Linked Life Data

14743368

Source:http://linkedlifedata.com/resource/pubmed/id/14743368

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-1-26
pubmed:abstractText
Mutations in the parkin gene (PRKN) are the commonest cause of juvenile and early-onset parkinsonism. However, the pathogenic mechanism by which loss of parkin protein results in degeneration of dopaminergic neurons remains elusive. Animal models provide a useful tool for the study of development and disease, and the recent production of transgenic fly and mouse parkin deficient models allows investigation of the molecular role of parkin in dopamine regulation and nigrostriatal function. We have identified the mouse mutant Quaking as a spontaneously occurring PRKN knockout. The quaking mutation is a deletion of approximately 1.17 Mb of mouse chromosome 17, resulting in the deletion of the entire promoter and first five coding exons of PRKN In addition, the recently described Parkin Co-Regulated Gene (PACRG) is completely deleted. Homozygous Quaking mice show a complete loss of PRKN and PACRG mRNA and protein. These mice will constitute a useful additional model for studies of the molecular role of parkin and PACRG in neurodegeneration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0885-3185
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Movement Disorder Society
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-4
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
It's a double knock-out! The quaking mouse is a spontaneous deletion of parkin and parkin co-regulated gene (PACRG).
pubmed:affiliation
Mayo Clinic Jacksonville, Jacksonville, Florida 32224, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't