Linked Life Data

12600719

Source:http://linkedlifedata.com/resource/pubmed/id/12600719

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-2-25
pubmed:abstractText
The expression of different cell cycle proteins in terminally differentiated neurons apparently precedes cell death or contributes to pathogenetic progression of Alzheimer's disease (AD). Cyclins and cyclin-dependent kinases (Cdks), physiologically involved in mitotic processes of proliferating cells, are elevated in neurons prone to dedifferentiation and degeneration. Previously, it was shown that even inhibitors of the Cdks as p16(INK4a), p18(INK4c) or p27(KIP1) are expressed in neurons of AD patients, indicating a rather complete involvement of cell cycle machinery in affected neurons. The aim of this study was to examine the involvement of the non-classical cyclin C in the pathogenetic process of AD. A marked elevated immunoreactivity of cyclin C was found both in neurons and astrocytes in AD. Increased levels of cyclin C RNA were detected by ribonuclease protection assay (RPA) in severe AD cases. Colocalization of cyclin C and its preferred binding partner, Cdk8, was only observed in astrocytes but not in neurons. The present observations suggest different cellular functions of cyclin C in neurons and astrocytes in AD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0197-4580
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
427-35
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:articleTitle
Cyclin C expression is involved in the pathogenesis of Alzheimer's disease.
pubmed:affiliation
Department of Neuroanatomy, Paul Flechsig Institute for Brain Research, University of Leipzig, Jahnallee 59, D-04109, Leipzig, Germany. uebu@medizin.uni-leipzig.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't