G Multhaup

Summary

Affiliation: University of Heidelberg
Country: Germany

Publications

  1. ncbi request reprint Copper-binding amyloid precursor protein undergoes a site-specific fragmentation in the reduction of hydrogen peroxide
    G Multhaup
    ZMBH Center for Molecular Biology Heidelberg, University of Heidelberg, Germany
    Biochemistry 37:7224-30. 1998
  2. ncbi request reprint Reactive oxygen species and Alzheimer's disease
    G Multhaup
    ZMBH Center for Molecular Biology Heidelberg, University of Heidelberg, Germany
    Biochem Pharmacol 54:533-9. 1997
  3. ncbi request reprint The amyloid precursor protein of Alzheimer's disease in the reduction of copper(II) to copper(I)
    G Multhaup
    ZMBH Center for Molecular Biology Heidelberg, University of Heidelberg, Germany
    Science 271:1406-9. 1996
  4. ncbi request reprint Homodimerization of amyloid precursor protein and its implication in the amyloidogenic pathway of Alzheimer's disease
    S Scheuermann
    ZMBH, Center for Molecular Biology, University of Heidelberg, Im Neuenheimer Feld 282, D 69120 Heidelberg, Germany
    J Biol Chem 276:33923-9. 2001
  5. ncbi request reprint Mutations in the transmembrane domain of APP altering gamma-secretase specificity
    S F Lichtenthaler
    Center for Molecular Biology Heidelberg ZMBH, University of Heidelberg, Im Neuenheimer Feld 282, D 69120 Heidelberg, Germany
    Biochemistry 36:15396-403. 1997
  6. ncbi request reprint A novel substrate for analyzing Alzheimer's disease gamma-secretase
    S F Lichtenthaler
    Center for Molecular Biology Heidelberg ZMBH, University of Heidelberg, Germany
    FEBS Lett 453:288-92. 1999
  7. ncbi request reprint Regulation of APP expression, biogenesis and metabolism by extracellular matrix and cytokines
    K Beyreuther
    ZMBH, Center for Molecular Biology, University of Heidelberg, Germany
    Ann N Y Acad Sci 777:74-6. 1996
  8. ncbi request reprint Regulation and expression of the Alzheimer's beta/A4 amyloid protein precursor in health, disease, and Down's syndrome
    K Beyreuther
    ZMBH, Center for Molecular Biology, University of Heidelberg, Germany
    Ann N Y Acad Sci 695:91-102. 1993
  9. ncbi request reprint Interaction of the CopZ copper chaperone with the CopA copper ATPase of Enterococcus hirae assessed by surface plasmon resonance
    G Multhaup
    Center for Molecular Biology (ZMBH, University of Heidelberg, Im Neuenheimer Feld 282, D-69120 Heidelberg, Germany
    Biochem Biophys Res Commun 288:172-7. 2001
  10. ncbi request reprint The A beta peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction
    X Huang
    Laboratory for Oxidation Biology, Genetics and Aging Unit, Massachusetts General Hospital, Charlestown 02129, USA
    Biochemistry 38:7609-16. 1999

Collaborators

Detail Information

Publications49

  1. ncbi request reprint Copper-binding amyloid precursor protein undergoes a site-specific fragmentation in the reduction of hydrogen peroxide
    G Multhaup
    ZMBH Center for Molecular Biology Heidelberg, University of Heidelberg, Germany
    Biochemistry 37:7224-30. 1998
    ..What significance such a perturbation may have for the pathogenesis of Alzheimer's disease remains to be determined...
  2. ncbi request reprint Reactive oxygen species and Alzheimer's disease
    G Multhaup
    ZMBH Center for Molecular Biology Heidelberg, University of Heidelberg, Germany
    Biochem Pharmacol 54:533-9. 1997
    ..Thus, copper-mediated toxicity of APP-Cu(II)/(I) complexes may contribute to neurodegeneration in AD...
  3. ncbi request reprint The amyloid precursor protein of Alzheimer's disease in the reduction of copper(II) to copper(I)
    G Multhaup
    ZMBH Center for Molecular Biology Heidelberg, University of Heidelberg, Germany
    Science 271:1406-9. 1996
    ..Thus, copper-mediated toxicity may contribute to neurodegeneration in Alzheimer's disease...
  4. ncbi request reprint Homodimerization of amyloid precursor protein and its implication in the amyloidogenic pathway of Alzheimer's disease
    S Scheuermann
    ZMBH, Center for Molecular Biology, University of Heidelberg, Im Neuenheimer Feld 282, D 69120 Heidelberg, Germany
    J Biol Chem 276:33923-9. 2001
    ..We suggest that dimerization could be a physiologically important mechanism for regulating the proposed signal activity of APP...
  5. ncbi request reprint Mutations in the transmembrane domain of APP altering gamma-secretase specificity
    S F Lichtenthaler
    Center for Molecular Biology Heidelberg ZMBH, University of Heidelberg, Im Neuenheimer Feld 282, D 69120 Heidelberg, Germany
    Biochemistry 36:15396-403. 1997
    ..These results suggest that the different Abeta- and p3-species are generated by gamma-cleavage activities with a similar enzymatic mechanism...
  6. ncbi request reprint A novel substrate for analyzing Alzheimer's disease gamma-secretase
    S F Lichtenthaler
    Center for Molecular Biology Heidelberg ZMBH, University of Heidelberg, Germany
    FEBS Lett 453:288-92. 1999
    ..This novel SPA4CT protein is processed by gamma-secretase in the same manner as APP-derived A4CT and might be valuable for the generation of transgenic animals showing amyloid pathology...
  7. ncbi request reprint Regulation of APP expression, biogenesis and metabolism by extracellular matrix and cytokines
    K Beyreuther
    ZMBH, Center for Molecular Biology, University of Heidelberg, Germany
    Ann N Y Acad Sci 777:74-6. 1996
    ....
  8. ncbi request reprint Regulation and expression of the Alzheimer's beta/A4 amyloid protein precursor in health, disease, and Down's syndrome
    K Beyreuther
    ZMBH, Center for Molecular Biology, University of Heidelberg, Germany
    Ann N Y Acad Sci 695:91-102. 1993
    ..This may be the case during pathological evolution of AD and DS when beta/A4 derived from synaptic APP is converted to beta/A4 amyloid by radical generation...
  9. ncbi request reprint Interaction of the CopZ copper chaperone with the CopA copper ATPase of Enterococcus hirae assessed by surface plasmon resonance
    G Multhaup
    Center for Molecular Biology (ZMBH, University of Heidelberg, Im Neuenheimer Feld 282, D-69120 Heidelberg, Germany
    Biochem Biophys Res Commun 288:172-7. 2001
    ....
  10. ncbi request reprint The A beta peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction
    X Huang
    Laboratory for Oxidation Biology, Genetics and Aging Unit, Massachusetts General Hospital, Charlestown 02129, USA
    Biochemistry 38:7609-16. 1999
    ..These findings indicate that the accumulation of A beta could be a direct source of oxidative stress in Alzheimer's disease...
  11. ncbi request reprint Regulation of amyloid protein precursor (APP) binding to collagen and mapping of the binding sites on APP and collagen type I
    D Beher
    Center for Molecular Biology Heidelberg ZMBH, University of Heidelberg, Federal Republic of Germany
    J Biol Chem 271:1613-20. 1996
    ..Taken together, the data suggest that the regulation of APP binding to collagen type I by heparin occurs through the competitive binding of heparin and APP to collagen...
  12. ncbi request reprint Human amyloid precursor-like protein 1--cDNA cloning, ectopic expression in COS-7 cells and identification of soluble forms in the cerebrospinal fluid
    K Paliga
    Center for Molecular Biology Heidelberg, Germany
    Eur J Biochem 250:354-63. 1997
    ..Using a novel hAPLP1-specific antiserum, we identified soluble hAPLP1 in the human cerebrospinal fluid, which suggests that secretion of hAPLP1 from brain cells also takes place in vivo...
  13. ncbi request reprint Amyloid precursor-like protein 1 accumulates in neuritic plaques in Alzheimer's disease
    T A Bayer
    Department of Neuropathology, University of Bonn Medical Center, Germany
    Acta Neuropathol 94:519-24. 1997
    ..Some astrocytes elicited perinuclear APLP1 staining, but this was observed in both AD and control brains. These findings raise the possibility that APLP1 may contribute to the pathogenesis of AD-associated neurodegeneration...
  14. ncbi request reprint The beta A4 amyloid precursor protein binding to copper
    L Hesse
    Center for Molecular Biology Heidelberg, University Heidelberg, Germany
    FEBS Lett 349:109-16. 1994
    ..Copper(II) binding is shown to inhibit homophilic APP binding. The identification of a copper(II) binding site in APP suggests that APP and APLP2 may be involved in electron transfer and radical reactions...
  15. ncbi request reprint Chelation and intercalation: complementary properties in a compound for the treatment of Alzheimer's disease
    R A Cherny
    The Department of Pathology, The University of Melbourne, Melbourne, Victoria, 3010, Australia
    J Struct Biol 130:209-16. 2000
    ..Such hybrid copper chelating and "chain breaking" properties may form the basis of a rational design for a therapy for Alzheimer's disease...
  16. pmc Identification, transmembrane orientation and biogenesis of the amyloid A4 precursor of Alzheimer's disease
    T Dyrks
    Center for Molecular Biology, University of Heidelberg, FRG
    EMBO J 7:949-57. 1988
    ....
  17. ncbi request reprint The Alzheimer's disease amyloid precursor protein modulates copper-induced toxicity and oxidative stress in primary neuronal cultures
    A R White
    Department of Pathology, The University of Melbourne, Parkville, 3052 Victoria, Australia
    J Neurosci 19:9170-9. 1999
    ..These data support a role for the APP copper-binding domain in APP-mediated copper (I) generation and toxicity in primary neurons, a process that has important implications for Alzheimer's disease and other neurodegenerative disorders...
  18. ncbi request reprint Crystal structure of the N-terminal, growth factor-like domain of Alzheimer amyloid precursor protein
    J Rossjohn
    The Ian Potter Foundation Protein Crystallography Laboratory, St Vincent s Institute of Medical Research, Fitzroy, Victoria, Australia
    Nat Struct Biol 6:327-31. 1999
    ..Structural similarities with cysteine-rich growth factors, taken together with its known growth-promoting properties, suggests the APP N-terminal domain could function as a growth factor in vivo...
  19. pmc Presenilin-dependent gamma-secretase processing of beta-amyloid precursor protein at a site corresponding to the S3 cleavage of Notch
    M Sastre
    Adolf Butenandt-Institute, Department of Biochemistry, Laboratory for Alzheimer's and Parkinson's Disease Research, Ludwig-Maximilians-University, Schillerstrasse 44, 80336 Munich, Germany
    EMBO Rep 2:835-41. 2001
    ..Sequence analysis revealed that CTFgamma is produced by a novel gamma-secretase cut, which occurs at a site corresponding to the S3 cleavage of Notch...
  20. ncbi request reprint A splice variant of beta-secretase deficient in the amyloidogenic processing of the amyloid precursor protein
    U Bodendorf
    Nervous System, Novartis Pharma AG, CH 4002 Basel, Switzerland
    J Biol Chem 276:12019-23. 2001
    ..Our findings suggest that tissue-specific splicing of the BACE mRNA may explain the observation that in the human pancreas robust transcription of the BACE gene does not translate into recovered enzymatic activity...
  21. ncbi request reprint Processing of beta-secretase by furin and other members of the proprotein convertase family
    J W Creemers
    Center for Human Genetics, Molecular Oncology and Neuronal Cell Biology Laboratories, Katholieke Universiteit Leuven, 3000 Leuven, Belgium
    J Biol Chem 276:4211-7. 2001
    ..We conclude that modulation of the conversion of pro-Bace to mature Bace is not a relevant drug target to treat Alzheimer's disease...
  22. ncbi request reprint Gender dependent APP processing in a transgenic mouse model of Alzheimer's disease
    S Schafer
    Department of Psychiatry, Division of Neurobiology, Saarland University, Homburg Saar, Germany
    J Neural Transm 114:387-94. 2007
    ....
  23. ncbi request reprint Phosphorylation regulates intracellular trafficking of beta-secretase
    J Walter
    Adolf Butenandt Institute, Department of Biochemistry, Laboratory for Alzheimer s and Parkinson s Disease Research, Ludwig Maximilians University, 44 Schillerstrasse, 80336 Munich, Germany
    J Biol Chem 276:14634-41. 2001
    ..In contrast, nonphosphorylatable BACE S498A is retained within early endosomes. Our results therefore demonstrate regulated trafficking of BACE within the secretory and endocytic pathway...
  24. ncbi request reprint A vicious circle: role of oxidative stress, intraneuronal Abeta and Cu in Alzheimer's disease
    T A Bayer
    Department of Neurobiology, Clinic of Psychiatry, University of the Saarland, Homburg, Germany
    Clin Neuropathol 25:163-71. 2006
    ..Thus, we conclude that bioavailability of Cu is a crucial point for the pathogenesis of AD...
  25. ncbi request reprint Cerebrospinal fluid diagnostic markers correlate with lower plasma copper and ceruloplasmin in patients with Alzheimer's disease
    H Kessler
    Department of Psychiatry and Psychotherapy, Saarland University, Homburg Saar, Germany
    J Neural Transm 113:1763-9. 2006
    ..Although only AD patients were included, the reduced plasma Cu and CB levels in patients with a CSF diagnosis of advanced AD supports previous observations that a mild Cu deficiency might contribute to AD progression...
  26. ncbi request reprint [The role of copper in the pathophysiology of Alzheimer's disease]
    H Kessler
    Klinik fur Psychiatrie und Psychotherapie, Universitatsklinikum des Saarlandes, Homburg Saar
    Nervenarzt 76:581-5. 2005
    ....
  27. ncbi request reprint The LPS receptor (CD14) links innate immunity with Alzheimer's disease
    K Fassbender
    Department of Neurology, University of Goettingen, 37075 Goettingen, FRG
    FASEB J 18:203-5. 2004
    ....
  28. ncbi request reprint Hohenheim consensus workshop: copper
    K Schumann
    Walther Straub Institut für Pharmakologie und Toxikologie der LMU, Munchen, Germany
    Eur J Clin Nutr 56:469-83. 2002
    ..The consensus statements were agreed on by all members. One of the conclusions is that a re-assessment of published data is necessary and future research is required...
  29. ncbi request reprint Reelin in plaques of beta-amyloid precursor protein and presenilin-1 double-transgenic mice
    O Wirths
    Department of Psychiatry, University of Bonn Medical Center, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Neurosci Lett 316:145-8. 2001
    ..This observation gives the first evidence for the association of reelin with amyloid deposits...
  30. ncbi request reprint Copper in disorders with neurological symptoms: Alzheimer's, Menkes, and Wilson diseases
    D Strausak
    Center for Cellular and Molecular Biology, School of Biological and Chemical Sciences, Deakin University, Burwood, Victoria, Australia
    Brain Res Bull 55:175-85. 2001
    ..This could provide a rationale for a link between severely dysregulated metal-ion homeostasis and the selective neuronal pathology...
  31. ncbi request reprint Intraneuronal Abeta accumulation precedes plaque formation in beta-amyloid precursor protein and presenilin-1 double-transgenic mice
    O Wirths
    Department of Psychiatry, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105, Bonn, Germany
    Neurosci Lett 306:116-20. 2001
    ..Interestingly, intraneuronal Abeta staining was no longer detected in the brain of aged double-transgenic mice, which correlates with the typical neuropathology in the brain of chronic AD patients...
  32. pmc Separation of presenilin function in amyloid beta-peptide generation and endoproteolysis of Notch
    L Kulic
    Adolf Butenandt Institute, Department of Biochemistry, Laboratory for Alzheimer s Disease Research, Ludwig Maximilians University, 80336 Munich, Germany
    Proc Natl Acad Sci U S A 97:5913-8. 2000
    ..These results demonstrate that the biological function of PS proteins in the endoproteolysis of beta-amyloid precursor protein and Notch can be separated...
  33. ncbi request reprint Maturation and pro-peptide cleavage of beta-secretase
    A Capell
    Adolf Butenandt Institute, Department of Biochemistry, Laboratory for Alzheimer s Disease Research, Ludwig Maximilians University, 80336 Munich, Germany
    J Biol Chem 275:30849-54. 2000
    ..Pro-BACE was predominantly located within the endoplasmic reticulum. Pro-peptide cleavage occurred immediately before full maturation and trafficking through the Golgi...
  34. ncbi request reprint Molecular characterization of two invariant surface glycoproteins specific for the bloodstream stage of Trypanosoma brucei
    K Ziegelbauer
    Max Planck Institut fur Biologie, Abteilung Membranbiochemie, Tubingen, Federal Republic of Germany
    J Biol Chem 267:10797-803. 1992
    ..They can be detected in all T. brucei brucei variant clones investigated. Both polypeptides are distributed over the entire surface of the parasite...
  35. ncbi request reprint Murine cyclophilin-S1: a variant peptidyl-prolyl isomerase with a putative signal sequence expressed in differentiating F9 cells
    A Schumacher
    Institute for Molecular Biology, Hannover Medical School, Germany
    Biochim Biophys Acta 1129:13-22. 1991
    ..Specific subcellular localization of PPIases is postulated to contribute to functional specificities of this class of enzymes...
  36. ncbi request reprint GABAA-receptor expressed from rat brain alpha- and beta-subunit cDNAs displays potentiation by benzodiazepine receptor ligands
    P Malherbe
    Research Department, F Hoffmann La Roche, Basel, Switzerland
    Brain Res Mol Brain Res 8:199-208. 1990
    ..Thus, alpha 1- and beta 1-subunits are sufficient to form GABAA-receptors which contain benzodiazepine binding sites, although in a functionally restricted form...
  37. ncbi request reprint Cloning and expression of the 58 kd beta subunit of the inhibitory glycine receptor
    G Grenningloh
    ZMBH, University of Heidelberg, Federal Republic of Germany
    Neuron 4:963-70. 1990
    ..Our data indicate a differential expression of GlyR alpha and beta subunits in the rat nervous system and support a structural role of the beta polypeptide in the native receptor complex...
  38. ncbi request reprint The Drosophila PROS-28.1 gene is a member of the proteasome gene family
    C Haass
    ZMBH Molekulare Genetik, University of Heidelberg, F R G
    Gene 90:235-41. 1990
    ..The data suggest that at least a subset of the proteasome-encoding genes belongs to a family of related genes (PROS gene family) which may have evolved from a common ancestral PROS gene...
  39. pmc The PROS-35 gene encodes the 35 kd protein subunit of Drosophila melanogaster proteasome
    C Haass
    ZMBH, Heidelberg, FRG
    EMBO J 8:2373-9. 1989
    ..These data suggest a tissue- and development-dependent distribution of the proteasome in D. melanogaster...
  40. pmc The PreA4(695) precursor protein of Alzheimer's disease A4 amyloid is encoded by 16 exons
    H G Lemaire
    Institute für Genetik, Universitat Koln, FRG
    Nucleic Acids Res 17:517-22. 1989
    ..The DNA sequence coding for the amyloid A4 protein is interrupted by an intron. This finding supports the idea that amyloid A4 protein arises by incomplete proteolysis of a larger precursor, and not by aberrant splicing...
  41. ncbi request reprint The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
    J Kang
    Nature 325:733-6. 1987
    ..This sequence, together with the localization of its gene on chromosome 21, suggests that the cerebral amyloid deposited in Alzheimer's disease and aged Down's syndrome is caused by aberrant catabolism of a cell-surface receptor...
  42. pmc Alzheimer's disease amyloidogenic glycoprotein: expression pattern in rat brain suggests a role in cell contact
    B D Shivers
    Zentrum fur Molekulare Biologie, Universitat Heidelberg, FRG
    EMBO J 7:1365-70. 1988
    ..Since amyloid deposits are rarely observed in rat brain, we conclude that high expression of AG is not the sole cause of amyloidosis...
  43. pmc Amyloid plaque core protein in Alzheimer disease and Down syndrome
    C L Masters
    Proc Natl Acad Sci U S A 82:4245-9. 1985
    ....
  44. ncbi request reprint Drosophila proteasome Dm25 subunit substitutes the mouse MC3 subunit in hybrid proteasomes. The N-terminal domain is essential for subunit incorporation
    A Seelig
    Center of Molecular Biology, University of Heidelberg, Federal Republic of Germany
    J Biol Chem 268:25561-7. 1993
    ..The ability to form hybrid proteasomes involving essential nondeletable subunits now opens the possibility for structural and also functional analysis of such subunits by mutagenesis in higher eukaryotes...
  45. ncbi request reprint A novel zinc(II) binding site modulates the function of the beta A4 amyloid protein precursor of Alzheimer's disease
    A I Bush
    Department of Pathology, University of Melbourne, Parkville, Victoria, Australia
    J Biol Chem 268:16109-12. 1993
    ..Egawa, H., Okubo, S., Yasunaga, K., and Murata, K. (1992) Thromb. Res. 66, 397-408) situated near the zinc binding region. Zinc is a factor that modulates the functional properties of the substrate for beta A4 amyloidogenesis...
  46. pmc Chicken NFI/TGGCA proteins are encoded by at least three independent genes: NFI-A, NFI-B and NFI-C with homologues in mammalian genomes
    R A Rupp
    Zentrum fur Molekulare Biologie der Universitat Heidelberg, FRG
    Nucleic Acids Res 18:2607-16. 1990
    ....
  47. ncbi request reprint Copper levels are increased in the cerebral cortex and liver of APP and APLP2 knockout mice
    A R White
    Department of Pathology, The University of Melbourne, Parkville, Victoria, 3052, Australia
    Brain Res 842:439-44. 1999
    ..These data support a novel mechanism in the APP/Abeta pathway which leads to AD...
  48. ncbi request reprint It all sticks together--the APP-related family of proteins and Alzheimer's disease
    T A Bayer
    Department of Psychiatry, University of Bonn Medical Center, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Mol Psychiatry 4:524-8. 1999
    ..We hypothesize that the functional loss of members of the APP family contributes to the gradual cognitive decline in Alzheimer's disease patients...
  49. ncbi request reprint Primary structure and alternative splice variants of gephyrin, a putative glycine receptor-tubulin linker protein
    P Prior
    Abteilung Neurochemie, Max Planck Institut für Hirnforschung, Frankfurt M, Germany
    Neuron 8:1161-70. 1992
    ..Thus, gephyrin may define a novel type of microtubule-associated protein involved in membrane protein-cytoskeleton interactions...