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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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    Activity patterns of human skeletal muscles: relation to muscle fiber type composition (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-04-21
    Description: The muscle activity of normal ambulatory individuals was recorded continuously for 8-hour (working day) periods. Parameters of activity patterns were defined and numerical outcomes for these parameters were compared across a diverse population of muscles. Several pattern parameters, such as the average percentage of time active, were highly correlated with the percentage of type I fibers of a muscle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monster, A W -- Chan, H -- O'Connor, D -- New York, N.Y. -- Science. 1978 Apr 21;200(4339):314-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/635587" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Electromyography ; Humans ; Male ; *Muscle Contraction ; Muscles/anatomy & histology/*physiology ; Time Factors
    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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