ArticleInternational journal of physiology, pathophysiology and pharmacology2012
Proteomic analysis of 14-3-3 zeta binding proteins in the mouse hippocampus.
Article in International journal of physiology, pathophysiology and pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Hippocampal Mitochondrial Dysfunction and Synaptic Disruption Link Organophosphate Exposure to Pre-Diabetes: An LC-MS/MS-Based Proteomics Approach.Biomolecules · 2026Article
- 14-3-3θ phosphorylation at S232 reduces its interactome and regulates axonal trafficking.Disease models & mechanisms · 2025Article
- 14-3-3ζ Constrains insulin secretion by regulating mitochondrial function in pancreatic β cells.JCI insight · 2022Article
- Redox proteomics and amyloid β-peptide: insights into Alzheimer disease.Journal of neurochemistry · 2019Review
- Molecular Cloning and Effects ofGenes · 2018Article
- Hippocampal Proteome of Rats Subjected to the Li-Pilocarpine Epilepsy Model and the Effect of Carisbamate Treatment.Pharmaceuticals (Basel, Switzerland) · 2017Article
- Posttranscriptional regulation of 14-3-3ζ by RNA-binding protein HuR modulating intestinal epithelial restitution after wounding.Physiological reports · 2016Article
- Differential expression of serum proteins in rats subchronically exposed to arsenic identified by iTRAQ-based proteomic technology-14-3-3 ζ protein to serve as a potential biomarker.Toxicology research · 2016Article
- 14-3-3ζ deficient mice in the BALB/c background display behavioural and anatomical defects associated with neurodevelopmental disorders.Scientific reports · 2015Article
- Overexpression of 14-3-3ζ Increases Brain Levels of C/EBP Homologous Protein CHOP.Journal of molecular neuroscience : MN · 2015Article
- Proteins recruited to exosomes by tau overexpression implicate novel cellular mechanisms linking tau secretion with Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2014Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
14-3-3 proteins are ubiquitous molecular chaperones with important roles in brain development and neuronal function. Altered expression of 14-3-3 proteins has been reported in several neurologic and neurodegenerative disorders and identifying 14-3-3 binding proteins may provide important insights into the physiologic and pathophysiologic roles of these proteins. Particular interest has emerged on 14-3-3 zeta (ζ) in the setting of neuronal injury because reducing 14-3-3ζ levels triggers an endoplasmic reticulum stress-like response in neurons and increases vulnerability to excitotoxicity. Here we examined the subcellular distribution of 14-3-3ζ in the mouse hippocampus. We then used recombinant His-tagged 14-3-3ζ to pull-down interacting proteins from the mouse hippocampus followed by identification by liquid chromatography-mass spectrometry. 14-3-3ζ protein was present in the cytoplasm, microsomal compartment, nucleus and mitochondrial fractions of the mouse hippocampus. Recombinant 14-3-3ζ eluted 13 known 14-3-3 binding partners, including three other 14-3-3 isoforms, and 16 other proteins which have not previously been reported to bind 14-3-3ζ. The present study identifies potentially novel 14-3-3ζ binding proteins and contributes to defining the 14-3-3ζ interactome in the mouse brain.
Indexed as
Identifiers
22837806PMC3403563W1837914011What OpenQuestion holds
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.