ArticleAnnals of clinical and translational neurology2017
Dysregulation of 14-3-3 proteins in neurodegenerative diseases with Lewy body or Alzheimer pathology.
Article in Annals of clinical and translational neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- 14-3-3σ up-regulation in the temporal cortex associates with tau pathology and reactive astroglia in Lewy body disorders.Brain pathology (Zurich, Switzerland) · 2026Article
- 14-3-3θ phosphorylation at S232 reduces its interactome and regulates axonal trafficking.Disease models & mechanisms · 2025Article
- 14-3-3 Proteins Negatively Regulate Microglial Activation via Inhibition of the NF-κB Pathway.Journal of neurochemistry · 2025Article
- Brain proteome changes after intracerebral hemorrhage in aged male and female mice.Neurobiology of disease · 2025Article
- A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects.Biology open · 2025Article
- Characterization of multiple binding sites on microtubule associated protein 2c recognized by dimeric and monomeric 14-3-3ζ.The FEBS journal · 2025Article
- 14-3-3θ phosphorylation exacerbates alpha-synuclein aggregation and toxicity.Neurobiology of disease · 2025Article
- 14-3-3 phosphorylation inhibits 14-3-3θ's ability to regulate LRRK2 kinase activity and toxicity.Human molecular genetics · 2024Article
- Toxic interactions between dopamine, α-synuclein, monoamine oxidase, and genes in mitochondria of Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Cortical thickness modeling and variability in Alzheimer's disease and frontotemporal dementia.Journal of neurology · 2024Article
- 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
- Pathways to Parkinson's disease: a spotlight on 14-3-3 proteins.NPJ Parkinson's disease · 2021Review
- 14-3-3 Proteins: Novel Pharmacological Targets in Neurodegenerative Diseases.Trends in pharmacological sciences · 2021Review
- 14-3-3 mitigates alpha-synuclein aggregation and toxicity in the in vivo preformed fibril model.Acta neuropathologica communications · 2021Article
- Inhibition of 14-3-3 Proteins Alters Neural Oscillations in Mice.Frontiers in neural circuits · 2021Article
- 14-3-3σ and Its Modulators in Cancer.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Genealogy of the neurodegenerative diseases based on a meta-analysis of age-stratified incidence data.Scientific reports · 2020Article
- 007 (x2)-3-3: 14-3-3 Targeted Compounds as Double Agents.Trends in pharmacological sciences · 2020Article
- The GTPase Rab27b regulates the release, autophagic clearance, and toxicity of α-synuclein.The Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe highly conserved 14-3-3 proteins interact with key players involved in Parkinson's disease (PD) and other neurodegenerative disorders. We recently demonstrated that 14-3-3 phosphorylation is increased in PD models and that increased 14-3-3 phosphorylation reduces the neuroprotective effects of 14-3-3 proteins. Here, we investigated whether 14-3-3 phosphorylation is altered in postmortem brains from control, PD, Alzheimer's Disease (AD), Alzheimer's with Lewy Bodies (ADLB), Dementia with Lewy Bodies (DLB), and Progressive Supranuclear Palsy (PSP) subjects at three conserved sites: serine 58 (S58), serine 185 (S185), and serine 232 (S232).
methodsS58, S185, and S232 phosphorylation was measured by western blot analysis of Triton X-100 soluble and insoluble fractions from postmortem temporal cortex.
resultsThe ratio of soluble phospho-S232 to insoluble phospho-S232 was reduced by 32%, 60%, 37%, and 52% in PD, AD, ADLB, and DLB, respectively. S185 and S58 phosphorylation were mildly elevated in the soluble fraction in DLB. We also noted a dramatic reduction in soluble pan 14-3-3 levels by ~35% in AD, ADLB, and DLB. Lower ratios of soluble to insoluble S232 phosphorylation (pointing to higher insoluble pS232) correlated with lower soluble pan 14-3-3 levels, suggesting that S232 phosphorylation may promote insolubilization of 14-3-3s. The phospho-S232 ratio and soluble pan 14-3-3 levels correlated with clinical and pathological severity.
interpretationThese data reveal dysregulation of 14-3-3 proteins in neurodegeneration associated with Lewy body or Alzheimer pathology. S232 phosphorylation may drive insolubilization of 14-3-3s and thus contribute to the pathophysiology in neurodegenerative disorders associated with Lewy body or Alzheimer pathology.
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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.