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  • 1
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    Mitochondria and the autophagy-inflammation-cell death axis in organismal aging (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Autophagy-dependent anticancer immune responses induced by chemotherapeutic agents in mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the release of adenosine triphosphate (ATP) from dying tumor cells. Conversely, inhibition of extracellular ATP-degrading enzymes increased pericellular ATP in autophagy-deficient tumors, reestablished the recruitment of immune cells, and restored chemotherapeutic responses but only in immunocompetent hosts. Thus, autophagy is essential for the immunogenic release of ATP from dying cells, and increased extracellular ATP concentrations improve the efficacy of antineoplastic chemotherapies when autophagy is disabled.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michaud, Mickael -- Martins, Isabelle -- Sukkurwala, Abdul Qader -- Adjemian, Sandy -- Ma, Yuting -- Pellegatti, Patrizia -- Shen, Shensi -- Kepp, Oliver -- Scoazec, Marie -- Mignot, Gregoire -- Rello-Varona, Santiago -- Tailler, Maximilien -- Menger, Laurie -- Vacchelli, Erika -- Galluzzi, Lorenzo -- Ghiringhelli, Francois -- di Virgilio, Francesco -- Zitvogel, Laurence -- Kroemer, Guido -- New York, N.Y. -- Science. 2011 Dec 16;334(6062):1573-7. doi: 10.1126/science.1208347.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, U848, Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174255" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Antineoplastic Agents/*pharmacology/therapeutic use ; Autophagy/drug effects/*physiology ; Calreticulin/pharmacology ; Cell Death/immunology ; Cell Line, Tumor ; Dendritic Cells/immunology ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mitoxantrone/pharmacology ; Neoplasms/drug therapy/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    An immunosurveillance mechanism controls cancer cell ploidy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-29
    Description: Cancer cells accommodate multiple genetic and epigenetic alterations that initially activate intrinsic (cell-autonomous) and extrinsic (immune-mediated) oncosuppressive mechanisms. Only once these barriers to oncogenesis have been overcome can malignant growth proceed unrestrained. Tetraploidization can contribute to oncogenesis because hyperploid cells are genomically unstable. We report that hyperploid cancer cells become immunogenic because of a constitutive endoplasmic reticulum stress response resulting in the aberrant cell surface exposure of calreticulin. Hyperploid, calreticulin-exposing cancer cells readily proliferated in immunodeficient mice and conserved their increased DNA content. In contrast, hyperploid cells injected into immunocompetent mice generated tumors only after a delay, and such tumors exhibited reduced DNA content, endoplasmic reticulum stress, and calreticulin exposure. Our results unveil an immunosurveillance system that imposes immunoselection against hyperploidy in carcinogen- and oncogene-induced cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Senovilla, Laura -- Vitale, Ilio -- Martins, Isabelle -- Tailler, Maximilien -- Pailleret, Claire -- Michaud, Mickael -- Galluzzi, Lorenzo -- Adjemian, Sandy -- Kepp, Oliver -- Niso-Santano, Mireia -- Shen, Shensi -- Marino, Guillermo -- Criollo, Alfredo -- Boileve, Alice -- Job, Bastien -- Ladoire, Sylvain -- Ghiringhelli, Francois -- Sistigu, Antonella -- Yamazaki, Takahiro -- Rello-Varona, Santiago -- Locher, Clara -- Poirier-Colame, Vichnou -- Talbot, Monique -- Valent, Alexander -- Berardinelli, Francesco -- Antoccia, Antonio -- Ciccosanti, Fabiola -- Fimia, Gian Maria -- Piacentini, Mauro -- Fueyo, Antonio -- Messina, Nicole L -- Li, Ming -- Chan, Christopher J -- Sigl, Verena -- Pourcher, Guillaume -- Ruckenstuhl, Christoph -- Carmona-Gutierrez, Didac -- Lazar, Vladimir -- Penninger, Josef M -- Madeo, Frank -- Lopez-Otin, Carlos -- Smyth, Mark J -- Zitvogel, Laurence -- Castedo, Maria -- Kroemer, Guido -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1678-84.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, U848, Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calreticulin/immunology ; Cell Line, Tumor ; Common Variable Immunodeficiency/genetics ; DNA, Neoplasm/analysis/genetics ; Endoplasmic Reticulum Stress/*immunology ; Eukaryotic Initiation Factor-2/metabolism ; Humans ; Immunocompetence ; *Immunologic Surveillance ; Mice ; Mice, Inbred BALB C ; Neoplasms/chemically induced/*genetics/*immunology ; Phosphorylation ; *Ploidies
    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)
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  • 4
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    Cell biology. Metabolic control of cell death (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-09-23
    Description: Beyond their contribution to basic metabolism, the major cellular organelles, in particular mitochondria, can determine whether cells respond to stress in an adaptive or suicidal manner. Thus, mitochondria can continuously adapt their shape to changing bioenergetic demands as they are subjected to quality control by autophagy, or they can undergo a lethal permeabilization process that initiates apoptosis. Along similar lines, multiple proteins involved in metabolic circuitries, including oxidative phosphorylation and transport of metabolites across membranes, may participate in the regulated or catastrophic dismantling of organelles. Many factors that were initially characterized as cell death regulators are now known to physically or functionally interact with metabolic enzymes. Thus, several metabolic cues regulate the propensity of cells to activate self-destructive programs, in part by acting on nutrient sensors. This suggests the existence of "metabolic checkpoints" that dictate cell fate in response to metabolic fluctuations. Here, we discuss recent insights into the intersection between metabolism and cell death regulation that have major implications for the comprehension and manipulation of unwarranted cell loss.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219413/" 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/PMC4219413/" 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 AI044828/AI/NIAID NIH HHS/ -- R01 AI047891/AI/NIAID NIH HHS/ -- R01 CA169291/CA/NCI NIH HHS/ -- R01 GM096208/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1250256. doi: 10.1126/science.1250256.〈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 kroemer@orange.fr. ; Equipe 11 labellisee par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, F-75006 Paris, France. Universite Paris Descartes/Paris V; Sorbonne Paris Cite; F-75005 Paris, France. INSERM, U1138, F-94805 Villejuif, France. ; Equipe 11 labellisee par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, F-75006 Paris, France. Universite Paris Descartes/Paris V; Sorbonne Paris Cite; F-75005 Paris, France. INSERM, U1138, F-94805 Villejuif, France. Metabolomics and Cell Biology Platforms, Gustave Roussy, F-94805 Villejuif, France. Pole de Biologie, Hopital Europeen Georges Pompidou, Assistance Publique-Hopitaux de Paris, F-75015 Paris, France. douglas.green@stjude.org kroemer@orange.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237106" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Acetyl Coenzyme A/metabolism ; Animals ; *Apoptosis ; *Autophagy ; *Energy Metabolism ; Humans ; *Metabolic Networks and Pathways ; Mitochondria/*metabolism ; Mitochondrial Membranes/metabolism ; Multiprotein Complexes/metabolism ; Permeability ; TOR Serine-Threonine Kinases/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)
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