Research Report 2003 - Max-Planck-Institut für molekulare Genetik

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Department of Vertebrate Genomics 42 • SFB 506, TP C8, CD30 als therapeutische Zielstruktur, 1997-2000 • SFB 506, TP R9, Humane Antikörper- Fusionsproteine zur Therapie des diffusen Magenkarzinoms, 2000-2003 Prof. Dr. Gerd Burmester & Dr. Karl Skriner, Charité, Humboldt University Berlin Prof. Dr. Reto Crameri, Swiss Institute of Asthma and Allergy Research (SIAF), Switzerland Prof. Dr. Hannelore Breitenbach-Koller, Paris- Lodron University Salzburg, Austria. Dr. Jens Coorssen, University of Calgary, Canada Dr. Sergei Tillib, Institute of Gene Biology RAN, Moscow, Russia
Neurodegenerative Disorders Group Head: Sylvia Krobitsch (since 2/02) Phone: +49 (0)30-8413 1351 Fax: +49 (0)30-8413 1380 Email: krobitsc@molgen.mpg.de Graduate students: Ute Nonhoff (since 5/02) Karolin Huckauf (since 9/02) Markus Ralser (since 7/03) Undergraduate student: Norbert Mehlmer (11/02-7/03) Students worker: Annika Quast (since 5/02) Dr. Anja Westram (since 10/02) Scientific overview The major focus of the group, established in 2002, is to identify pathogenic pathways underlying neurodegenerative disorders like spinocerebellar ataxia 2 (SCA2), which accounts for nearly 14% and 29% of autosomal dominant SCAs in Germany and Italy, respectively, and Parkinson´s disease (PD), the second most frequent neurodegenerative disorder. SCA2 is a member of the so-called polyglutamine disorder family that includes Huntington’s disease (HD), dentatorubral-pallidoluysian atrophy (DRPLA), spinal and bulbar muscular atrophy (SBMA) and spinocerebellar ataxia 1, 3, 6, 7, 12 and 17. The basic underlying mutation is an expansion of CAG repeats encoding polyglutamine in the respective disease-causing proteins, that otherwise do not share any homology. In PD different mutations in several genes are responsible for onset and progression of disease. Conformational changes of the disease-causing proteins are mainly responsible for the formation of abnormal protein deposits in different regions of the brain of affected humans leading to a specific neuropathology in each disorder and for the formation of abnormal protein-protein interactions. The processes leading to these abnormal protein deposits as well as the cellular function of the relevant proteins and their role and involvement in the whole cellular network are far from being entirely understood. Exploring cellular mechanisms underlying formation of these abnormal protein deposits is one necessary step to take, but in addition, elucidating the cellular function of the proteins is crucial to open new perspectives for the development of therapeutic strategies for these so far untreatable neurodegenerative disorders. MPI for Molecular Genetics Research Report 2003 43
Page 1 and 2: Max-Planck-Institut für molekulare
Page 3 and 4: Table of Contents The Max Planck In
Page 5 and 6: MPI for Molecular Genetics Research
Page 7 and 8: The Max Planck Institute for Molecu
Page 9 and 10: Department of Vertebrate Genomics I
Page 11 and 12: To generate high resolution express
Page 13 and 14: Competitive position Since a long t
Page 15 and 16: the Protein Structure Factory. Fina
Page 17 and 18: Mass Spectrometry Group Head: Dr. J
Page 19 and 20: different tissues of A. thaliana, w
Page 21 and 22: Bioinformatics Group Heads: Ralf He
Page 23 and 24: a) Evolutionary studies In a recent
Page 25 and 26: Fuchs T, Malecova B, Linhart C, Sha
Page 27 and 28: Mouse, Medaka & MHC Group Head: Dr.
Page 29 and 30: General information Publications 19
Page 31 and 32: Jochen Wittbrodt, EMBL, Heidelberg
Page 35 and 36: THETA - Two Hybrid Transfected-cell
Page 37 and 38: Academical co-operations Andreas Ra
Page 39 and 40: The investigation of signaling path
Page 41 and 42: In vitro Ligand Screening Group Hea
Page 43: General information Publications 19
Page 47 and 48: Automation Group Graduate students:
Page 49 and 50: In addition, novel methods for the
Page 51 and 52: Sittler A, Walter S, Wedemeyer N, H
Page 53 and 54: Prof. Dr. Joachim Klose, Institut f
Page 55 and 56: eral years. This ambiguity is partl
Page 57 and 58: Clark MD, Panopoulou GD, Cahill DJ,
Page 59 and 60: integrations were passaged to the g
Page 63 and 64: Protein Group Scientists: Sabine Ba
Page 65 and 66: Kersten B, Bürkle L, Kuhn EJ, Giav
Page 67 and 68: Cardiovascular Genetics Group Head:
Page 69 and 70: protein interaction partners and at
Page 73 and 74: Chromosome 21 Group Head: Marie-Lau
Page 77 and 78: Department of Human Molecular Genet
Page 79 and 80: Network (NGFN). Recently, DNA from
Page 81 and 82: Finally, several of these groups ar
Page 83 and 84: Neurochemistry Group & Mouse Lab Gr
Page 85 and 86: studies. Furthermore, these mice wi
Page 87 and 88: Noonan syndrome and related disorde
Page 89 and 90: Chromosome Rearrangements & Disease
Page 91 and 92: General information Selected Public
Page 93 and 94: DNA Microarrays Scientists: Dr. Fik
Page 95 and 96:
General information Publications He
Page 97 and 98:
that in addition to reduced prolife
Page 99 and 100:
Christoph Redies, Prof. Dr., Instit
Page 101 and 102:
Since my move to the MPIMG in 11/20
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Biochemistry of Inherited Brain Dis
Page 105 and 106:
Schweiger S, Chaoui R, Tennstedt C,
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Until 2002, 13 genes have been impl
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General information Selected public
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Department of Computational Molecul
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EU: The European Molecular Biology
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EST tissue distribution Besides the
Page 117 and 118:
Protein Families & Evolution Group
Page 119 and 120:
General information Publications 20
Page 121 and 122:
We make use of the well-known HMMer
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Theses Benjamin Georgi: A graph-bas
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wide analysis of tyrosine as well a
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Further projects include multiple t
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Co-operations Identification and fu
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upstream of the translational start
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Department of Developmental Genetic
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2000; see figure 1). So far, we hav
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partners are. We also want to find
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Emeritus Group General Molecular Ge
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Sethmann S, Ceglowski P, Willert J,
Page 143 and 144:
Research Group Development & Diseas
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MPI for Molecular Genetics Research
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Goals An important future goal is t
Page 149 and 150:
Independent Junior Research Groups
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over, daf-9 is tightly regulated by
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European C.elegans Meeting, Blanken
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and at the ribosomal DNA locus. One
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lencer, has so far remained unchara
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Molecular control of skeletal devel
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BMPs, into a common control network
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this end I plan to analyze mouse mu
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Ribosome Group The Ribosome group c
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General information Selected Public
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group during the same period. In ad
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11) Agmon I, Auerbach T, Baram D, B
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Reconstitution & function The ribos
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Wendrich TM, Blaha G, Wilson DN, Ma
Page 177 and 178:
Miscellaneous Research Groups There
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vealed that the extraordinary stabi
Page 181 and 182:
34. Thorsted PB, Macartney DP, Akht
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esis and DNA packaging of this phag
Page 185 and 186:
Other launched projects concern con
Page 187 and 188:
BMBF 01GR0105, Plattform 1.1: NGFN
Page 189 and 190:
DNA synthesis, lipid biosynthesis,
Page 191 and 192:
Administration & Research Support H
Page 193 and 194:
Technical Management and Workshops
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tion based on the simplified GOOD a
Page 197 and 198:
Library Librarians: Dipl.-Fachinf.
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How to get to the Institute Max Pla
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