ArticleNeurobiology of disease2005
Transcriptional repression and cell death induced by nuclear aggregates of non-polyglutamine protein.
Article in Neurobiology of disease, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
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- Autophagy Dysfunction and Neurodegeneration: Where Does It Go Wrong?Journal of molecular biology · 2025Review
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Article
- Identification of a multienzyme complex for glucose metabolism in living cells.The Journal of biological chemistry · 2017Article
- Sequestration-Mediated Downregulation of de Novo Purine Biosynthesis by AMPK.ACS chemical biology · 2016Article
- Dynamic architecture of the purinosome involved in human de novo purine biosynthesis.Biochemistry · 2015Article
- Calpain 5 is highly expressed in the central nervous system (CNS), carries dual nuclear localization signals, and is associated with nuclear promyelocytic leukemia protein bodies.The Journal of biological chemistry · 2014Article
- Cellular maintenance of nuclear protein homeostasis.Cellular and molecular life sciences : CMLS · 2014Review
- Misfolded proteins recognition strategies of E3 ubiquitin ligases and neurodegenerative diseases.Molecular neurobiology · 2013Review
- Overexpression of the transcriptional repressor complex BCL-6/BCoR leads to nuclear aggregates distinct from classical aggresomes.PloS one · 2013Article
- Dab2 is a key regulator of endocytosis and post-endocytic trafficking of the cystic fibrosis transmembrane conductance regulator.The Biochemical journal · 2012Article
- Efficient induction of nuclear aggresomes by specific single missense mutations in the DNA-binding domain of a viral AP-1 homolog.The Journal of biological chemistry · 2011Article
- Human cytomegalovirus UL97 kinase prevents the deposition of mutant protein aggregates in cellular models of Huntington's disease and ataxia.Neurobiology of disease · 2011Article
- A short polypeptide from the herpes simplex virus type 2 ICP10 gene can induce antigen aggregation and autophagosomal degradation for enhanced immune presentation.Human gene therapy · 2010Article
- Progressive multifocal leukoencephalopathy and promyelocytic leukemia nuclear bodies: a review of clinical, neuropathological, and virological aspects of JC virus-induced demyelinating disease.Acta neuropathologica · 2010Review
- Puromycin-based vectors promote a ROS-dependent recruitment of PML to nuclear inclusions enriched with HSP70 and Proteasomes.BMC cell biology · 2009Article
- Localization and importance of the adenovirus E4orf4 protein during lytic infection.Journal of virology · 2009Article
- Human cytomegalovirus UL97 kinase activity is required for the hyperphosphorylation of retinoblastoma protein and inhibits the formation of nuclear aggresomes.Journal of virology · 2008Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear aggregates of polyglutamine (polyQ)-expanded proteins are associated with a number of neurodegenerative diseases including Huntington's disease (HD) and spinocerebellar ataxias (SCAs). The nuclear deposition of polyQ proteins correlates with rearrangements of nuclear matrix, transcriptional dysregulation, and cell death. To explore the requirement for polyQ tracks in educing such cellular responses, we examined whether a non-polyQ protein can deposit as nuclear aggregates and elicit similar responses. We report that a protein chimera (GFP170*) composed of the green fluorescent protein (GFP) fused to an internal fragment of the Golgi Complex Protein (GCP-170) forms nuclear aggregates analogous to those formed by polyQ proteins. Like the polyQ nuclear aggregates, GFP170* inclusions recruit molecular chaperones and proteasomal components, alter nuclear structures containing the promyelocytic leukemia protein (PML), recruit transcriptional factors such as CREB-binding protein (CBP) and p53, repress p53 transcriptional activity, and induce cell death. Our results indicate that nuclear aggregation and transcriptional effects are not unique to polyQ-containing proteins and may represent a general response to misfolded proteins in the nucleus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.