ReviewCerebellum (London, England)2010
14-3-3 proteins and spinocerebellar ataxia type 1: from molecular interaction to human neuropathology.
Review in Cerebellum (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 20 citations in OpenAlex.
- 14-3-3 proteins-a moonlight protein complex with therapeutic potential in neurological disorder: in-depth review with Alzheimer's disease.Frontiers in molecular biosciences · 2024Review
- Epilepsy as the symptom of a spinocerebellar ataxia 13 in a patient presenting with a mutation in the KCNC3 gene.BMC neurology · 2023Article
- On the identification of potential novel therapeutic targets for spinocerebellar ataxia type 1 (SCA1) neurodegenerative disease using EvoPPI3.Journal of integrative bioinformatics · 2023Article
- Beyond the glutamine expansion: influence of posttranslational modifications of ataxin-1 in the pathogenesis of spinocerebellar ataxia type 1.Molecular neurobiology · 2014Review
- The importance of serine 776 in Ataxin-1 partner selection: a FRET analysis.Scientific reports · 2012Article
- Application of systems biology approach identifies and validates GRB2 as a risk gene for schizophrenia in the Irish Case Control Study of Schizophrenia (ICCSS) sample.Schizophrenia research · 2011Article
- Dopamine D2 receptor signaling modulates mutant ataxin-1 S776 phosphorylation and aggregation.Journal of neurochemistry · 2010Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This mini-review focuses on the possible relevance of 14-3-3 proteins in spinocerebellar ataxia type 1 (SCA1). 14-3-3 proteins are mainly localized in the synapses and neuronal cytoplasm, and seven isoforms have been identified in mammals. This family of proteins was initially identified as adaptor proteins which bind to phosphoserine-containing motifs. Binding motifs and potential functions of 14-3-3 proteins are now recognized to have a wide range of functional relevance. SCA1 is an autosomal-dominant neurodegenerative disorder and is linked to polyglutamine expansion (ataxin-1 protein). The Zoghbi and Orr group showed direct interaction of 14-3-3 proteins with ataxin-1 where nuclear recruitment of the ataxin-1 protein is dependent on its phosphorylation. This targeted binding of 14-3-3 protein to phosphorylated ataxin-1 to stabilize ataxin-1 in cellular models was corroborated by our double-labeling study for expanded polyglutamine and 14-3-3 proteins which demonstrated colocalization of these two epitopes in the neuronal nuclei in human autopsied brains with SCA1. Ataxin-1/14-3-3 protein interaction is a new potential target for therapeutic intervention in the treatment of SCA1.
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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.