Visit our Expo - Redox and Inflammation signaling 2012

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Session XVII : Cell signaling in health and disease Poster XVII, 55 PI3 kinase inhibition provides a novel mechanism for the action of valproic acid Xuehua Xu1, Helmut Kae2, Annette Müller-Taubenberger3, Kathryn Adley4, Nadine Pawolleck5, Vivian Lee6, Talvinder Sihra6, Claudia Wiedemann7, Gerry Weeks2, Jan Faix8, Markus Maniak5, Tian Jin1 and Robin S.B. Williams4 1. Chemotaxis Signal Sect, NIAID, Rockville, MD20852, USA. TJIN@niaid.nih.gov. 2. Microbiol. Immunol. UBC, Vancouver, V6T1Z3, Canada. weeks@ciml.univ-mrs.fr. 3. M-Plank Biochem, LRZ, Munich, 80336, Germany. amueller@lrz.uni-muenchen.de. 4. Dept Biol and WIBR, UCL, London, WC1E 6BT, UK. robin.williams@ucl.ac.uk. 5. Inst Cell Bio, University of Kasse, Kassel, 34132, Germany. maniak@uni-kassel.de. 6. Dept Pharmacol., UCL, London, WC1E6BT, UK. t.sihra@ucl.ac.uk. 7. Mol Cell Bio, UCL Med. School, NW32PF, UK. c.wiedemann@medsch.ucl.ac.uk. 8. Hanover Med School, Hanover, D-30623, Germany. hans@imap.bpc.mh-hannover.de. Valproic acid (VPA, 2 propyl pentanoic acid) is a short chain fatty acid that was accidentally found to be an effective treatment for epilepsy in 1962, and is now also used to treat bipolar disorder and migraine, and is undergoing trials for cancer therapy. Despite its wide use, the therapeutic targets of VPA are not clear. We have identified an effect of VPA in blocking chemotaxis, a process controlled by phosphoinositide 3-kinase (PI3K) signalling, using the social amoeba Dictyostelium discoideum. In this model, we show that VPA attenuates PI3K activity by inhibiting signal-induced PIP3 production, that both VPA and a PI3K inhibitor reverse the phenotype of activated Rac1A, reduce Ras activation and VPA also inhibits vesicle trafficking. These results suggest that VPA functions through the reduction of PIP3 production to modulate downstream effectors including small GTPases and vesicle release. To examine the therapeutic potential of this effect, we show that the human PI3Kgamma enzyme is weakly but directly inhibited by VPA and that both VPA and a PI3K inhibitor suppress depolarization-dependent neurotransmitter release in purified rat nerve terminals. These results thus suggest that VPA may function to reduce PI3K activity as a therapeutic mechanism for the treatment of epilepsy, bipolar disorder, migraine, and cancer. - 662 -
Session XVII : Cell signaling in health and disease Poster XVII, 56 Determination of oxidative stress status and concentration of TGF-B1 in the blood and saliva of osteoporotic patients 1Gholamreza Yousefzadeh, 1Bagher Larijani, 2Azadeh Mohammadirad, 1Ramin Heshmat, 2Roja Rahimi, and 2Mohammad Abdollahi 1Endocrinology and Metabolism Research Centre, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran Email: mohammad.abdollahi@utoronto.ca Introduction: The maintenance of bone mass is influenced by genetic, race, hormonal, mechanical and nutritional factors which modulate the local and systemic mechanisms regulating bone turnover. It seems that oxidative stress and interleukins particularly TGF-#1 also influences bone mass. Objectives: to determine if oxidative stress and TGF-#1 have any role in the bone mass density. Methods: Blood and saliva samples of twenty two osteoporotic patients were collected. TBARS and FRAP assay respectively were used to determine levels of lipid peroxidation and antioxidant status in these samples. The concentration of TGF-#1 antigen was measured by using the capture sandwich ELISA. Results: Total antioxidant power in blood and saliva of osteoporotic patients was lower (p
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- 1 - Luxembourg, January 25th to 2
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Table of content PREFACE ..........
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Preface In 1998, we organized the f
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Acknowledgments This meeting has be
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Group B (15h00 - 17h00) Session V.
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- 11 - Exhibition
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Visit our Expo (in alphabetical ord
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Thursday January 26th, 2006 (Early
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Thursday January 26th, 2006 (Evenin
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Regulation of inflammation and gluc
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Saturday January 28th, 2006 (Early
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Oral presentations (by alphabetical
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4: : Lottin S, Vercoutter-Edouart A
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the B-Raf/mitogen-activated/extrace
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Albertini MC, Accorsi A, Citterio B
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AP-1-dependent gene expression in s
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Jaks and cytokine receptors - an in
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The Role of Met-Gab1 Signalling in
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The mammalian tumor suppressor Scri
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SIGNAL TRANSDUCTION BY STRESS-ACTIV
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Title to be announced Caroline Dive
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Mechanisms of DNA methylation in ma
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Blocking the "4 Integrin-Paxillin I
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Regulation of NF-kB-dependent trans
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The immunomodulator AS101 induces g
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Signaling pathways leading to the a
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Boute, N., Jockers, R. and Issad, T
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Jespsen JS, Sorensen MD and Wengel
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8. Nishikawa, H., Kawai, K., Tanaka
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9) Proteome analysis of rat pancrea
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MicroRNA is an anti-apoptotic facto
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Resveratrol inhibits phorbol ester-
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Cross-talk between angiotensin II a
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Multiple role of histamine H 1 rece
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PI3K Targeting by the Beta-GBP Cyto
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D.P. Chopra, R.E. Menard, J. Janusz
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[2] Meijer, L., Flajolet, M. and Gr
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[4] Niemand, C., Nimmesgern, A., Ha
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Oncogenic signaling by mutant p53 M
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activity of the Peroxisome Prolifer
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Restauration of SHIP-1 activity in
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Hypoxia Signaling. Impact on Tumor
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5. Sokolov EI, Zykov KA, Pukhalsky
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HOW ANTITOXIC AND ANTICANCER AGENTS
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Listeria monocytogenes induced Rac1
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Epigenetic Regulation of Stem Cell
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Survey on in vitro cell death induc
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Distinct roles of IRF-3 and IRF-7 i
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Redox-Sensitive Transcription Facto
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Epigenic control of MHC2TA transcri
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Attenuation of MSK1-driven NF-kB ge
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Talking to chromatin: Silencers Sil
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Ubiquitin ligase Smurf1 controls os
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Workshop presentations (by alphabet
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Ambion MicroRNAs (miRNAs) are small
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Organizer: BIOBASE GmbH Date: Janua
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Reliable and efficient gene Knock-d
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Exploring ubiquitin signaling with
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Poster presentations Poster are cla
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Session I : protein domains Poster
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Session II. Receptor signaling and
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Session II : Receptor signaling and
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Session III. Protein kinase cascade
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Session III : Protein kinase cascad
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Session IV. Protein kinase inhibito
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IV. Protein kinase inhibitors: insi
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IV. Protein kinase inhibitors: insi
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V. Phosphatases as key cell signali
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VI. Proteasome degradation pathways
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VI. Proteasome degradation pathways
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Session VII. Stem cell specific cel
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VIII. Inflammation specific signali
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Session IX. Novel compounds targeti
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Session X : Cell death in cancer -
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Session X : Cell death in cancer Po
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Session XI : Cell death and cardiov
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Session XI: Cell death and cardiova
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Session XII : Cell death and neurod
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Session XIII : Cell signaling pathw
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Session XIV : Transcriptional and t
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Session XV : Reactive oxygen specie
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Session XVI : Chemopreventive agent
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Session XVII : Cell signaling in he
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Page 675 and 676: Dr. Nassera Aouali L-1526 Luxembour
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Pr. Moncef ZOUALI Centre Viggo Pete
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