P4-154: THE PROTEIN QUALITY CONTROL PROTEIN, UBIQUILIN-2, REGULATES TAU ACCUMULATION
نویسندگان
چکیده
منابع مشابه
Ubiquilin-1 and protein quality control in Alzheimer disease
Single nucleotide polymorphisms in the ubiquilin-1 gene may confer risk for late-onset Alzheimer disease (AD). We have shown previously that ubiquilin-1 functions as a molecular chaperone for the amyloid precursor protein (APP) and that protein levels of ubiquilin-1 are decreased in the brains of AD patients. We have recently found that ubiquilin-1 regulates APP trafficking and subsequent secre...
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Tau is one of several types of microtubule-associated proteins (MAPs), responsible for the assembly and stability of microtubule networks that is present only in neurons and predominantly localized in axons which its functions are tightly regulated by phosphorylation. Via as yet unknown mechanisms, tau becomes hyperphosphorylated and accompanies with neuronal degeneration, loss of synapses...
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Accumulation of aberrant proteins in inclusion bodies is a hallmark of many neurodegenerative diseases. Impairment of proteolytic systems is a common event in these protein misfolding diseases. Recently, mutations in the UBQLN 2 gene encoding ubiquilin 2 have been identified in X-linked amyotrophic lateral sclerosis (ALS). Furthermore, ubiquilin 2 is associated with inclusions in familial and s...
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Cellular toxicity introduced by protein misfolding threatens cell fitness and viability. Failure to eliminate these polypeptides is associated with various aggregation diseases. In eukaryotes, the ubiquitin proteasome system (UPS) plays a vital role in protein quality control (PQC), by selectively targeting misfolded proteins for degradation. While the assembly of the proteasome can be naturall...
متن کاملIdentification of Ubiquilin, a Novel Presenilin Interactor That Increases Presenilin Protein Accumulation
Mutations in the highly homologous presenilin genes encoding presenilin-1 and presenilin-2 (PS1 and PS2) are linked to early-onset Alzheimer's disease (AD). However, apart from a role in early development, neither the normal function of the presenilins nor the mechanisms by which mutant proteins cause AD are well understood. We describe here the properties of a novel human interactor of the pre...
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ژورنال
عنوان ژورنال: Alzheimer's & Dementia
سال: 2019
ISSN: 1552-5260
DOI: 10.1016/j.jalz.2019.06.3816