Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2010-9-7
pubmed:abstractText
The article by McConoughey et al in the current issue of EMBO Molecular Medicine examines the contribution of transglutaminase 2 (TG2) to Huntington's disease (HD) pathogenesis. The authors find that TG2 inhibition can ameliorate HD neurodegeneration, and thereby elevate the status of transglutaminases (TGs) to a major therapeutic target-not because of their well-known activity in mutant protein aggregation, but instead based upon their ability to epigenetically modulate transcription and energy production. While the reintroduction of TG inhibition as a therapy for HD may evoke feelings of déjà vu, the outcome this time around could go in a dramatically different direction.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1757-4684
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
335-7
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Déjà vu with a twist: transglutaminases in bioenergetics and transcriptional dysfunction in Huntington's disease.
pubmed:affiliation
Division of Genetics, Department of Pediatrics, University of California, San Diego - La Jolla, CA, USA.
pubmed:publicationType
Journal Article, Comment, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural