pubmed-article:16959241 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16959241 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:16959241 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:16959241 | lifeskim:mentions | umls-concept:C0105770 | lld:lifeskim |
pubmed-article:16959241 | lifeskim:mentions | umls-concept:C0814002 | lld:lifeskim |
pubmed-article:16959241 | lifeskim:mentions | umls-concept:C2610344 | lld:lifeskim |
pubmed-article:16959241 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
pubmed-article:16959241 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:16959241 | pubmed:dateCreated | 2006-10-31 | lld:pubmed |
pubmed-article:16959241 | pubmed:abstractText | During vertebrate retinal development, the seven retinal cell types differentiate sequentially from a single population of retinal progenitor cells (RPCs) and organize themselves into a distinct laminar structure. The purpose of this study was to determine whether beta-catenin, which functions both as a nuclear effector for the canonical Wnt signaling pathway and as a regulator of cell adhesion, is required for retinal neurogenesis or lamination. We used the Cre-loxP system to either eliminate beta-catenin or to express a constitutively active form during retinal neurogenesis. Eliminating beta-catenin did not affect cell differentiation, but did result in the loss of the radial arrangement of RPCs and caused abnormal migration of differentiated neurons. As a result, the laminar structure was massively disrupted in beta-catenin-null retinas, although all retinal cell types still formed. In contrast to other neural tissues, eliminating beta-catenin did not significantly reduce the proliferation rate of RPCs; likewise, activating beta-catenin ectopically in RPCs did not result in overproliferation, but loss of neural retinal identity. These results indicate that beta-catenin is essential during retinal neurogenesis as a regulator of cell adhesion but not as a nuclear effector of the canonical Wnt signaling pathway. The results further imply that retinal lamination and retinal cell differentiation are genetically separable processes. | lld:pubmed |
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pubmed-article:16959241 | pubmed:language | eng | lld:pubmed |
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pubmed-article:16959241 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:16959241 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16959241 | pubmed:month | Nov | lld:pubmed |
pubmed-article:16959241 | pubmed:issn | 0012-1606 | lld:pubmed |
pubmed-article:16959241 | pubmed:author | pubmed-author:MuXiuqianX | lld:pubmed |
pubmed-article:16959241 | pubmed:author | pubmed-author:KleinWilliam... | lld:pubmed |
pubmed-article:16959241 | pubmed:author | pubmed-author:FuXueyaoX | lld:pubmed |
pubmed-article:16959241 | pubmed:author | pubmed-author:SunHongxiaH | lld:pubmed |
pubmed-article:16959241 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16959241 | pubmed:day | 15 | lld:pubmed |
pubmed-article:16959241 | pubmed:volume | 299 | lld:pubmed |
pubmed-article:16959241 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16959241 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16959241 | pubmed:pagination | 424-37 | lld:pubmed |
pubmed-article:16959241 | pubmed:dateRevised | 2011-9-22 | lld:pubmed |
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pubmed-article:16959241 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16959241 | pubmed:articleTitle | Beta-catenin is essential for lamination but not neurogenesis in mouse retinal development. | lld:pubmed |
pubmed-article:16959241 | pubmed:affiliation | Department of Biochemistry and Molecular Biology, Unit 1000, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA. | lld:pubmed |
pubmed-article:16959241 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16959241 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:16959241 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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