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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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    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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  • 4
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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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  • 5
    Electronic Resource
    Electronic Resource
    Different regulatory pathways involved in ATP-stimulated chloride secretion in rat epididymal epithelium (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 164 (1995), S. 271-276 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The regulatory pathways involved in the ATP-stimulated CI- secretion across rat epididymal epithelium were investigated by the short-circuit current (ISC) technique. Biphasic characteristic was observed in the ISC responded to ATP (0.01-10 m̈M). Inhibitor of P1 receptor, 8-phenyltheophylline (up to 100 m̈M), did not have any effect on both phases of the ATP-stimulated ISC. The order of potency for stimulation of the two phases in ISC was ATP〉ADP〉 AMP, adenosine, consistent with the presence of P2-purinoceptors. CI- channel blocker, disulfonic acid stilbene (DIDS, 300 m̈M), only inhibited the first peak of the ATP-stimulated ISC while diphenylamine-dicarboxylic acid (DPC, 1 mM) reduced both, indicating the involvement of different conductance pathways. DIDS was found to have an inhibitory effect on Ca2+-activated ISC (induced by ionomycin, 10 m̈M) but not cAMP-activated ISC (induced by forskolin, 1 m̈M) which could only be blocked by DPC. Both peaks of the ATP-activated ISC could be significantly inhibited by pretreatment with a Ca2+-chelating agent, BAPTA-AM (50 m̈M). An increase in cellular cAMP content upon stimulation of ATP was measured by radioimmunoassay. No significant increase in cAMP production was observed in cells stimulated with adenosine. The ATP-induced cAMP increase was prevented by pretreatment with BAPTA-AM (100 m̈M) indicating that cAMP production upon ATP stimulation was secondary to an increase in intracellular Ca2+ concentration. These results indicate that the ATP-stimulated CI- secretion could be mediated by Ca2+ and cAMP-dependent regulatory pathways giving rise to the biphasic nature of the ATP-induced ISC. © 1995 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041640207
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  • 6
    Electronic Resource
    Electronic Resource
    Homogeneous embedding for orientated monolayer cell cultures (1991)
    New York, NY : Wiley-Blackwell
    Journal of Electron Microscopy Technique 19 (1991), S. 271-272 
    Details
    ISSN: 0741-0581
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Natural Sciences in General
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jemt.1060190212
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