https://transhumanist.ru/index.php?action=history&feed=atom&title=PQBP1 2026-06-20T18:10:54Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=PQBP1&diff=5538&oldid=prev 2021-05-12T13:48:45Z

<p>Новая страница: «Polyglutamine-binding protein 1 (PQBP-1) (38 kDa nuclear protein containing a WW domain) (Npw38) (Polyglutamine tract-binding protein 1) [NPW38] [JM26] ==Publica...»</p> <p><b>Новая страница</b></p><div>Polyglutamine-binding protein 1 (PQBP-1) (38 kDa nuclear protein containing a WW domain) (Npw38) (Polyglutamine tract-binding protein 1) [NPW38] [JM26]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=A restricted level of [[PQBP1]] is needed for the best longevity of Drosophila.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22901698<br /> |abstract=A number of neurological diseases are caused by mutations of RNA metabolism-related genes. A complicating issue is that whether under- or overfunction of such genes is responsible for the phenotype. Polyglutamine tract binding protein-1, a causative gene for X-linked mental retardation, is also involved in RNA metabolism, and both mutation and duplication of the gene were reported in human patients. In this study, we first report a novel phenotype of d[[PQBP1]] (drosophila homolog of Polyglutamine tract binding protein-1)-mutant flies, lifespan shortening. We next address the gene dose-phenotype relationship in lifespan shortening and in learning disability, a previously described phenotype. The 2 phenotypes are rescued by d[[PQBP1]] but in different dose-phenotype relationships. Either insufficient or excessive expression of d[[PQBP1]] does not recover lifespan, while excessive expression recovers learning ability. We finally address the mechanism of lifespan shortening. Tissue-specific expression of d[[PQBP1]]-RNA interference construct reveals both neural and nonneural d[[PQBP1]] contribute to the lifespan, while the latter has a dominant effect. Gene expression profiling suggested retinophilin/MORN repeat containing 4, a gene promoting axonal degeneration, to contribute to lifespan shortening by neural d[[PQBP1]]. Systems biology analysis of the gene expression profiles revealed indirect influence of d[[PQBP1]] on insulin-like growth factor 1, insulin receptor, and peroxisome proliferator-activated receptorα/γ signaling pathways in nonneural tissues. Collectively, given that d[[PQBP1]] affects multiple pathways in different dose-dependent and tissue-specific manners, d[[PQBP1]] at a restricted expression level is needed for the best longevity.<br /> |mesh-terms=* Age Factors<br /> * Animals<br /> * Animals, Genetically Modified<br /> * Caenorhabditis elegans<br /> * Carrier Proteins<br /> * DNA-Binding Proteins<br /> * Drosophila<br /> * Enzyme Inhibitors<br /> * Gene Regulatory Networks<br /> * Humans<br /> * Hydroxamic Acids<br /> * Learning Disabilities<br /> * Longevity<br /> * Mutation<br /> * Neuroglia<br /> * Neurons<br /> * Nuclear Proteins<br /> * Phenotype<br /> <br /> |full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2012.07.015<br /> }}</div>

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