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  • 1
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    Skp2 targeting suppresses tumorigenesis by Arf-p53-independent cellular senescence (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-20
    Description: Cellular senescence has been recently shown to have an important role in opposing tumour initiation and promotion. Senescence induced by oncogenes or by loss of tumour suppressor genes is thought to critically depend on induction of the p19(Arf)-p53 pathway. The Skp2 E3-ubiquitin ligase can act as a proto-oncogene and its aberrant overexpression is frequently observed in human cancers. Here we show that although Skp2 inactivation on its own does not induce cellular senescence, aberrant proto-oncogenic signals as well as inactivation of tumour suppressor genes do trigger a potent, tumour-suppressive senescence response in mice and cells devoid of Skp2. Notably, Skp2 inactivation and oncogenic-stress-driven senescence neither elicit activation of the p19(Arf)-p53 pathway nor DNA damage, but instead depend on Atf4, p27 and p21. We further demonstrate that genetic Skp2 inactivation evokes cellular senescence even in oncogenic conditions in which the p19(Arf)-p53 response is impaired, whereas a Skp2-SCF complex inhibitor can trigger cellular senescence in p53/Pten-deficient cells and tumour regression in preclinical studies. Our findings therefore provide proof-of-principle evidence that pharmacological inhibition of Skp2 may represent a general approach for cancer prevention and therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928066/" 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/PMC2928066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Hui-Kuan -- Chen, Zhenbang -- Wang, Guocan -- Nardella, Caterina -- Lee, Szu-Wei -- Chan, Chia-Hsin -- Yang, Wei-Lei -- Wang, Jing -- Egia, Ainara -- Nakayama, Keiichi I -- Cordon-Cardo, Carlos -- Teruya-Feldstein, Julie -- Pandolfi, Pier Paolo -- R01 CA082328/CA/NCI NIH HHS/ -- R01 CA082328-13/CA/NCI NIH HHS/ -- R01 MD004038/MD/NIMHD NIH HHS/ -- England -- Nature. 2010 Mar 18;464(7287):374-9. doi: 10.1038/nature08815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237562" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 4/metabolism ; Adenovirus E1A Proteins/genetics/metabolism ; Animals ; *Cell Aging/drug effects ; *Cell Transformation, Neoplastic/drug effects ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Fibroblasts ; Male ; Mice ; PTEN Phosphohydrolase/deficiency/genetics/metabolism ; Prostate/cytology/metabolism ; Prostatic Neoplasms/drug therapy/pathology/prevention & control ; Proto-Oncogene Proteins p21(ras)/genetics/metabolism ; S-Phase Kinase-Associated Proteins/antagonists & inhibitors/genetics/*metabolism ; SKP Cullin F-Box Protein Ligases/metabolism ; Tumor Suppressor Protein p53/deficiency/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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  • 2
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    TLR recognition of self nucleic acids hampers glucocorticoid activity in lupus (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-19
    Description: Glucocorticoids are widely used to treat patients with autoimmune diseases such as systemic lupus erythematosus (SLE). However, regimens used to treat many such conditions cannot maintain disease control in the majority of SLE patients and more aggressive approaches such as high-dose methylprednisolone pulse therapy are used to provide transient reductions in disease activity. The primary anti-inflammatory mechanism of glucocorticoids is thought to be NF-kappaB inhibition. Recognition of self nucleic acids by toll-like receptors TLR7 and TLR9 on B cells and plasmacytoid dendritic cells (PDCs) is an important step in the pathogenesis of SLE, promoting anti-nuclear antibodies and the production of type I interferon (IFN), both correlated with the severity of disease. Following their activation by self-nucleic acid-associated immune complexes, PDCs migrate to the tissues. We demonstrate, in vitro and in vivo, that stimulation of PDCs through TLR7 and 9 can account for the reduced activity of glucocorticoids to inhibit the IFN pathway in SLE patients and in two lupus-prone mouse strains. The triggering of PDCs through TLR7 and 9 by nucleic acid-containing immune complexes or by synthetic ligands activates the NF-kappaB pathway essential for PDC survival. Glucocorticoids do not affect NF-kappaB activation in PDCs, preventing glucocorticoid induction of PDC death and the consequent reduction of systemic IFN-alpha levels. These findings unveil a new role for self nucleic acid recognition by TLRs and indicate that inhibitors of TLR7 and 9 signalling could prove to be effective corticosteroid-sparing drugs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964153/" 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/PMC2964153/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guiducci, Cristiana -- Gong, Mei -- Xu, Zhaohui -- Gill, Michelle -- Chaussabel, Damien -- Meeker, Thea -- Chan, Jean H -- Wright, Tracey -- Punaro, Marilynn -- Bolland, Silvia -- Soumelis, Vassili -- Banchereau, Jacques -- Coffman, Robert L -- Pascual, Virginia -- Barrat, Franck J -- 2R44AI066483-02/AI/NIAID NIH HHS/ -- P50 AR054083/AR/NIAMS NIH HHS/ -- P50 AR054083-01/AR/NIAMS NIH HHS/ -- P50 AR054083-010001/AR/NIAMS NIH HHS/ -- P50 AR054083-010002/AR/NIAMS NIH HHS/ -- P50 AR054083-019001/AR/NIAMS NIH HHS/ -- P50 AR054083-02/AR/NIAMS NIH HHS/ -- P50 AR054083-020001/AR/NIAMS NIH HHS/ -- P50 AR054083-020002/AR/NIAMS NIH HHS/ -- P50 AR054083-029001/AR/NIAMS NIH HHS/ -- P50 AR054083-03/AR/NIAMS NIH HHS/ -- P50 AR054083-030001/AR/NIAMS NIH HHS/ -- P50 AR054083-030002/AR/NIAMS NIH HHS/ -- P50 AR054083-04/AR/NIAMS NIH HHS/ -- P50 AR054083-040001/AR/NIAMS NIH HHS/ -- P50 AR054083-040002/AR/NIAMS NIH HHS/ -- P50 AR054083-04S1/AR/NIAMS NIH HHS/ -- P50 AR054083-05/AR/NIAMS NIH HHS/ -- P50 AR054083-050001/AR/NIAMS NIH HHS/ -- P50 AR054083-050002/AR/NIAMS NIH HHS/ -- P50-ARO54083-01CORT/PHS HHS/ -- R44 AI066483/AI/NIAID NIH HHS/ -- R44 AI066483-02/AI/NIAID NIH HHS/ -- U19 AI082715/AI/NIAID NIH HHS/ -- U19 AI082715-01/AI/NIAID NIH HHS/ -- U19 AI082715-017348/AI/NIAID NIH HHS/ -- U19 AI082715-017351/AI/NIAID NIH HHS/ -- U19 AI082715-02/AI/NIAID NIH HHS/ -- U19 AI082715-027348/AI/NIAID NIH HHS/ -- U19 AI082715-027351/AI/NIAID NIH HHS/ -- U19 AI082715-03/AI/NIAID NIH HHS/ -- U19-AI082715-01/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Jun 17;465(7300):937-41. doi: 10.1038/nature09102.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dynavax Technologies Corporation, 2929 Seventh Street, Suite 100, Berkeley, California 94710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20559388" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Autoantibodies/immunology ; Cell Survival/drug effects ; Cells, Cultured ; Child ; Dendritic Cells/*drug effects ; Disease Models, Animal ; Female ; Glucocorticoids/*pharmacology ; Humans ; Interferon-alpha/immunology ; Interferons/immunology ; Lupus Erythematosus, Systemic/*physiopathology ; Male ; Membrane Glycoproteins/immunology ; Mice ; Mice, Inbred C57BL ; NF-kappa B/immunology ; Nucleic Acids/*immunology ; Toll-Like Receptor 7/*immunology ; Toll-Like Receptor 9/*immunology ; Up-Regulation
    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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  • 3
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    How cells know the size of their organelles (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: Cells have developed ways to sense and control the size of their organelles. Size-sensing mechanisms range from direct measurements provided by dedicated reporters to indirect functional readouts, and they are used to modify organelle size under both normal and stress conditions. Organelle size can also be controlled in the absence of an identifiable size sensor. Studies on flagella have dissected principles of size sensing and control, and it will be exciting to see how these principles apply to other organelles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625396/" 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/PMC3625396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, Yee-Hung M -- Marshall, Wallace F -- 1F32GM090442-01A1/GM/NIGMS NIH HHS/ -- P50 GM081879/GM/NIGMS NIH HHS/ -- P50GM081879/GM/NIGMS NIH HHS/ -- R01 GM097017/GM/NIGMS NIH HHS/ -- R01GM097017/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 7;337(6099):1186-9. doi: 10.1126/science.1223539.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, UCSF Center for Systems and Synthetic Biology, University of California, San Francisco, San Francisco, CA 94158, USA. yhmchan@ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22955827" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; *Cell Physiological Phenomena ; Flagella/metabolism/physiology/ultrastructure ; Humans ; Models, Biological ; *Organelle Size ; *Organelles/chemistry/metabolism/ultrastructure
    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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    Fungal pathogen reduces potential for malaria transmission (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-11
    Description: Using a rodent malaria model, we found that exposure to surfaces treated with fungal entomopathogens following an infectious blood meal reduced the number of mosquitoes able to transmit malaria by a factor of about 80. Fungal infection, achieved through contact with both solid surfaces and netting for durations well within the typical post-feed resting periods, was sufficient to cause 〉90% mortality. Daily mortality rates escalated dramatically around the time of sporozoite maturation, and infected mosquitoes showed reduced propensity to blood feed. Residual sprays of fungal biopesticides might replace or supplement chemical insecticides for malaria control, particularly in areas of high insecticide resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blanford, Simon -- Chan, Brian H K -- Jenkins, Nina -- Sim, Derek -- Turner, Ruth J -- Read, Andrew F -- Thomas, Matt B -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1638-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institutes of Evolution, Immunology, and Infection Research, School of Biological Sciences, Ashworth Laboratories, University of Edinburgh, Edinburgh EH9 3JT Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15947189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/*microbiology/*parasitology/physiology ; Blood ; Feeding Behavior ; *Hypocreales/pathogenicity/physiology ; Insect Vectors/microbiology/parasitology/physiology ; Malaria/parasitology/prevention & control/*transmission ; Mice ; *Mitosporic Fungi/pathogenicity/physiology ; *Pest Control, Biological ; Plasmodium chabaudi/*growth & development/physiology ; Spores, Fungal ; Virulence
    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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  • 5
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    The E3 ligase TRAF6 regulates Akt ubiquitination and activation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-29
    Description: Akt signaling plays a central role in many biological functions, such as cell proliferation and apoptosis. Because Akt (also known as protein kinase B) resides primarily in the cytosol, it is not known how these signaling molecules are recruited to the plasma membrane and subsequently activated by growth factor stimuli. We found that the protein kinase Akt undergoes lysine-63 chain ubiquitination, which is important for Akt membrane localization and phosphorylation. TRAF6 was found to be a direct E3 ligase for Akt and was essential for Akt ubiquitination, membrane recruitment, and phosphorylation upon growth-factor stimulation. The human cancer-associated Akt mutant displayed an increase in Akt ubiquitination, in turn contributing to the enhancement of Akt membrane localization and phosphorylation. Thus, Akt ubiquitination is an important step for oncogenic Akt activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008763/" 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/PMC3008763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Wei-Lei -- Wang, Jing -- Chan, Chia-Hsin -- Lee, Szu-Wei -- Campos, Alejandro D -- Lamothe, Betty -- Hur, Lana -- Grabiner, Brian C -- Lin, Xin -- Darnay, Bryant G -- Lin, Hui-Kuan -- R01 CA149321/CA/NCI NIH HHS/ -- R01 CA149321-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 28;325(5944):1134-8. doi: 10.1126/science.1175065.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713527" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Apoptosis ; Cell Line ; Cell Line, Tumor ; Cell Membrane/*metabolism ; Humans ; Insulin-Like Growth Factor I/pharmacology ; Interleukin-1beta/pharmacology ; Lipopolysaccharides/pharmacology ; Mice ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/chemistry/*metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 6/genetics/*metabolism ; Transplantation, Heterologous ; Ubiquitin-Protein Ligases/*metabolism ; Ubiquitination
    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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  • 6
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    Brain edema: induction in cortical slices by polyunsaturated fatty acids (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-07-28
    Description: The presence of polyunsaturated and saturated fatty acids in leukocytic membranes prompted study of their possible role in the induction of brain edema. Polyunsaturated fatty acids including sodium arachidonate, sodium linoleate, sodium linolenate, and docasahexaenoic acids induced edma in slices of rat brain cortex. This cellular edema was specific, since neither saturated fatty acids nor a fatty acid containing a single double bond had such effect.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, P H -- Fishman, R A -- New York, N.Y. -- Science. 1978 Jul 28;201(4353):358-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/663662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acids ; Brain Edema/*chemically induced ; Cerebral Cortex ; Detergents ; Dose-Response Relationship, Drug ; *Fatty Acids, Unsaturated ; Granulocytes/physiology ; Hydroxy Acids ; In Vitro Techniques ; Prostaglandins ; Rats ; Sodium Dodecyl Sulfate ; Water-Electrolyte Imbalance/chemically induced
    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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