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Authordc.contributor.authorMendoza Naranjo, Ariadna 
Authordc.contributor.authorGonzález Billault, Christian es_CL
Authordc.contributor.authorMaccioni Baraona, Ricardo es_CL
Admission datedc.date.accessioned2011-03-23T17:11:33Z
Available datedc.date.available2011-03-23T17:11:33Z
Publication datedc.date.issued2006-10-30
Cita de ítemdc.identifier.citationJOURNAL OF CELL SCIENCE, Volume: 120, Issue: 2, Pages: 279-288, 2007en_US
Identifierdc.identifier.issn0021-9533
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/119105
Abstractdc.description.abstractA number of psychiatric and neurodegenerative disorders, such as Alzheimer’s disease, are characterized by abnormalities in the neuronal cytoskeleton. Here, we find that the enhancement in actin polymerization induced by fibrillar amyloid-beta peptide (A ) is associated with increased activity of Rac1/Cdc42 Rho GTPases. Rac1 upregulation involves the participation of Tiam1, a Rac guanine-nucleotide exchange factor, where A exposure leads to Tiam1 activation by a Ca2+-dependent mechanism. These results point to Rho GTPases as one of the targets in A -induced neurodegeneration in Alzheimer’s disease pathology, with a role in mediating changes in the actin cytoskeletal dynamics.en_US
Patrocinadordc.description.sponsorshipThis work was supported by grants from FONDECYT 1050198 to R.B.M. and by the Millennium Institute CBB. A.M.-N. was supported by a doctoral fellowship from the Millennium Institute for Advanced Studies in Cell Biology and Biotechnology (CBB).en_US
Lenguagedc.language.isoenen_US
Publisherdc.publisherCOMPANY OF BIOLOGISTS LTDen_US
Keywordsdc.subjectAlzheimer’s diseaseen_US
Títulodc.titleA beta(1-42) stimulates actin polymerization in hippocampal neurons through Rac1 and Cdc42 Rho GTPasesen_US
Document typedc.typeArtículo de revista


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