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Impaired voltage-gated K+ channel expression in brain during experimental cancer cachexia

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dc.contributor.author Coma Camprodón, Mireia
dc.contributor.author Vicente García, Rubén, 1978-
dc.contributor.author Busquets, Silvia
dc.contributor.author Carbó, Neus
dc.contributor.author Tamkun, Michael M.
dc.contributor.author López Soriano, Francisco J.
dc.contributor.author Argilés, Josep M.
dc.contributor.author Felipe, Antonio
dc.date.accessioned 2016-01-20T19:28:12Z
dc.date.available 2016-01-20T19:28:12Z
dc.date.issued 2003
dc.identifier.citation Coma M, Vicente R, Busquets S, Carbó N, Tamkun MM, López-Soriano FJ et al. Impaired voltage-gated K+ channel expression in brain during experimental cancer cachexia. FEBS Letters. 2003;536(1-3):45-50. DOI: 10.1016/S0014-5793(03)00009-7
dc.identifier.issn 0014-5793
dc.identifier.uri http://hdl.handle.net/10230/25611
dc.description.abstract Cancer-induced cachexia affects most advanced cancer patients. It is characterized by anorexia, profound metabolic dysfunctions, and severe neurological disorders. Here we show that voltage-gated potassium channel (Kv) expression is impaired in the brain of tumor-bearing animals. Expression of both delayed rectifier (Kv1.1, Kv1.2, Kv1.3, Kv1.5, Kv1.6, Kv2.1, Kv3.1, Kv4.2) and A-type potassium channels (Kv1.4, Kv3.3, Kv3.4) was greatly down-regulated in brain from animals bearing a Yoshida AH-130 ascites hepatoma. The possible compensatory mechanisms (Kv1.4/Kv4.2), expression of redundant genes (Kv3.1/Kv3.3) and heteromultimeric channel formation (Kv2.1/Kv9.3) were also affected. The high circulating levels of TNFalpha and the reduced expression of the anti-apoptotic protein Bcl-XL found in the brain of tumor-bearing animals indicate that this response could be mediated by an increase in brain cell death due to apoptosis. The results suggest that brain function is impaired during cancer cachexia, and may account for the cancer-induced anorectic response and other neurological alterations.
dc.description.sponsorship This study was supported by grants from the Ministerio de Ciencia y Tecnología (BFI2002-00764 to A.F., BFI2002-02186 to J.M.A.) and Ministerio de Sanidad (FIS, 00/1116 to J.M.A.), Spain, and Universitat de Barcelona (to A.F.). R.V. holds a fellowship from the Universitat de Barcelona.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Elsevier
dc.relation.ispartof FEBS Letters. 2003;536(1-3):45-50
dc.rights © Elsevier. This is the published version of an article http://dx.doi.org/10.1016/S0014-5793(03)00009-7 that appeared in the journal FEBS Letters. It is published in an Open Archive under an Elsevier user license. Details of this licence are available here: http://www.elsevier.com/about/open-access/open-access-policies/oa-license-policy/elsevier-user-license
dc.subject.other Cervell -- Metabolisme
dc.subject.other Canals de potassi
dc.title Impaired voltage-gated K+ channel expression in brain during experimental cancer cachexia
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1016/S0014-5793(03)00009-7
dc.subject.keyword Potassium channel
dc.subject.keyword Cancer cachexia
dc.subject.keyword Apoptosis
dc.subject.keyword Brain
dc.subject.keyword Anorexia
dc.relation.projectID info:eu-repo/grantAgreement/ES/1PN/BFI2002-00764
dc.relation.projectID info:eu-repo/grantAgreement/ES/1PN/BFI2002-02186
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion

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