Visit our Expo - Redox and Inflammation signaling 2012

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Session II : Receptor signaling and G proteins Poster II, 35 Involvement of Kv1.5 channel endocytosis in serotonin-induced inhibition of voltagegated K+ currents and contraction in pulmonary arteries. Laura Moreno, Angel Cogolludo, Laura Cobeño, Federica Lodi, Giovanna Frazziano, Juan Tamargo, and Francisco Perez-Vizcaino. Department Pharmacology. School Medicine. Universidad Complutense de Madrid. 28040 Madrid. SPAIN. E-mail: lmoreno@ift.csic.es Serotonin (5-HT) and voltage-gated K+ (Kv) channels play a central role in the pathogenesis of pulmonary hypertension (PH). We showed (abstract, this meeting) that 5-HT inhibits Kv channels in rat pulmonary artery smooth muscle cells (PASMC) establishing a link between these pathogenetic factors in PH. These effects were mediated by activation of 5-HT(2A) receptors via PLC, classic PKC and tyrosine kinase. Herein we analyzed whether 5-HT inhibited human Kv1.5 channels stably expressed in Ltk- and the possible role of Kv1.5 endocytosis in native PASMC. 5-HT reduced Kv1.5 currents and this effect was prevented by the 5-HT(2A) receptor antagonist ketanserin and by the tyrosine kinase inhibitor tyrphostin 23. However, we did not find changes in the Kv1.5 protein phosphorylation in tyrosine residues using an anti-phosphotyrosine antibody in Kv1.5 immunoprecipitates after treatment with 5-HT. Inhibition of caveolar disruption (#-cyclodextrin) or inhibition of endocytotic processes (concanavalin A), prevented the inhibitory effects of 5-HT on Kv currents in native PASMC. Concanavalin A also inhibited the vasoconstrictor effect of 5-HT in isolated rat pulmonary arteries. In homogenates from pulmonary arteries, 5-HT(2A) receptors and caveolin-1 co-immunoprecipitated with Kv1.5 channels and this was increased upon stimulation with 5-HT. Moreover, confocal microscopy revealed that Kv1.5 channels were internalized when PASMC were stimulated with 5-HT. In conclusion, activation of 5-HT(2A) receptors inhibits rat native Kv currents as well as cloned human Kv1.5 currents. 5-HTinduced inhibition of Kv currents and the subsequent vasoconstriction of PA result from the interaction of 5-HT(2A) receptors with Kv1.5 channels within caveolar membrane microdomains and involve tyrosine phosphorylation and endocytotic processes. - 162 -
Session II : Receptor signaling and G proteins Poster II, 36 CLA/PUFA and Deoxycholic Acid (DCA)-Induced Signaling in Colorectal Cancer via the Insulin-Like Growth Factor 1 Receptor (IGF-1R). Sherif S Morgan, Shawna Comer, and Emmanuelle J Meuillet. The Cancer Biology Graduate Interdisciplinary Program, Nutritional Sciences Department, and Molecular and Cellular Biology Department. University of Arizona, Tucson, Arizona 85721 Colorectal cancer is the second leading cause of cancer-related deaths in the US. Clinical studies have shown that colorectal cancer patients have higher levels of bile acids (BA) in colonic lumen, and animal studies substantiate the role of BA as tumor promoters. The molecular mechanism of deoxycholic acid (DCA), which is a hydrophobic cholesterol derivative remains unclear. Recently, DCA has been shown to perturb the plasma membrane, which leads to EGFR activation. We sought to investigate a link between the presence of DCA and IGF-IR activity in colorectal cancer cells. Conjugated linoleic acid (CLA) and n-3 polyunsaturated fatty acids (PUFA) have been shown to have anti-tumorigenic effects. We hypothesize that DCA can perturb the plasma membrane, leading to the activation of the IGF- IR and its downstream signaling pathways, promoting survival and proliferation of colorectal cancer cells. Conversely, nutritional modulation by increasing intake of PUFA/CLA may counteract these effects by restoring normal IGF-IR signaling. We show that treatment with DCA leads to activation of IGF-IR and ERK-1/2 through the MEK-1 pathway. Counterintuitively, DCA does not activate AKT; in fact, it counteracts the IGF-induced AKT activation. DCA appears to preferentially activate ERK, while inhibiting AKT. Treatment with CLA, on the other hand, activates both ERK and AKT. Further studies are required to identify the functional role of activating these pathways, because they may lead to different cellular responses. These results support the role of DCA as a tumor promoter and sheds light on the potential mechanisms of CLA chemoprevention. These data have important implications since they support the significant role of nutrition in the prevention and treatment of colorectal cancer. - 163 -
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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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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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Mrs. Jessica Wagener 40225 Duesseld
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Pr. Moncef ZOUALI Centre Viggo Pete
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