Journal of neurochemistry
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Journal of neurochemistry · May 2017
Retraction Of PublicationRetraction Statement: CXCL12/CXCR4 chemokine signaling in spinal glia induces pain hypersensitivity through MAPKs-mediated neuroinflammation in bone cancer rats.
'CXCL12/CXCR4 chemokine signaling in spinal glia induces pain hypersensitivity through MAPKs-mediated neuroinflammation in bone cancer rats' by Hu X.-M., Liu Y.-N., Zhang H.-L., Cao S.-B., Zhang T., Chen L.-P. and Shen W. The above article from Journal of Neurochemistry, published online on 26 January 2015 and in volume 132, issue 4, pages 452-463 (available through www.onlinelibrary.wiley.com), and its subsequent Corrigendum, published online on 5 February 2015 and in volume 132, issue 4, p. 487, have been retracted by agreement between the Journal's Editor-in-Chief, Jörg Schulz, corresponding author Wen Shen on behalf of the authors, and John Wiley & Sons Ltd. The retraction has been agreed as the same GFAP immunostaining image was used to represent different experimental conditions in two different publications (Shen et al. [2014] in the Journal of Neuroinflammation and Hu et al. [2015] in the Journal of Neurochemistry), with apparent brightness changes between the images. ⋯ C. and Song C. (2014) CXCL12 in astrocytes contributes to bone cancer pain through CXCR4-mediated neuronal sensitization and glial activation in rat spinal cord. J. Neuroinflammation 11, 75. doi:10.1186/1742-2094-11-75.
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Retraction: "Aging is associated with altered inflammatory, arachidonic acid cascade, and synaptic markers, influenced by epigenetic modifications, in the human frontal cortex" by Keleshian VL, Modi HR, Rapoport SI, Rao JS. The above article from Journal of Neurochemistry, published online on 17 February 2013 in Wiley Online Library (wileyonlinelibrary.com) and in volume 121, issue 1, pp. 63-73, has been retracted by agreement between the corresponding author Stanley Rapoport, the Journal's Editor-in-Chief, Jörg Schulz, and John Wiley & Sons Ltd. The Editorial Office was contacted by the author Stanley Rapoport with the request to retract this and a related publication (see below), informing the Editor-in-Chief that the National Institutes of Health (NIH) had found Dr. Jagadeesh S. ⋯ J. (2007) Chronic NMDA administration to rats up-regulates frontal cortex cytosolic phospholipase A2 and its transcription factor, activator protein-2. J. Neurochem. 102, 1918-1927.
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Retraction: "Chronic NMDA administration to rats up-regulates frontal cortex cytosolic phospholipase A2 and its transcription factor, activator protein-2" by Rao JS, Ertley RN, Rapoport SI, Bazinet RP, Lee HJ. The above article from Journal of Neurochemistry, published online on 13 April 2007 in Wiley Online Library (wileyonlinelibrary.com) and in volume 102, issue 6, pp. 1918-1927, has been retracted by agreement between the corresponding author Stanley Rapoport, co-author Richard Bazinet, the Journal's Editor-in-Chief Jörg Schulz, and John Wiley & Sons Ltd. The Editorial Office was contacted by the author Stanley Rapoport with the request to retract this and a related publication (see below), informing the Editor-in-Chief that the National Institutes of Health (NIH) had found Dr. Jagadeesh S. ⋯ J. (2007) Chronic NMDA administration to rats up-regulates frontal cortex cytosolic phospholipase A2 and its transcription factor, activator protein-2. J. Neurochem. 102, 1918-1927.
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Journal of neurochemistry · Nov 2012
Retracted PublicationEthanol disrupts axon outgrowth stimulated by netrin-1, GDNF, and L1 by blocking their convergent activation of Src family kinase signaling.
Pre-natal alcohol exposure causes fetal alcohol spectrum disorders (FASD), the most common, preventable cause of developmental disability. The developing cerebellum is particularly vulnerable to the effects of ethanol. We reported that ethanol inhibits the stimulation of axon outgrowth in cerebellar granule neurons (CGN) by NAP, an active motif of activity-dependent neuroprotective protein (ADNP), by blocking NAP activation of Fyn kinase and its downstream signaling molecule, the scaffolding protein Cas. ⋯ Clinically relevant concentrations of ethanol inhibited axon outgrowth and the activation of the SFK-Cas-ERK1/2 pathway by netrin-1, GDNF, and L1, but did not disrupt BDNF-induced axon outgrowth or ERK1/2 activation. These results indicate that SFK, but not ERK1/2, is a primary target for ethanol inhibition of axon outgrowth. The ability of ethanol to block the convergent activation of the SFK-Cas-ERK1/2 pathway by netrin-1, GDNF, L1, and ADNP could contribute significantly to the pathogenesis of FASD.