Déjà vu with a twist: transglutaminases in bioenergetics and transcriptional dysfunction in Huntington's disease.

Abstract

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.

• Authors: Parsa Kazemi-Esfarjani, Albert R La Spada
• Journal: EMBO molecular medicine (EMBO Mol Med) Vol. 2 Issue 9 Pg. 335-7 (Sep 2010) ISSN: 1757-4684 [Electronic] England
• PMID: 20730854 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Comment)

Chemical References

• Enzyme Inhibitors
• Histones
• Peptides
• Polyamines
• Protein Glutamine gamma Glutamyltransferase 2
• Transglutaminases
• GTP-Binding Proteins

Topics

• Animals
• Disease Models, Animal
• Drosophila
• Energy Metabolism
• Enzyme Inhibitors (pharmacology)
• GTP-Binding Proteins (antagonists & inhibitors, genetics, metabolism)
• Histones (metabolism)
• Humans
• Huntington Disease (enzymology, genetics, metabolism)
• Peptides (pharmacology)
• Polyamines (metabolism)
• Protein Glutamine gamma Glutamyltransferase 2
• Transcription, Genetic
• Transglutaminases (antagonists & inhibitors, genetics, metabolism)