Visit our Expo - Redox and Inflammation signaling 2012

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Session II : Receptor signaling and G proteins Poster II, 13 The tyrosine 974 within the LIF-R-chain of the gp130/LIF-R heteromeric receptor mediates negative regulation of LIF signalling Thomas Clahsen1, Ute Lehmann1, Claudia Stross1, Heike M. Hermanns1, Rudolf Volkmer-Engert2, Jens Schneider-Mergener2, Peter C. Heinrich1, Fred Schaper1 1 Department of Biochemistry, RWTH Aachen, Pauwelsstraße 30, D-52074 Aachen, Germany, E-mail: Thomas.Clahsen@post.rwth-aachen.de 2 Department of Medical Immunology, Universitätsklinikum Charité, Molecular Libraries and Recognition, Ziegelerstrasse 5-9, Berlin D-10117, Germany Signalling of interleukin-6 and interleukin-11 through gp130 homodimeric receptor complexes has been analysed with respect to initiation and termination of signalling in great detail. Gp130 contains a crucial motif around tyrosine Y759 which mediates negative regulation through the feedback inhibitor SOCS3 and the protein tyrosine phosphatase SHP2. Signalling of LIF, CNTF, CT-1, CLC or OSM through gp130/LIF-R is believed to be similar due to the presence of the common signal transducer gp130 within the receptor complexes utilized, but the difference in the composition of gp130/gp130-homodimers and gp130/LIF-Rheterodimers is likely to be reflected in different signalling. Here, we analysed the contribution of the LIF-R within the gp130/LIF-R complex to negative regulation mediated by SHP2 and SOCS3. We show that SHP2 contributes to the negative regulation of signalling through gp130/LIF-R complexes. The inhibitory tyrosine motifs within the cytoplasmic parts of gp130 and the LIF-R act independently. Whereas SHP2 and SOCS3 bind directly to the inhibitory motif of gp130, only SHP2 was found to bind to the corresponding inhibitory sequence of the LIF-R. This observation was further corroborated by experiments indicating that mainly gp130 contributes to the inhibition of signalling by SOCS3. - 140 -
Session II : Receptor signaling and G proteins Poster II, 14 Serotonin-induced inhibition of voltage-gated K+ currents and contraction in pulmonary arteries. Signalling via 5-HT(2A) receptors. Laura Cobeño, Angel Cogolludo, Laura Moreno, Giovanna Frazziano, Tizziana Russo, Juan Tamargo and Francisco Perez-Vizcaino. Department Pharmacology. School Medicine. Universidad Complutense de Madrid. 28040 Madrid. SPAIN. E-mail: acogolludo@ift.csic.es Multiple lines of evidence indicate that serotonin (5-HT) and voltage-gated potassium (Kv) channels independently play a central role in the pathogenesis of pulmonary hypertension (PH). We hypothesized that 5-HT might module the activity of Kv channels, therefore, establishing a link between these pathogenetic factors in PH. We studied the effects of 5-HT on Kv currents in rat pulmonary artery smooth muscle cells (PASMC) and on contractile force in isolated pulmonary arteries (PA). 5-HT reduced native Kv currents, depolarized PASMC and caused a contraction of PA. The 5-HT(2A) receptor antagonist ketanserin and the 5-HT(1B) receptor antagonist SB224289 inhibited 5-HT-induced contraction by 72 ± 4% and 22 ± 2%, respectively. The contraction induced by 5-HT was also attenuated by the 5-HT transporter (5-HTT) inhibitor fluoxetine, which also antagonizes 5-HT(2A) receptors, but not by other 5-HTT inhibitors such as fluvoxamine or citalopram. The inhibitory effects of 5-HT on Kv currents were prevented by ketanserin and fluoxetine, but not by any of the other drugs. Furthermore, ketanserin inhibited the depolarizing effect induced by 5-HT. 5-HT induced inhibition of Kv current was insensitive to the PKCzeta pseudosubstrate inhibitor. In contrast, inhibition of phospholipase C (PLC, U-73122), classic PKCs (Go-6976) or tyrosine kinases (genistein and tyrphostin 23) prevented the effects of 5-HT on Kv currents and contractions. Altogether these results indicate that 5-HT inhibits native Kv currents following the activation of 5-HT(2A) receptors via PLC, classic PKCs and tyrosine kinase. The inhibition of Kv channels contributes to 5-HT-induced pulmonary vasoconstriction and might play a role in PH. - 141 -
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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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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 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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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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