pubmed-article:16005638 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16005638 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
pubmed-article:16005638 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:16005638 | lifeskim:mentions | umls-concept:C0079419 | lld:lifeskim |
pubmed-article:16005638 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:16005638 | lifeskim:mentions | umls-concept:C1328865 | lld:lifeskim |
pubmed-article:16005638 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:16005638 | pubmed:dateCreated | 2005-8-15 | lld:pubmed |
pubmed-article:16005638 | pubmed:abstractText | Abnormal activation of CXCR 4 during inflammatory/infectious states may lead to neuronal dysfunction or damage. The major goal of this study was to determine the coupling of CXCR 4 to p53-dependent survival pathways in primary neurons. Neurons were stimulated with the HIV envelope protein gp120(IIIB) or the endogenous CXCR 4 agonist, SDF-1 alpha. We found that gp120 stimulates p53 activity and induces expression of the p53 pro-apoptotic target Apaf-1 in cultured neurons. Inhibition of CXCR 4 by AMD 3100 abrogates the effect of gp120 on both p53 and Apaf-1. Moreover, gp120 neurotoxicity is markedly reduced by the p53-inhibitor, pifithrin-alpha. The viral protein also regulates p53 phosphorylation and expression of other p53-responsive genes, such as MDM 2 and p21. Conversely, SDF-1 alpha, which can promote neuronal survival, increases p53 acetylation and p21 expression in neurons. Thus, the stimulation of different p53 targets could be instrumental in determining the outcome of CXCR 4 activation on neuronal survival in neuro-inflammatory disorders. | lld:pubmed |
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pubmed-article:16005638 | pubmed:language | eng | lld:pubmed |
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pubmed-article:16005638 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:16005638 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16005638 | pubmed:month | Sep | lld:pubmed |
pubmed-article:16005638 | pubmed:issn | 1044-7431 | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:MeucciOlimpia... | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:BrandimartiRe... | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:FatatisAlessa... | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:ShimizuSaoriS | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:KhanMuhammad... | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:PatelJeegar... | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:NelsonAutumnA | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:LeMy-ThaoMT | lld:pubmed |
pubmed-article:16005638 | pubmed:author | pubmed-author:Mullen-Przewo... | lld:pubmed |