Increase in bax expression and apoptosis are associated in Huntington's disease progression
dc.contributor.author | Teles, A. V. F. F. [UNIFESP] | |
dc.contributor.author | Rosenstock, T. R. [UNIFESP] | |
dc.contributor.author | Okuno, C. S. [UNIFESP] | |
dc.contributor.author | Lopes, G. S. [UNIFESP] | |
dc.contributor.author | Bertoncini, C. R. A. [UNIFESP] | |
dc.contributor.author | Smaili, Soraya Soubhi [UNIFESP] | |
dc.contributor.institution | Universidade Federal de São Paulo (UNIFESP) | |
dc.date.accessioned | 2016-01-24T13:51:28Z | |
dc.date.available | 2016-01-24T13:51:28Z | |
dc.date.issued | 2008-06-13 | |
dc.description.abstract | Huntington's disease (HD) is a hereditary dominant neurodegenerative disorder and the progression of the disease may be associated with apoptosis and altered expression of apoptotic proteins. the aim of this study was to investigate gene expression of bax and bcl-2 in tissues from R6/1 transgenic (TGN) mice of different ages (3, 6 and 9 months). the mRNA expression was investigated and related to apoptotic cells measured by TUNEL Results showed a significant and progressive increase in box levels in the cortex of TGN (from 10 to 33%) when compared to control (CT) (8 to 20%) mice with 3, 6 and 9-month-old. the increase in box was correlated with the elevation in the number of apoptotic nuclei, especially in the cortex of 6 (10%) and 9 (18%)-month-old mice. Increase in bax expression might be related to an apoptotic induction which contributes to the HD progression. (C) 2008 Elsevier Ireland Ltd. All rights reserved. | en |
dc.description.affiliation | Universidade Federal de São Paulo, Dept Pharmacol, BR-04044020 São Paulo, Brazil | |
dc.description.affiliation | Universidade Federal de São Paulo, CEDEME, BR-04044020 São Paulo, Brazil | |
dc.description.affiliationUnifesp | Universidade Federal de São Paulo, Dept Pharmacol, BR-04044020 São Paulo, Brazil | |
dc.description.affiliationUnifesp | Universidade Federal de São Paulo, CEDEME, BR-04044020 São Paulo, Brazil | |
dc.description.source | Web of Science | |
dc.format.extent | 59-63 | |
dc.identifier | http://dx.doi.org/10.1016/j.neulet.2008.03.062 | |
dc.identifier.citation | Neuroscience Letters. Clare: Elsevier B.V., v. 438, n. 1, p. 59-63, 2008. | |
dc.identifier.doi | 10.1016/j.neulet.2008.03.062 | |
dc.identifier.issn | 0304-3940 | |
dc.identifier.uri | http://repositorio.unifesp.br/handle/11600/30730 | |
dc.identifier.wos | WOS:000257152000014 | |
dc.language.iso | eng | |
dc.publisher | Elsevier B.V. | |
dc.relation.ispartof | Neuroscience Letters | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.rights.license | http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy | |
dc.subject | bcl-2 | en |
dc.subject | bax | en |
dc.subject | mRNA | en |
dc.subject | apoptosis | en |
dc.subject | aging | en |
dc.subject | Huntington's disease | en |
dc.subject | neurodegeneration | en |
dc.subject | cell death | en |
dc.title | Increase in bax expression and apoptosis are associated in Huntington's disease progression | en |
dc.type | info:eu-repo/semantics/article |