ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
Quantitative phosphoproteomic analysis of neuronal intermediate filament proteins (NF-M/H) in Alzheimer's disease by iTRAQ.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 70 citations in OpenAlex.
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- A Proteome-Wide Effect of PHF8 Knockdown on Cortical Neurons Shows Downregulation of Parkinson's Disease-Associated Protein Alpha-Synuclein and Its Interactors.Biomedicines · 2023Article
- Posttranscriptional regulation of neurofilament proteins and tau in health and disease.Brain research bulletin · 2023Review
- Unraveling axonal mechanisms of traumatic brain injury.Acta neuropathologica communications · 2022Article
- Neurofilament Proteins as Biomarkers to Monitor Neurological Diseases and the Efficacy of Therapies.Frontiers in neuroscience · 2021Review
- Review
- TFP5, a Peptide Inhibitor of Aberrant and Hyperactive Cdk5/p25, Attenuates Pathological Phenotypes and Restores Synaptic Function in CK-p25Tg Mice.Journal of Alzheimer's disease : JAD · 2017Article
- Mechanisms and Consequences of Dopamine Depletion-Induced Attenuation of the Spinophilin/Neurofilament Medium Interaction.Neural plasticity · 2017Article
- Quantitative Proteomic Analysis Reveals Similarities between Huntington's Disease (HD) and Huntington's Disease-Like 2 (HDL2) Human Brains.Journal of proteome research · 2016Article
- Specialized roles of neurofilament proteins in synapses: Relevance to neuropsychiatric disorders.Brain research bulletin · 2016Review
- Mass spectrometric phosphoproteome analysis of HIV-infected brain reveals novel phosphorylation sites and differential phosphorylation patterns.Proteomics. Clinical applications · 2016Article
- Neurodegeneration and Alzheimer's disease (AD). What Can Proteomics Tell Us About the Alzheimer's Brain?Molecular & cellular proteomics : MCP · 2016Review
- Approaches for targeted proteomics and its potential applications in neuroscience.Journal of biosciences · 2015Review
- Dynamic self-guiding analysis of Alzheimer's disease.Oncotarget · 2015Review
- Quantitative phosphoproteomics of Alzheimer's disease reveals cross-talk between kinases and small heat shock proteins.Proteomics · 2015Article
- Quantitative phosphoproteomic profiling of fiber differentiation and initiation in a fiberless mutant of cotton.BMC genomics · 2014Article
- New insight into neurodegeneration: the role of proteomics.Molecular neurobiology · 2014Review
- Post-translational modifications of intermediate filament proteins: mechanisms and functions.Nature reviews. Molecular cell biology · 2014Review
- Regulation of Sox6 by cyclin dependent kinase 5 in brain.PloS one · 2014Article
- Searching for novel Cdk5 substrates in brain by comparative phosphoproteomics of wild type and Cdk5-/- mice.PloS one · 2014Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Aberrant hyperphosphorylation of neuronal cytoskeletal proteins is one of the major pathological hallmarks of neurodegenerative disorders such as Alzheimer disease (AD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD). Human NF-M/H display a large number of multiple KSP repeats in the carboxy-terminal tail domain, which are phosphorylation sites of proline-directed serine/threonine (pSer/Thr-Pro, KS/T-P) kinases. The phosphorylation sites of NF-M/H have not been characterized in AD brain. Here, we use quantitative phosphoproteomic methodology, isobaric tag for relative and absolute quantitation (iTRAQ), for the characterization of NF-M/H phosphorylation sites in AD brain. We identified 13 hyperphosphorylated sites of NF-M; 9 Lys-Ser-Pro (KSP) sites; 2 variant motifs, Glu-Ser-Pro (ESP) Ser-736 and Leu-Ser-Pro (LSP) Ser-837; and 2 non-S/T-P motifs, Ser-783 and Ser-788. All the Ser/Thr residues are phosphorylated at significantly greater abundance in AD brain compared with control brain. Ten hyperphosphorylated KSP sites have been identified on the C-terminal tail domain of NF-H, with greater abundance of phosphorylation in AD brain compared with control brain. Our data provide the direct evidence that NF-M/H are hyperphosphorylated in AD compared with control brain and suggest the role of both proline-directed and non-proline-directed protein kinases in AD. This study represents the first comprehensive iTRAQ analyses and quantification of phosphorylation sites of human NF-M and NF-H from AD brain and suggests that aberrant hyperphosphorylation of neuronal intermediate filament proteins is involved in AD.
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