Linked Life Data

20732420

Source:http://linkedlifedata.com/resource/pubmed/id/20732420

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-11-16
pubmed:abstractText
The endoplasmic reticulum-stress response is induced in several neurodegenerative diseases and in cellular models of Huntington's disease. However, here we report that the processing of ATF6? to its active nuclear form, one of the three branches of endoplasmic reticulum-stress activation, is impaired in both animal models and Huntington's disease patients. ATF6? has been reported to be essential for the survival of dormant tumour cells that, like neurons, are arrested in the G0-G1 phase of the cell cycle. This effect is mediated by the small GTPase Rheb (Ras-homologue enriched in brain). Our results suggest that the ATF6?/Rheb pathway is altered in Huntington's disease as the decrease in ATF6? processing is accompanied by a decrease in the accumulation of Rheb. These alterations correlate with the aberrant accumulation of cell cycle re-entry markers in post-mitotic neurons which is accompanied by death of a subset of neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1095-953X
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
23-32
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Impaired ATF6? processing, decreased Rheb and neuronal cell cycle re-entry in Huntington's disease.
pubmed:affiliation
Centro de Biología Molecular Severo Ochoa-CSIC, UAM and CIBERNED, C/Nicolás Cabrera, 1 28049 Cantoblanco, Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't