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Title:
Regulation of Neuronal Ferritin Heavy Chain, A New Player in Opiate-Induced Chemokine Dysfunction | Journal of Neuroimmune Pharmacology
Description:
The heavy chain subunit of ferritin (FHC), a ubiquitous protein best known for its iron-sequestering activity as part of the ferritin complex, has recently been described as a novel inhibitor of signaling through the chemokine receptor CXCR4. Levels of FHC as well as its effects on CXCR4 activation increase in cortical neurons exposed to mu-opioid receptor agonists such as morphine, an effect likely specific to neurons. Major actions of CXCR4 signaling in the mature brain include a promotion of neurogenesis, activation of pro-survival signals, and modulation of excitotoxic pathways; thus, FHC up-regulation may contribute to the neuronal dysfunction often associated with opiate drug abuse. This review summarizes our knowledge of neuronal CXCR4 function, its regulation by opiates and the role of FHC in this process, and known mechanisms controlling FHC production. We speculate on the mechanism involved in FHC regulation by opiates and offer FHC as a new target in opioid-induced neuropathology.
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Keywords {π}
article, google, scholar, pubmed, cas, ferritin, chemokine, biol, cxcr, torti, regulation, meucci, iron, receptor, chem, protein, cell, heavy, sci, chain, human, biochem, usa, signaling, cells, regulatory, acad, neuronal, neurons, brain, gene, neurosci, receptors, zhang, miller, proc, natl, research, fhc, activity, role, regulates, costanzo, factor, mol, rogers, morphine, access, pharmacol, bevilacqua,
Topics {βοΈ}
iron-responsive element-binding protein month download article/chapter mu-opioid receptor-stimulated synthesis mu-opioid receptor-deficient glia human h-ferritin-encoding gene tumor necrosis factor-alpha hydrogen peroxide-dependent inhibition opiate-induced chemokine dysfunction calcium/calmodulin kinase-ii beta-amyloid peptide toxicity high-affinity rna binding mu-opioid receptor agonists g-protein-coupled receptors micro-opioid agonist damgo p300/cbp adaptor proteins morphine-induced analgesic tolerance bi-directional heterologous desensitization sdf-1alpha reveals opioid-induced heterologous desensitization tumor necrosis factor related subjects /caf/p300 complex binds hiv-induced metalloproteinase processing nuclear factor bbf full article pdf endothelial progenitor cells ferritin heavy chain iron-responsive elements post-transcriptional level mu-opioid receptor cxcr4-mediated survival signaling iron regulatory proteins iron-regulatory proteins neural stem cells nih grants r01-da19808 human immunodeficiency virus privacy choices/manage cookies alters cxcr4 signaling chemokine receptor cxcr4 cxcr4 chemokine receptor central nervous system khan mz ligand stabilization histone deacetylase inhibitors fer-1 enhancer activity cysteine oxidation regulates heavy chain subunit article abt translational research training ferritin mrna translation
Questions {β}
- Bresgen N, Ohlenschlager I, Fiedler B, Wacht N, Zach S, Dunkelmann B, Arosio P, Kuffner E, Lottspeich F, Eckl PM (2007) Ferritinβa mediator of apoptosis?
- Khan MZ, Brandimarti R, Patel JP, Huynh N, Wang J, Huang Z, Fatatis A, Meucci O (2004) Apoptotic and antiapoptotic effects of CXCR4: is it a matter of intrinsic efficacy?
- Sargeant TJ, Miller JH, Day DJ (2008) Opioidergic regulation of astroglial/neuronal proliferation: where are we now?
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headline:Regulation of Neuronal Ferritin Heavy Chain, A New Player in Opiate-Induced Chemokine Dysfunction
description:The heavy chain subunit of ferritin (FHC), a ubiquitous protein best known for its iron-sequestering activity as part of the ferritin complex, has recently been described as a novel inhibitor of signaling through the chemokine receptor CXCR4. Levels of FHC as well as its effects on CXCR4 activation increase in cortical neurons exposed to mu-opioid receptor agonists such as morphine, an effect likely specific to neurons. Major actions of CXCR4 signaling in the mature brain include a promotion of neurogenesis, activation of pro-survival signals, and modulation of excitotoxic pathways; thus, FHC up-regulation may contribute to the neuronal dysfunction often associated with opiate drug abuse. This review summarizes our knowledge of neuronal CXCR4 function, its regulation by opiates and the role of FHC in this process, and known mechanisms controlling FHC production. We speculate on the mechanism involved in FHC regulation by opiates and offer FHC as a new target in opioid-induced neuropathology.
datePublished:2011-04-05T00:00:00Z
dateModified:2011-04-05T00:00:00Z
pageStart:466
pageEnd:476
sameAs:https://doi.org/10.1007/s11481-011-9278-3
keywords:
Opioids
Chemokine
Neurons
CXCR4
Neuroprotection
Ferritin
Neurosciences
Immunology
Pharmacology/Toxicology
Virology
Cell Biology
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headline:Regulation of Neuronal Ferritin Heavy Chain, A New Player in Opiate-Induced Chemokine Dysfunction
description:The heavy chain subunit of ferritin (FHC), a ubiquitous protein best known for its iron-sequestering activity as part of the ferritin complex, has recently been described as a novel inhibitor of signaling through the chemokine receptor CXCR4. Levels of FHC as well as its effects on CXCR4 activation increase in cortical neurons exposed to mu-opioid receptor agonists such as morphine, an effect likely specific to neurons. Major actions of CXCR4 signaling in the mature brain include a promotion of neurogenesis, activation of pro-survival signals, and modulation of excitotoxic pathways; thus, FHC up-regulation may contribute to the neuronal dysfunction often associated with opiate drug abuse. This review summarizes our knowledge of neuronal CXCR4 function, its regulation by opiates and the role of FHC in this process, and known mechanisms controlling FHC production. We speculate on the mechanism involved in FHC regulation by opiates and offer FHC as a new target in opioid-induced neuropathology.
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dateModified:2011-04-05T00:00:00Z
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keywords:
Opioids
Chemokine
Neurons
CXCR4
Neuroprotection
Ferritin
Neurosciences
Immunology
Pharmacology/Toxicology
Virology
Cell Biology
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