ArticleJournal of biomedical science2015
Identification of lipocalin-2 as a PKCδ phosphorylation substrate in neutrophils.
Article in Journal of biomedical science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Macrophage migration inhibitory factor of zoonoticiScience · 2026Article
- Article
- Single-Cell Transcriptome Reveals Cell Type-Specific Molecular Pathology in a 2VO Cerebral Ischemic Mouse Model.Molecular neurobiology · 2024Article
- Lipocalin 2 receptors: facts, fictions, and myths.Frontiers in immunology · 2023Review
- Post-stroke Impairment of the Blood-Brain Barrier and Perifocal Vasogenic Edema Is Alleviated by Endovascular Mesenchymal Stem Cell Administration: Modulation of the PKCδ/MMP9/AQP4-Mediated Pathway.Molecular neurobiology · 2022Article
- Are Physicochemical Properties Shaping the Allergenic Potency of Animal Allergens?Clinical reviews in allergy & immunology · 2022Review
- The role of lipocalin 2 in brain injury and recovery after ischemic and hemorrhagic stroke.Frontiers in molecular neuroscience · 2022Review
- Deregulated Protein Kinases: Friend and Foe in Ischemic Stroke.Molecular neurobiology · 2021Review
- Neutralization of Lipocalin-2 Diminishes Stroke-Reperfusion Injury.International journal of molecular sciences · 2020Article
- Protein kinase C in cancer: The top five unanswered questions.Molecular carcinogenesis · 2017Review
- Lipocalin-2 as an Infection-Related Biomarker to Predict Clinical Outcome in Ischemic Stroke.PloS one · 2016Article
- Lipocalin-2 in Stroke.Neuro : open journal · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPKCδ expressed in neutrophils is implicated in promoting reperfusion injury after ischemic stroke. To understand the molecular and cellular actions of PKCδ, we employed a chemical-genetics approach to identify PKCδ substrates in neutrophils.
resultsWe recently generated knock-in mice endogenously expressing analog-specific PKCδ (AS-PKCδ) that can utilize ATP analogs as phosphate donors. Using neutrophils isolated from the knock-in mice, we identified several PKCδ substrates, one of which was lipocalin-2 (LCN2), which is an iron-binding protein that can trigger apoptosis by reducing intracellular iron concentrations. We found that PKCδ phosphorylated LCN2 at T115 and this phosphorylation was reduced in Prkcd (-/-) mice. PKCδ colocalized with LCN2 in resting and stimulated neutrophils. LCN2 release from neutrophils after cerebral ischemia was reduced in PKCδ null mice.
conclusionsThese findings suggest that PKCδ phosphorylates LCN2 and mediates its release from neutrophils during ischemia-reperfusion injury.
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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.