Visit our Expo - Redox and Inflammation signaling 2012

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Session XIII : Cell signaling pathways leading to regulated chromatin modifications Poster XIII, 6 Combinatorial histone deacetylase inhibitors effect to the differentiation of human promyelocytic leukemia HL-60 cell Rasa Merzvinskyte1, Grazina Treigyte1, Jurate Savickiene1, Karl-Eric Magnusson2 and Ruta Navakauskiene1 1Department of Developmental Biology, Institute of Biochemistry, LT-08662 Vilnius, Lithuania. E-mail: rasa_merzvinskyte@yahoo.com grazina.treigyte@bchi.lt savickiene@bchi.lt ruta.navakauskiene@bchi.lt 2Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Linköping University, SE-581 85 Linköping, Sweden. E-mail: karma@imk.liu.se Recently, a novel strategy for the treatment of leukemias through the modulation of chromatin structure has been applied. In this study, we conducted an analysis of anti-leukemic efects of the histone deacetylase (HDAC) inhibitors, phenyl butyrate (PB) and vitamin B3, and in combination with the differentiation agent, retinoic acid (RA), on the promyelocytic leukemia cell line HL-60. We found that the HDACI combinations exert different effects on cell cycle arrest, differentiation and apoptosis. We also assessed the expression of the early granulocytic differentiation marker CD11b on the cells treated with different combination of HDACI and RA. The most promising treatment for differentiation therapy was defined using a 6-h pretreatment with phenyl butyrate and vitamin B3 before the combined exposition to RA with vitamin B3. This significantly accelerated and increased cell differentiation (up to 95%) during the 48-h treatment. The examined HDAC inhibitors, in combination with the differentiation agent caused rapid histone H3 and H4 modifications in HL-60 cells. The increased level of histone H4 acetylation was associated with the initiation and maturation stages of HL-60 cell differentiation. Our results suggest that the chromatin remodeling using HDAC inhibitors provides a rationale for the treatment of acute promyelocytic leukemia. - 494 -
Session XIII : Cell signaling pathways leading to regulated chromatin modifications Poster XIII, 7 Histone acetylation-targeted differential responses of leukemia cells HL-60 and NB4 to histone deacetylase inhibitor FK228 Jurate Savickiene1, Grazina Treigyte1, Ruta Navakauskiene1 and Karl-Eric Magnusson2 1Department of Developmental Biology, Institute of Biochemistry, LT-2600 Vilnius, Lithuania. E-mail: grazina.treigyte@bchi.lt savickiene@bchi.lt ruta.navakauskiene@bchi.lt 2Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Linköping University, SE-58185 Linköping, Sweden. E-mail: karma@imk.liu.se The histone deacetylase inhibitor (HDACI), depsipeptide (FK228), was shown previously as a chemopreventive agent for the treatment of adult T-cell lymphomas. In this report, we investigated the in vitro antileukemic activity of FK228 alone, and in combination with alltrans retinoic acid (RA), on the human leukemia cell lines, NB4 and HL-60. The results show that FK228 induced a dose-dependent (0.2-1 ng/ml) cell growth arrest and death by apoptosis in NB4 and HL-60. The combined treatment with RA accelerated and enhanced granulocytic differentiation in both cell lines distinctly; the 6 h - pretreatment with HDACI had an additive differentiating effect in HL-60 cells only. These effects were accompanied by a time- and dose-dependent histone H4 hyper-acetylation and histone H3 dephosphorylation, occuring after 2-8 h exposure to HDACI. FK228 up-regulated NF-!B binding to the FasL promoter, and in combination with RA it altered the DNA binding of NF-!B linking the findings to cell death and differentiation. Pifithrin-" (PFT), an inhibitor of p53 transcriptional activity, protected from apoptosis only in NB4 cells with functional p53, i.e. when used 4 h before treatment with FK228 only or together with HDACI. In NB4 cells, PFT inhibited p53 binding to the p21 (Waf1/Cip1) promoter and induced DNA binding of NF-!B leading to enhanced cell survival. Thus, FK228 may be a promising antileukemic agent in combination with RA, since it exerts antiproliferative, differentiating and apoptotic effects in leukemia cells without and with functional p53, acting via histone modifications and selective involvement of transcription factors, like NF-!B and p53. - 495 -
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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 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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Dr. Jochen Hefl Division of Signal
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Mr. Jan Jepsen 2100 Copenhagen DNK
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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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