ArticleThe Journal of biological chemistry2010
Endotoxin conditioning induces VCP/p97-mediated and inducible nitric-oxide synthase-dependent Tyr284 nitration in protein phosphatase 2A.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- PME-1 sensitizes glioblastoma cells to oxidative stress-induced cell death by attenuating PP2A-B55α-mediated inactivation of MAPKAPK2-RIPK1 signaling.Cell death discovery · 2023Article
- Is Nucleoredoxin a Master Regulator of Cellular Redox Homeostasis? Its Implication in Different Pathologies.Antioxidants (Basel, Switzerland) · 2022Review
- Editorial: The Roles of Mitochondria in Immunity.Frontiers in immunology · 2022Article
- Regulation of Cardiac PKA Signaling by cAMP and Oxidants.Antioxidants (Basel, Switzerland) · 2021Review
- Taurine Antagonizes Macrophages M1 Polarization by Mitophagy-Glycolysis Switch BlockageFrontiers in immunology · 2021Article
- Redox inhibition of protein phosphatase PP2A: Potential implications in oncogenesis and its progression.Redox biology · 2019Review
- The role of SET/I2PP2A in canine mammary tumors.Scientific reports · 2017Article
- Article
- Quantitative proteomics reveals novel protein interaction partners of PP2A catalytic subunit in pancreatic β-cells.Molecular and cellular endocrinology · 2016Article
- Blocking protein phosphatase 2A signaling prevents endothelial-to-mesenchymal transition and renal fibrosis: a peptide-based drug therapy.Scientific reports · 2016Article
- The therapeutic effects of SET/I2PP2A inhibitors on canine melanoma.The Journal of veterinary medical science · 2015Article
- Protein Phosphatase Methyl-Esterase PME-1 Protects Protein Phosphatase 2A from Ubiquitin/Proteasome Degradation.PloS one · 2015Article
- Characterization of SET/I2PP2A isoforms in dogs.The Journal of veterinary medical science · 2014Article
- Evaluation of vitamin C for adjuvant sepsis therapy.Antioxidants & redox signaling · 2013Review
- The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013Review
- Nitric oxide-dependent downregulation of BRCA1 expression promotes genetic instability.Cancer research · 2013Article
- A dual role for receptor-interacting protein kinase 2 (RIP2) kinase activity in nucleotide-binding oligomerization domain 2 (NOD2)-dependent autophagy.The Journal of biological chemistry · 2012Article
- Ascorbate protects against vascular leakage in cecal ligation and puncture-induced septic peritonitis.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Article
- Protein tyrosine nitration in cellular signal transduction pathways.Journal of receptor and signal transduction research · 2010Review
- Mammalian Ste20-like kinase (Mst2) indirectly supports Raf-1/ERK pathway activity via maintenance of protein phosphatase-2A catalytic subunit levels and consequent suppression of inhibitory Raf-1 phosphorylation.The Journal of biological chemistry · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Endotoxins activate Toll-like receptors and reprogram cells to be refractory to secondary exposure. Here we found that activation of different Toll-like receptors elicited a time- and dose-dependent increase in the levels of the protein phosphatase 2A catalytic subunit (PP2Ac) but not its partner A subunit. We purified the lipopolysaccharide-induced form of PP2A by chromatography plus immunoprecipitation and used mass spectrometry to identify VCP/p97 as a novel partner for PP2Ac. Endogenous VCP/p97 and PP2Ac were co-immunoprecipitated from primary murine macrophages and human lymphocytes. GST-VCP/p97 bound purified PP2A in pulldown assays, showing direct protein-protein interaction. Endotoxin conditioning of macrophages induced formation of 3-nitrotyrosine in the PP2Ac associated with VCP/p97, a response severely reduced in macrophages from iNOS knock-out mice. The reaction of purified PP2A with peroxynitrite dissociated the A subunit, and 3-nitro-Tyr(284) was identified in PP2Ac by mass spectrometry. Myc-PP2Ac (Y284F) expressed in cells was resistant to peroxynitrite-induced nitration and reduction of A subunit binding. Transient expression of either VCP/p97 or PP2Ac was sufficient to elevate levels of the dual specificity phosphatase DUSP1, reduce p38 MAPK activation, and suppress tumor necrosis factor-alpha release. We propose that VCP/p97-mediated Tyr nitration of PP2A increases the levels of phosphatases PP2A and DUSP1 to contribute to the refractory response of conditioned cells.
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