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http://dx.doi.org/10.1084/jem.2014228803082017c | DOI Listing |
Biochim Biophys Acta Mol Basis Dis
January 2024
Institute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, Aveiro, Portugal. Electronic address:
Alzheimer's Disease (AD) is a neurodegenerative disorder characterized by accumulation of β-amyloid aggregates and loss of proteostasis. Transfer RNA (tRNA) modifications play a crucial role in maintaining proteostasis, but their impact in AD remains unclear. Here, we report that expression of the tRNA modifying enzyme ELP3 is reduced in the brain of AD patients and amyloid mouse models and negatively correlates with amyloid plaque mean density.
View Article and Find Full Text PDFPLoS Genet
January 2010
C. elegans Genetics, IFOM, Fondazione Istituto FIRC di Oncologia Molecolare, Milan, Italy.
Although acetylated alpha-tubulin is known to be a marker of stable microtubules in neurons, precise factors that regulate alpha-tubulin acetylation are, to date, largely unknown. Therefore, a genetic screen was employed in the nematode Caenorhabditis elegans that identified the Elongator complex as a possible regulator of alpha-tubulin acetylation. Detailed characterization of mutant animals revealed that the acetyltransferase activity of the Elongator is indeed required for correct acetylation of microtubules and for neuronal development.
View Article and Find Full Text PDFMol Genet Genomics
May 2005
Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, PR China.
Functions of the Elp3 subunit of the recently purified human Elongator were studied using an in vivo yeast complementation system. We demonstrated that the human ELP3 gene (hELP3) was able partially to complement functional defects of yeast elp3Delta cells. Furthermore, a chimeric ELP3 gene (yhELP3) encoding a protein in which the putative histone acetyltransferase (HAT) domain of hELP3 fused to the remainder of the yeast Elp3p corrected the growth defects of elp3Delta cells and complemented the slow activation of some inducible genes.
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