1. ZHAW digitalcollection
  2. Life Sciences und Facility Management
  3. Publikationen
  4. Publikationen Life Sciences und Facility Management
Full metadata record
DC FieldValueLanguage
dc.contributor.authorMathews, Paul M.-
dc.contributor.authorGuerra, Carolyn B.-
dc.contributor.authorJiang, Ying-
dc.contributor.authorGrbovic, Olivera M.-
dc.contributor.authorKao, Benjamin H.-
dc.contributor.authorSchmidt, Stephen D.-
dc.contributor.authorDinakar, Ravi-
dc.contributor.authorMercken, Marc-
dc.contributor.authorHille-Rehfeld, Annette-
dc.contributor.authorRohrer, Jack-
dc.contributor.authorMehta, Pankaj-
dc.contributor.authorCataldo, Anne M.-
dc.contributor.authorNixon, Ralph A.-
dc.date.accessioned2018-06-13T08:43:01Z-
dc.date.available2018-06-13T08:43:01Z-
dc.date.issued2002-09-10-
dc.identifier.issn1083-351Xde_CH
dc.identifier.urihttps://digitalcollection.zhaw.ch/handle/11475/6807-
dc.description.abstractProminent endosomal and lysosomal changes are an invariant feature of neurons in sporadic Alzheimer's disease (AD). These changes include increased levels of lysosomal hydrolases in early endosomes and increased expression of the cation-dependent mannose 6-phosphate receptor (CD-MPR), which is partially localized to early endosomes. To determine whether AD-associated redistribution of lysosomal hydrolases resulting from changes in CD-MPR expression affects amyloid precursor protein (APP) processing, we stably transfected APP-overexpressing murine L cells with human CD-MPR. As controls for these cells, we also expressed CD-MPR trafficking mutants that either localize to the plasma membrane (CD-MPRpm) or to early endosomes (CD-MPRendo). Expression of CD-MPR resulted in a partial redistribution of a representative lysosomal hydrolase, cathepsin D, to early endosomal compartments. Turnover of APP and secretion of sAPPalpha and sAPPbeta were not altered by overexpression of any of the CD-MPR constructs. However, secretion of both human Abeta40 and Abeta42 into the growth media nearly tripled in CD-MPR- and CD-MPRendo-expressing cells when compared with parental or CD-MPRpm-expressing cells. Comparable increases were confirmed for endogenous mouse Abeta40 in L cells expressing these CD-MPR constructs but not overexpressing human APP. These data suggest that redistribution of lysosomal hydrolases to early endocytic compartments mediated by increased expression of the CD-MPR may represent a potentially pathogenic mechanism for accelerating Abeta generation in sporadic AD, where the mechanism of amyloidogenesis is unknown.de_CH
dc.language.isoende_CH
dc.publisherAmerican Society for Biochemistry and Molecular Biologyde_CH
dc.relation.ispartofJournal of Biological Chemistryde_CH
dc.rightsLicence according to publishing contractde_CH
dc.subject.ddc571: Physiologie und verwandte Themende_CH
dc.subject.ddc572: Biochemiede_CH
dc.titleAlzheimer's disease-related overexpression of the cation-dependent mannose 6-phosphate receptor increases Aβ secretion : role for altered lysosomal hydrolase distribution in β-amyloidogenesisde_CH
dc.typeBeitrag in wissenschaftlicher Zeitschriftde_CH
dcterms.typeTextde_CH
zhaw.departementLife Sciences und Facility Managementde_CH
zhaw.organisationalunitInstitut für Chemie und Biotechnologie (ICBT)de_CH
dc.identifier.doi10.1074/jbc.M108161200de_CH
zhaw.funding.euNode_CH
zhaw.issue7de_CH
zhaw.originated.zhawYesde_CH
zhaw.pages.end5307de_CH
zhaw.pages.start5299de_CH
zhaw.publication.statuspublishedVersionde_CH
zhaw.volume277de_CH
zhaw.publication.reviewPeer review (Publikation)de_CH
zhaw.webfeedZellphysiologiede_CH
Appears in collections:Publikationen Life Sciences und Facility Management

Files in This Item:
There are no files associated with this item.
Show simple item record
Mathews, P. M., Guerra, C. B., Jiang, Y., Grbovic, O. M., Kao, B. H., Schmidt, S. D., Dinakar, R., Mercken, M., Hille-Rehfeld, A., Rohrer, J., Mehta, P., Cataldo, A. M., & Nixon, R. A. (2002). Alzheimer’s disease-related overexpression of the cation-dependent mannose 6-phosphate receptor increases Aβ secretion : role for altered lysosomal hydrolase distribution in β-amyloidogenesis. Journal of Biological Chemistry, 277(7), 5299–5307. https://doi.org/10.1074/jbc.M108161200
Mathews, P.M. et al. (2002) ‘Alzheimer’s disease-related overexpression of the cation-dependent mannose 6-phosphate receptor increases Aβ secretion : role for altered lysosomal hydrolase distribution in β-amyloidogenesis’, Journal of Biological Chemistry, 277(7), pp. 5299–5307. Available at: https://doi.org/10.1074/jbc.M108161200.
P. M. Mathews et al., “Alzheimer’s disease-related overexpression of the cation-dependent mannose 6-phosphate receptor increases Aβ secretion : role for altered lysosomal hydrolase distribution in β-amyloidogenesis,” Journal of Biological Chemistry, vol. 277, no. 7, pp. 5299–5307, Sep. 2002, doi: 10.1074/jbc.M108161200.
MATHEWS, Paul M., Carolyn B. GUERRA, Ying JIANG, Olivera M. GRBOVIC, Benjamin H. KAO, Stephen D. SCHMIDT, Ravi DINAKAR, Marc MERCKEN, Annette HILLE-REHFELD, Jack ROHRER, Pankaj MEHTA, Anne M. CATALDO und Ralph A. NIXON, 2002. Alzheimer’s disease-related overexpression of the cation-dependent mannose 6-phosphate receptor increases Aβ secretion : role for altered lysosomal hydrolase distribution in β-amyloidogenesis. Journal of Biological Chemistry. 10 September 2002. Bd. 277, Nr. 7, S. 5299–5307. DOI 10.1074/jbc.M108161200
Mathews, Paul M., Carolyn B. Guerra, Ying Jiang, Olivera M. Grbovic, Benjamin H. Kao, Stephen D. Schmidt, Ravi Dinakar, et al. 2002. “Alzheimer’s Disease-Related Overexpression of the Cation-Dependent Mannose 6-Phosphate Receptor Increases Aβ Secretion : Role for Altered Lysosomal Hydrolase Distribution in β-Amyloidogenesis.” Journal of Biological Chemistry 277 (7): 5299–5307. https://doi.org/10.1074/jbc.M108161200.
Mathews, Paul M., et al. “Alzheimer’s Disease-Related Overexpression of the Cation-Dependent Mannose 6-Phosphate Receptor Increases Aβ Secretion : Role for Altered Lysosomal Hydrolase Distribution in β-Amyloidogenesis.” Journal of Biological Chemistry, vol. 277, no. 7, Sept. 2002, pp. 5299–307, https://doi.org/10.1074/jbc.M108161200.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.