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FORMER RESEARCH GROUP OF PROF. M. SCHWEIGER |
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Institute of Chemistry - Biochemistry
Freie Universität Berlin
Thielallee 63
Room:
Prof. Schweiger has retired
E-Mail: mschweig@chemie.fu-berlin.de |
FURTHER INFORMATION
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KEYWORDSPoly(ADP-ribosyl) Transferase (ADPRT): protein-protein interaction and binding to specific DNA structures of the human enyzme. Isolation and cloning of ADPRT from lower eucaryotes. Defense mechanisms against "reactive oxygen species" (ROS): pathological defects: Fanconi anaemia. NAD+-Glycohydrolase: mode of action, isolation, cloning; ROS and Ca2+ homeostasis in the cell. Defects of DNA repair: Relationship of DNA repair/senescence; Cockayne Syndrome, Werner Syndrome, Down Syndrome. |
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ABSTRACTStructure and Function of poly(ADP-ribosyl) Transferase (ADPRT): ADPRT catalyzes the transfer of ADP-ribose moieties onto nuclear proteins utilizing NAD. This modification serves a regulatory function in a number of nuclear processes. So far neither the exact catalytic mechanism nor the physiologically important acceptor proteins have been established. The crystallization of the recombinant human protein as well as the characterization of the phylogeny of the enzyme (by detecting and isolating it from lower organisms) are in progress. Domains involved in protein-protein interactions have been detected within the human enzyme. Knowledge of these domains will facilitate the discovery of potential acceptor proteins and also the characterization of dimerization of the enzyme itself.Regulation of Mitochondrial Calcium Fluxes by ADP-Ribosylation: Oxidative damage of mitochondria causes pyridine nucleotide oxidation, degradation of NAD(P), ADP-ribosylation and calcium efflux. These processes appear to be causally linked. The studies of the molecular mechanisms include isolation, characterization, cloning and sequencing of the mitochondrial enzymes involved (NADase, ADP-ribosyl transferase, acceptors of ADP-ribose and the calcium channel). Molecular characterization of genetic diseases associated with DNA repair defects: Fanconi's anaemia (FA) and Werner's syndrome (WS) are rare autosomal recessively inherited diseases with typical phenotypes. On the cellular level, the rate of spontaneous and induced chromosome breaks is drastically increased. FA cells exhibit a high sensitivity towards oxygen. Identification of the impaired gene (by molecular biological approaches such as subtractive hybridization) will lead to the discovery of novel mechanisms of DNA repair. |
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