HHS/ -- R01 GM096208/GM/NIGMS NIH HHS/ -- R37 GM052735/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1109-12. doi: 10.1126/science.1201940.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. douglas.green@stjude.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21868666" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Apoptosis ; *Autophagy ; Cell Aging ; *Cell Death ; Humans ; Inflammation/*physiopathology ; Mitochondria/*physiology ; Necrosis ; Neurodegenerative Diseases/physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 10
    facet.materialart.
    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2010-05-28
    Description: 〈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〉
    Keywords: 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
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...