Title | Transglutaminases and neurodegeneration. |
Publication Type | Journal Article |
Year of Publication | 2009 |
Authors | Jeitner TM, Pinto JT, Krasnikov BF, Horswill M, Cooper AJL |
Journal | J Neurochem |
Volume | 109 Suppl 1 |
Pagination | 160-6 |
Date Published | 2009 May |
ISSN | 1471-4159 |
Keywords | Animals, Brain, Humans, Nerve Degeneration, Neurodegenerative Diseases, Transglutaminases |
Abstract | Transglutaminases (TGs) are Ca2+-dependent enzymes that catalyze a variety of modifications of glutaminyl (Q) residues. In the brain, these modifications include the covalent attachment of a number of amine-bearing compounds, including lysyl (K) residues and polyamines, which serve to either regulate enzyme activity or attach the TG substrates to biological matrices. Aberrant TG activity is thought to contribute to Alzheimer disease, Parkinson disease, Huntington disease, and supranuclear palsy. Strategies designed to interfere with TG activity have some benefit in animal models of Huntington and Parkinson diseases. The following review summarizes the involvement of TGs in neurodegenerative diseases and discusses the possible use of selective inhibitors as therapeutic agents in these diseases. |
DOI | 10.1111/j.1471-4159.2009.05843.x |
Alternate Journal | J Neurochem |
PubMed ID | 19393023 |
PubMed Central ID | PMC2752967 |
Grant List | P01 AG014930 / AG / NIA NIH HHS / United States P01 AG014930-05A20004 / AG / NIA NIH HHS / United States P01 AG14930 / AG / NIA NIH HHS / United States |
Related Institute:
Molecular Imaging Innovations Institute (MI3)