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The genome of Drosophila contains a single UBQLN homolog (dUbqn) that shows high similarity to UBQLN1 and UBQLN2; therefore, the fly is a useful model for characterizing the role of UBQLN in vivo in neurological disorders affecting locomotion and learning abilities.
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Thus, UBQLN1 plays an important role in clearing mislocalized mitochondrial proteins upon cell stimulation, and its absence leads to suppression of protein synthesis and cell cycle arrest.
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UBQLN1 variant was not associated with the risk of Alzheimer's disease.
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The STI and UBA Domains of UBQLN1 Are Critical Determinants of Substrate Interaction and Proteostasis.
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Following the loss of UBQLN1 in lung adenocarcinoma cells, there is an accelerated loss of IGF1R.
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Ubiquilins are a family of chaperones for cytosolically exposed transmembrane domains and use ubiquitin to triage clients for degradation via coordinated intra- and intermolecular interactions.
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The evidence of genetic associations has been found for the multivariate response phenotype that involves trans effects modulating expression of genes following heat shock, including HSF1 and UBQLN1.
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Results suggest that ubiquilin-1 may mechanistically participate in Alzheimer's disease molecular pathogenesis by affecting BACE1 and thereby APP processing and Abeta accumulation
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The expression level of UBQLN1 and prognosis in breast cancer is clarified for the first time and UBQLN1 seems to be a novel molecular marker to predict poor prognosis in breast cancer.
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The results suggest that UBQ-8i polymorphism may contribute to Alzheimer's disease susceptibility, but does not synergize with APOEepsilon4 status to increase Alzheimer's disease risk.
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These results suggest that the UBQ-8i polymorphism is associated with Alzheimer's disease risk.
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found that ZEB1 is required for induction of mesenchymal-like properties following loss of UBQLN1 and ZEB1 is capable of repressing expression of UBQLN1
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High UBQLN1 expression is associated with low radiosensitivity in breast cancer.
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Ubiquilin-1 immunoreactivity is concentrated on Hirano bodies and dystrophic neurites in Alzheimer's disease
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Human ubiquilin-1 overexpression in transgenic mice increases the lifespan and delays accumulation of Huntingtin aggregates in the R6/2 mouse model of Huntington's disease.
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The results demonstrate that in Alzheimer's disease hippocampus, ubiquilin-1 immunoreactivity increases in the neuronal nucleoplasm and is associated with region-specific neurofibrillary changes.
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results were confirmed by similar findings for ubiquilin-1 and -2 in human brain tissue sections, where accumulation was observed in huntingtin inclusions
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Targeting of Ubqln1 to autophagosomes requires the Ubqln4 UBL domain and the Ubqln1 UBA domain.
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data suggest that ubiquilin-1 modulates gamma-secretase-mediated epsilon-site cleavage and thus may play a role in regulating gamma-secretase cleavage of various substrates.
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Genetic variants in UBQLN1 are not commonly associated with amyotrophic lateral sclerosis
