| pubmed-article:19443652 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19443652 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
| pubmed-article:19443652 | lifeskim:mentions | umls-concept:C0068563 | lld:lifeskim |
| pubmed-article:19443652 | lifeskim:mentions | umls-concept:C1336789 | lld:lifeskim |
| pubmed-article:19443652 | lifeskim:mentions | umls-concept:C1254042 | lld:lifeskim |
| pubmed-article:19443652 | pubmed:issue | 28 | lld:pubmed |
| pubmed-article:19443652 | pubmed:dateCreated | 2009-7-6 | lld:pubmed |
| pubmed-article:19443652 | pubmed:abstractText | Transcription is essential for neurite and axon outgrowth during development. Recent work points to the involvement of nuclear factor of activated T cells (NFAT) in the regulation of genes important for axon growth and guidance. However, NFAT has not been reported to directly control the transcription of axon outgrowth-related genes. To identify transcriptional targets, we performed an in silico promoter analysis and found a putative NFAT site within the GAP-43 promoter. Using in vitro and in vivo experiments, we demonstrated that NFAT-3 regulates GAP-43, but unexpectedly, does not promote but represses the expression of GAP-43 in neurons and in the developing brain. Specifically, in neuron-like PC-12 cells and in cultured cortical neurons, the overexpression of NFAT-3 represses GAP-43 activation mediated by neurotrophin signaling. Using chromatin immunoprecipitation assays, we also show that prior to neurotrophin activation, endogenous NFAT-3 occupies the GAP-43 promoter in PC-12 cells, in cultured neurons, and in the mouse brain. Finally, we observe that NFAT-3 is required to repress the physiological expression of GAP-43 and other pro-axon outgrowth genes in specific developmental windows in the mouse brain. Taken together, our data reveal an unexpected role for NFAT-3 as a direct transcriptional repressor of GAP-43 expression and suggest a more general role for NFAT-3 in the control of the neuronal outgrowth program. | lld:pubmed |
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| pubmed-article:19443652 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19443652 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19443652 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19443652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19443652 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19443652 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:19443652 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:19443652 | pubmed:author | pubmed-author:GreenAndrewA | lld:pubmed |
| pubmed-article:19443652 | pubmed:author | pubmed-author:NguyenTuanT | lld:pubmed |
| pubmed-article:19443652 | pubmed:author | pubmed-author:Di... | lld:pubmed |
| pubmed-article:19443652 | pubmed:author | pubmed-author:LindnerRiccoR | lld:pubmed |
| pubmed-article:19443652 | pubmed:author | pubmed-author:TedeschiAndre... | lld:pubmed |
| pubmed-article:19443652 | pubmed:author | pubmed-author:ForsbergKirsi... | lld:pubmed |
| pubmed-article:19443652 | pubmed:author | pubmed-author:WuttkeAnjaA | lld:pubmed |
| pubmed-article:19443652 | pubmed:author | pubmed-author:GaubPerrineP | lld:pubmed |
| pubmed-article:19443652 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:19443652 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:19443652 | pubmed:volume | 284 | lld:pubmed |
| pubmed-article:19443652 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19443652 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19443652 | pubmed:pagination | 18816-23 | lld:pubmed |
| pubmed-article:19443652 | pubmed:dateRevised | 2010-9-27 | lld:pubmed |
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| pubmed-article:19443652 | pubmed:meshHeading | pubmed-meshheading:19443652... | lld:pubmed |
| pubmed-article:19443652 | pubmed:meshHeading | pubmed-meshheading:19443652... | lld:pubmed |
| pubmed-article:19443652 | pubmed:meshHeading | pubmed-meshheading:19443652... | lld:pubmed |
| pubmed-article:19443652 | pubmed:meshHeading | pubmed-meshheading:19443652... | lld:pubmed |
| pubmed-article:19443652 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19443652 | pubmed:articleTitle | NFAT-3 is a transcriptional repressor of the growth-associated protein 43 during neuronal maturation. | lld:pubmed |
| pubmed-article:19443652 | pubmed:affiliation | Laboratory for NeuroRegeneration and Repair, Department of Neurology, Hertie Institute for Clinical Brain Research, Germany. | lld:pubmed |
