| pubmed-article:18005957 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18005957 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:18005957 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:18005957 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:18005957 | lifeskim:mentions | umls-concept:C0085140 | lld:lifeskim |
| pubmed-article:18005957 | lifeskim:mentions | umls-concept:C0040691 | lld:lifeskim |
| pubmed-article:18005957 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:18005957 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:18005957 | lifeskim:mentions | umls-concept:C0079411 | lld:lifeskim |
| pubmed-article:18005957 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18005957 | pubmed:dateCreated | 2007-12-27 | lld:pubmed |
| pubmed-article:18005957 | pubmed:abstractText | The generation of Cajal-Retzius (CR) neurons is restricted to discrete sites in the telencephalon. Most of these sites do not express Foxg1, a transcription factor that inhibits transforming growth factor (TGF)beta-dependent upregulation of p21. We tested the hypothesis that TGFbeta signaling triggers CR neurogenesis in Foxg1-deficient zones through p21 induction. In Foxg1(+/+) mice, p21 (a) was expressed in select cycling cells in CR neuron-producing areas and (b) was co-localized in newly generated CR neurons. Zones of CR neuronal production and p21 expression were expanded in the forebrains of Foxg1(Cre/Cre) mice. Manipulation of TGFbeta signaling in explants from cortical hems of wild-type mice altered p21 expression and the production of CR neurons. Furthermore, despite continued TGFbeta activity, p21 immunoreactivity diminished in CR neurons with distance from their generation site. This implicated a second pathway controlling p21 expression. We provide evidence that Foxo3a, which has been shown to translocate into the nucleus to act as a transcriptional co-activator of TGFbeta-dependent upregulation of p21, is strategically expressed to be involved in controlling p21 expression in CR neurons. Specifically, Foxo3a was nuclear in p21+/reelin+ cells in sites of CR neuronal generation, however, nuclear Foxo3a immunoreactivity was absent in p21-/reelin+ cells distal from sites of CR neurogenesis. Thus, TGFbeta and Foxo3a may work in concert to regulate expression of p21 during CR neuronal generation. | lld:pubmed |
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| pubmed-article:18005957 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18005957 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18005957 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18005957 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:18005957 | pubmed:issn | 1095-564X | lld:pubmed |
| pubmed-article:18005957 | pubmed:author | pubmed-author:MillerMichael... | lld:pubmed |
| pubmed-article:18005957 | pubmed:author | pubmed-author:SiegenthalerJ... | lld:pubmed |
| pubmed-article:18005957 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18005957 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:18005957 | pubmed:volume | 313 | lld:pubmed |
| pubmed-article:18005957 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18005957 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18005957 | pubmed:pagination | 35-46 | lld:pubmed |
| pubmed-article:18005957 | pubmed:dateRevised | 2011-3-8 | lld:pubmed |
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| pubmed-article:18005957 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18005957 | pubmed:articleTitle | Generation of Cajal-Retzius neurons in mouse forebrain is regulated by transforming growth factor beta-Fox signaling pathways. | lld:pubmed |
| pubmed-article:18005957 | pubmed:affiliation | Department of Neuroscience and Physiology, State University of New York-Upstate Medical University, Syracuse, NY 13210, USA. | lld:pubmed |
| pubmed-article:18005957 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18005957 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:18005957 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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