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60 Prof. Dr. Christophe Erneux I.R.I.B.H.N., Free University of Brussels, Campus Erasme, Bldg. C, 808, route de Lennik, B-1070 Brussels, Belgium Phone: +32.2.555.41.62 - Fax: +32.2.555.46.55 - e-mail: cerneux@ulb.ac.be Collaborations with: Isabelle Pirson and Valérie Dewaste
The metabolism of inositol phosphates and phosphoinositides in neuronal cells The metabolism of inositol phosphates and phosphoinositides is particularly important in brain and is implicated in various signaling cascades involving inositol trisphosphate, inositol tetrakisphosphate and phosphatidylinositol trisphosphate. Those molecules are second messengers in various cell events such as cell proliferation, apoptosis or Ca 2+ dependent control mechanisms and Ca 2+ itself. They are controlled by various members of the inositol 5-phosphatase family and 3-kinase family (Erneux et al., 1998). Cloning a cDNA encoding human inositol trisphosphate isoenzyme C (Dewaste et al., 2000) Inositol 1,4,5-trisphosphate (Ins(1,4,5)P 3) 3-kinases are enzymes which catalyse the phosphorylation of Ins(1,4,5)P 3 to inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P 4), both potential modulators of calcium homeostasis (Berridge and Irvine, 1989). Data presented by Irvine and colleagues indicated that Ins(1,3,4,5)P 4 binds to a protein of the GAP1 family and thereby modulates Ca 2+ mobilisation by Ins(1,4,5)P 3 (Cullen et al. 1995). Another indication of a key regulatory role for the Ins(1,4,5)P 3 3-kinase(s) comes from recent data indicating that Ins(1,3,4,5)P 4 controls the frequency of calcium oscillations in HeLa cells (Zhu et al., 2000). cDNAs encoding two 3-kinase isoenzymes have been reported to be present in rat and in human (referred to as Ins(1,4,5)P 3 3-kinases A and B) and these have been expressed in bacteria or in COS-7 cells (Takazawa et al., 1990 and 1991). 3-kinase A was shown to be expressed at high levels in the hippocampal CA1 pyramidal and in Purkinje cells (Mailleux et al., 1991). Recent data obtained in our laboratory have shown that Ins(1,4,5)P 3 3-kinase B is expressed in astrocytes and is phosphorylated in response to purinergic agonists (Communi et al., 1999). In general, Ca 2+ in a complex with calmodulin stimulates mammalian Ins(1,4,5)P 3 3-kinase activity despite the presence of proteolytic fragments often obtained during extraction and purification of the enzyme (Takazawa et al., 1989). This stimulating effect was attributed to the presence of a calmodulin binding domain at the N-terminal end of the protein (Takazawa and Erneux, 1991). However, there is considerable cell-to-cell variability in the sensitivity of Ins(1,4,5)P 3 3-kinase activity to Ca 2+/calmodulin activation. This could result from the existence of different isoforms and/or splice variants of a single gene. This difference in sensitivity of Ca 2+ was indeed also shown for the two previously reported Ins(1,4,5)P 3 3-kinase A and B isoforms when expressed in E. coli: the A isoform was stimulated two to three fold by Ca 2+/calmodulin whereas the B isoform was stimulated up to 10 fold (Takazawa et al., 1990 and 1991). The specificity of Ins(1,4,5)P 3 phosphorylation by recombinant 3-kinases A and B at the 3-position of the inositol ring has been resolved by HPLC (Craxton et al., 1994). Recently, a new family of inositol polyphosphate kinases has been reported and several cDNAs encoding these enzymes have been cloned: three of them (KIAA0263, PiUS and KCS1) are inositol hexakisphosphate (InsP 6) kinases (Voglmaier et al., 1996 and Schell et al., 1999) while ArgRIII (also known as Arg82) was shown to be a multifunctional kinase (IPMK) which phosphorylates Ins(1,4,5)P 3 and Ins(1,4,5,6)P 4 in Saccharomyces cerevisiae (Saiardi et al., 1999). In vitro, ArgRIII catalyses the phosphorylation of Ins(1,4,5)P 3 at both the 3- and 6-posi- 61
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Geneeskundige Stichting Koningin El
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Fondation Médicale Reine Elisabeth
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L’abondance et la qualité des pu
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Prof. Dr. A. Bossuyt Secrétaire du
Page 9 and 10: Prof. Dr. G. Orban Lab. voor Neuro-
Page 11: Reports of the University Research
Page 14 and 15: 14 Members of the team: Christophe
Page 16 and 17: 16 domains, most notably that of N-
Page 19 and 20: Report of the Research Group of Pro
Page 21 and 22: Part 1: Characterisation of noradre
Page 23 and 24: Part 2 : Chromogranins as neuro-imm
Page 25: Publications 2000 : • J. Depreite
Page 28 and 29: 28 Collaborations with: A. Volny-Lu
Page 30 and 31: 30 MATERIALS AND METHODS Surgery an
Page 32 and 33: 32 RESULTS Recordings were obtained
Page 34 and 35: 34 Responses to brush stimuli The s
Page 36 and 37: 36 DISCUSSION This experimental stu
Page 41 and 42: PART 1: Molecular Pharmacology of A
Page 43 and 44: c) Most insurmountable AT 1 recepto
Page 45 and 46: dy tested biphenyl-tetrazole derive
Page 47 and 48: ii) More distant functional respons
Page 49 and 50: References •Aiyar N, Baker E, Vic
Page 51 and 52: •Olins GM, Chen ST, McMahon EG, P
Page 53 and 54: PART 2: The use of Endothelin 1 in
Page 55 and 56: vasoconstriction, peaked 20 minutes
Page 57: ACCEPTED • Vanderheyden P.M.L., F
Page 62 and 63: 62 tion forming Ins(1,3,4,5)P 4 and
Page 64: 64 Bibliography •Berridge, M.J. a
Page 68 and 69: 68 University of Mons-Hainaut Labor
Page 70 and 71: 70 Works carried out in 2000 1. We
Page 75 and 76: Genetic definition of brain tumours
Page 77 and 78: Analysing this way these 48 tumours
Page 83 and 84: Genetic determinants of mouse brain
Page 85 and 86: Genomic organization of the Dab1 ge
Page 91 and 92: In vitro studies of the hypothalami
Page 93 and 94: vitro GnRH release by intact male g
Page 99 and 100: Study on the functional regulation
Page 101 and 102: Elucidation of the DAT primary sequ
Page 103 and 104: The role of presenilin-1 in the gam
Page 107 and 108: INTRODUCTION As usual, this activit
Page 109 and 110: The acquisitions for this study sho
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not lead to the integrative process
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REFERENCES Thesis •Steven Laureys
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• Positron emission tomography in
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Before scanning, subjects practised
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RESEARCH PROGRAM ON MEMORY FUNCTION
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Corticobasal degeneration, motor sl
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Figure 2. Brain Areas Disclosed Dur
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• Cognitive Neuropsychological an
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Report of the Research Group of Pro
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Neuregulin signaling regulates neur
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tein present in neural precursor ce
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Cell biology for prevention and tre
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Functional significance of neurorec
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Spinal Cord Traumatic Lesion Martin
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A.Schulman, and T.R.Van De Water, B
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•Identification of PSF, the PTB-a
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143
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Brain activations in a dot pattern
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References •R Vogels, G Sary, P D
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A Scientific activities 1. Overview
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4. Purinergic receptors. Purinergic
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mals also scored higher in anxiety
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cell clones have been used in these
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•Ledent C, Valverde O, Cossu G, P
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• Snell BJ, Short JL, Drago J, Le
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I. Physiology and physiopathology o
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nuclei, which are involved in respo
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Natl. Acad. Sci. USA, 96: 5257-5262
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in those who did not. In rats sacri
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(Poster). Abstract of the 4th EURON
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Positional cloning of the neuronal
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fragments, 18 expressed-sequence-ta
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Philadelphia, USA, 3-7 October 2000
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I. FMRI in Awake Behaving Macaques
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gressively higher levels of the cor
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MION was injected into the femoral
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Future Possibilities Future contras
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FIGURES Figure 1: FMRI responses in
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Figure 5: Average percent signal ch
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FUNCTIONAL MAGNETIC RESONANCE IMAGI
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explain these search processes. Par
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205
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Investigation of the molecular mech
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tral) cortex compared to non-depriv
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By comparing the percentual increas
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altered amino acid residue is equal
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BIBLIOGRAPHY - 2000 Publications in
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Soc. Neurosci. Abstr., 2000, vol. 2
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1. Coding of 3D-shape in macaque in
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3. Position sensitivity of macaque
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Publications: •JANSSEN P., VOGELS
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