Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/17980
DC FieldValueLanguage
dc.contributorDepartment of Applied Biology and Chemical Technology-
dc.creatorChen, X-
dc.creatorLan, X-
dc.creatorMo, S-
dc.creatorQin, J-
dc.creatorLi, W-
dc.creatorLiu, P-
dc.creatorHan, Y-
dc.creatorPi, R-
dc.date.accessioned2015-05-26T08:10:47Z-
dc.date.available2015-05-26T08:10:47Z-
dc.identifier.issn0006-291Xen_US
dc.identifier.urihttp://hdl.handle.net/10397/17980-
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.subjectCerebellar granule neuronsen_US
dc.subjectCopperen_US
dc.subjectMitogen-activated protein kinasesen_US
dc.subjectNimodipineen_US
dc.subjectReactive oxygen speciesen_US
dc.titlep38 and ERK, but not JNK, are involved in copper-induced apoptosis in cultured cerebellar granule neuronsen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage944en_US
dc.identifier.epage948en_US
dc.identifier.volume379en_US
dc.identifier.issue4en_US
dc.identifier.doi10.1016/j.bbrc.2008.12.177en_US
dcterms.abstractCopper (Cu 2+) is an essential element for a variety of cellular functions; however, it is involved in neurotoxic events at excessive doses. Mechanisms of Cu 2+-induced neurotoxicity are not well understood. Here, we studied the toxic effects of Cu 2+ on cultured cerebellar granule neurons (cCGNs). Treatment of cCGNs with CuCl 2 (50 and 75 μM) caused a concentration- and time-dependent cell death with apoptotic characters, including chromatin condensation and DNA ladder. Cu 2+ potently induced reactive oxygen species (ROS), and quickly and slightly increased the intracellular concentration of calcium. Western blot assay showed that Cu 2+ increased phosphorylation of p38 mitogen-activated protein kinase (MAPK) and ERK1/2, but not that of JNK-1. Pharmacological inhibition of calcium influx, p38 MAPK and ERK1/2 attenuated the Cu 2+ toxicity in cCGNs. These findings demonstrate that p38 MAPK and ERK1/2, but not JNK, are involved in apoptosis of cCGNs induced by copper, and p38 and ERK may be the downstream effectors of ROS and calcium signaling.-
dcterms.bibliographicCitationBiochemical and biophysical research communications, 2009, v. 379, no. 4, p. 944-948-
dcterms.isPartOfBiochemical and biophysical research communications-
dcterms.issued2009-
dc.identifier.isiWOS:000263336700028-
dc.identifier.scopus2-s2.0-58949087366-
dc.identifier.pmid19138669-
dc.identifier.eissn1090-2104en_US
dc.identifier.rosgroupidr42537-
dc.description.ros2008-2009 > Academic research: refereed > Publication in refereed journal-
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