Visit our Expo - Redox and Inflammation signaling 2012

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Session III : Protein kinase cascades as therapeutic targets Poster III, 1 Cyclic nucleotide-dependent inhibition of ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (E-NPP1) expression. I. Aerts1, P.P. De Deyn2and H. Slegers1 Department of Biomedical Sciences, Cellular Biochemistry1, Neurochemistry and behaviour2, University of Antwerp, Belgium Ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (E-NPP1) is a member of a multigen family which contains NPP1 (PC-1), NPP2 (autotaxine) and NPP3 (B10; gp130RB13-6). These are type II transmembrane metalloenzymes that hydrolyse ATP into AMP and PPi or lysophosphatidylcholine into lysophosphatidic acid. NPP1 is expressed in different tissues and abnormal expression is observed in several pathologies (1). Glioblastoma multiforme (GBM) is the most aggressive glioma with an expected lifespan of less than one year. Immunohistochemistry demonstrated that NPP1 expression is not detected in normal tissue while its expression increased with the gradation of glioma. NPP1 is highly expressed in reactive astrocytes of GBM. The rat C6 glioma cell line, an experimental ‘in vitro’ and ‘in vivo’ model system for GBM (2), is used for the study of the expression of NPP1. Cyclic AMP-dependent induction of differentiation resulted in inhibition of NPP1 expression. The use of specific PKA inhibitors indicated that this decrease in expression is PKA-dependent. Nitroprusside, a nitric oxide (NO) donor, inhibited the expression of NPP1 suggesting that NO may be involved in the latter mechanism. BAY 41-2272, a NO-independent activator of soluble guanylate cyclase (sGC), attenuated NPP1 expression. The presented data indicated that inhibition of NPP1 expression may be due to NO-induced activation of sGC. In addition dibutyryl cGMP, also attenuated the expression of NPP1, characterizing that NO/sGC/cGMP as elements of the signal transduction pathway that modulates the expression of NPP1. The signal transduction components of the NO-dependent pathway that effects NPP1 expression remain to be determined. The elucidation of the mechanism of NPP1 expression may lead to new medications or therapies for the treatment of patients with GBM. - 184 -
Session III : Protein kinase cascades as therapeutic targets Poster III, 2 Multiple roles of PI-3’ kinase / Akt signaling in human hepatoma cell proliferation and drug-induced apoptosis Catherine alexia 3, Marlène Bras 2, Guillaume Fallot 3, Nathalie Vadrot 3, Fanny Daniel 3, Malika Lasfer 3, Houda Tamouza 3 & André Groyer 1 1 Inserm U.683 and 3 Inserm U.481, Faculté de Médecine Xavier Bichat, 75870 Paris Cédex 18, France ; 2 Institut Pasteur, Département d'Immunologie, 75724 Paris Cedex 15, France. e-mail: groyer@bichat.inserm.fr IGF-II and type I-IGF receptor (IGF-IR) gene expression is increased in primary liver tumours and transgenic mice over-expressing IGF-II in the liver develop hepatocarcinoma (HCC) spontaneously, suggesting that alterations of IGF-IR signaling in vivo may play a role in the auto/paracrine control of hepatocarcinogenesis. We have addressed the contribution of PI-3’K/Akt signaling on the proliferation of HepG2 human hepatoma cells and on their protection against doxorubicin-induced apoptosis. Both basal HepG2 cell DNA replication and that stimulated by IGF-IR signaling were inhibited by the specific PI-3’K inhibitor Ly294002 (Ly). In the former case, PI-3’K signaling overcame cell cycle arrest in G1 via increased cyclin D1 protein and decreased p130Rb and p27kip1 gene expression. Doxorubicin treatment induced apoptosis in HepG2 cells and was concomitant with the proteolytic cleavage of Akt-1 and -2. Drug-induced apoptosis was reversed by IGF-I and was (i) dependent on Akt-1 and -2 phosphorylation and (ii) accompanied by the inhibition of initiator caspase-9 activity, suggesting that IGF-IR signaling interferes with mitochondria-dependent apoptosis. Accordingly, Ly enhanced doxorubicin-induced apoptosis and suppressed its reversal by IGF-I. Altogether, the data emphasize the crucial role of PI-3’K/Akt signaling (i) in basal as well as IGF-IR-stimulated HepG2 cell proliferation and (ii) in controlling both doxorubicin-induced apoptosis (e.g., drug-induced cleavage of Akt) and its reversal by IGF-I (protection against apoptosis parallels the extent of Akt phosphorylation). They suggest that targeting Akt activity or downstream Akt effectors (e.g. GSK3-beta, FOXO transcription factors) may help define novel therapeutic strategies of increased efficacy in the treatment of HCC-bearing patients. - 185 -
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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 II : Receptor signaling and
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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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Dr. Nassera Aouali L-1526 Luxembour
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Dr. Giordano Bianchi Clinic of inte
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Mrs. Isabel Burghardt Laboratory of
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Pr. Czeslaw Cierniewski 92-215 Lodz
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Mr. Igotz Delgado Biochemistry 4894
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Mrs. Anissa Fergani INSERM U-692 67
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Dr. Mark Ginsberg Mail code 0726 92
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Dr. Jochen Hefl Division of Signal
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Mr. Jan Jepsen 2100 Copenhagen DNK
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Pr. Young Min Kim Division of Biolo
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Mr. Christoph Lahtz AG Tumorgenetik
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Pr. Etta Livneh 84105 Beer Sheva IS
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Mrs. Rasa Merzvinskyte Department o
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Mr. Gustav Nilsonne Department of L
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Mrs. Christel Péqueux Tumour and D
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Dr. Gabriella Regis Tumor Immunolog
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Dr. Carsten Scheller 97078 Wuerzbur
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Mr. Yoo-Cheol Song Laboratory of Gy
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Pr. Moncef ZOUALI Centre Viggo Pete
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