Overexpression of amyloid precursor protein increases copper content in HEK293 cells
dc.catalogador | jlo | |
dc.contributor.author | Suazo, Miriam | |
dc.contributor.author | Hodar, Christián | |
dc.contributor.author | Morgan, Carlos | |
dc.contributor.author | Cerpa Nebott, Francisco Waldo | |
dc.contributor.author | Cambiazo, Verónica | |
dc.contributor.author | Inestrosa Cantín, Nibaldo | |
dc.contributor.author | González, Mauricio | |
dc.date.accessioned | 2024-01-29T17:48:31Z | |
dc.date.available | 2024-01-29T17:48:31Z | |
dc.date.issued | 2009 | |
dc.description.abstract | Amyloid precursor protein (APP) is a transmembrane glycoprotein widely expressed in mammalian tissues and plays a central role in Alzheimer’s disease. However, its physiological function remains elusive. Cu2+ binding and reduction activities have been described in the extracellular APP135–156 region, which might be relevant for cellular copper uptake and homeostasis. Here, we assessed Cu2+ reduction and 64Cu uptake in two human HEK293 cell lines overexpressing APP. Our results indicate that Cu2+ reduction increased and cells accumulated larger levels of copper, maintaining cell viability at supra-physiological levels of Cu2+ ions. Moreover, wild-type cells exposed to both Cu2+ ions and APP135–155 synthetic peptides increased copper reduction and uptake. Complementation of function studies in human APP751 transformed Fre1 defective Saccharomyces cerevisiae cells rescued low Cu2+ reductase activity and increased 64Cu uptake. We conclude that Cu2+ reduction activity of APP facilitates copper uptake and may represent an early step in cellular copper homeostasis. | |
dc.fuente.origen | ORCID-ene24 | |
dc.identifier.doi | 10.1016/j.bbrc.2009.03.096 | |
dc.identifier.issn | 1090-2104 | |
dc.identifier.uri | http://www.scopus.com/inward/record.url?eid=2-s2.0-64749108284&partnerID=MN8TOARS | |
dc.identifier.uri | https://repositorio.uc.cl/handle/11534/81032 | |
dc.information.autoruc | Facultad de Ciencias Biológicas; Cerpa Nebott, Waldo Francisco; 0000-0001-7344-0144; 16584 | |
dc.information.autoruc | Facultad de Ciencias Biológicas; Inestrosa Cantín, Nibaldo Manuel; 0000-0003-3118-9726; 99331 | |
dc.issue.numero | 4 | |
dc.language.iso | en | |
dc.nota.acceso | Contenido parcial | |
dc.pagina.final | 744 | |
dc.pagina.inicio | 740 | |
dc.revista | Biochemical and Biophysical Research Communications | |
dc.rights | acceso restringido | |
dc.subject | Alzheimer | |
dc.subject | Copper homeostasis | |
dc.subject | Reduction | |
dc.subject | Uptake | |
dc.subject | Yeast | |
dc.subject.ddc | 610 | |
dc.subject.dewey | Medicina y salud | es_ES |
dc.title | Overexpression of amyloid precursor protein increases copper content in HEK293 cells | |
dc.type | artículo | |
dc.volumen | 382 | |
sipa.codpersvinculados | 16584 | |
sipa.codpersvinculados | 99331 | |
sipa.trazabilidad | ORCID;2024-01-15 |