| pubmed-article:16107726 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16107726 | lifeskim:mentions | umls-concept:C0013935 | lld:lifeskim |
| pubmed-article:16107726 | lifeskim:mentions | umls-concept:C2750249 | lld:lifeskim |
| pubmed-article:16107726 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
| pubmed-article:16107726 | lifeskim:mentions | umls-concept:C1425015 | lld:lifeskim |
| pubmed-article:16107726 | lifeskim:mentions | umls-concept:C0205197 | lld:lifeskim |
| pubmed-article:16107726 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:16107726 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:16107726 | pubmed:dateCreated | 2005-8-18 | lld:pubmed |
| pubmed-article:16107726 | pubmed:abstractText | Regulation of cytoplasmic dynein and microtubule dynamics is crucial for both mitotic cell division and neuronal migration. NDEL1 was identified as a protein interacting with LIS1, the protein product of a gene mutated in the lissencephaly. To elucidate NDEL1 function in vivo, we generated null and hypomorphic alleles of Ndel1 in mice by targeted gene disruption. Ndel1(-/-) mice were embryonic lethal at the peri-implantation stage like null mutants of Lis1 and cytoplasmic dynein heavy chain. In addition, Ndel1(-/-) blastocysts failed to grow in culture and exhibited a cell proliferation defect in inner cell mass. Although Ndel1(+/-) mice displayed no obvious phenotypes, further reduction of NDEL1 by making null/hypomorph compound heterozygotes (Ndel1(cko/-)) resulted in histological defects consistent with mild neuronal migration defects. Double Lis1(cko/+)-Ndel1(+/-) mice or Lis1(+/-)-Ndel1(+/-) mice displayed more severe neuronal migration defects than Lis1(cko/+)-Ndel1(+/)(+) mice or Lis1(+/-)-Ndel1(+/+) mice, respectively. We demonstrated distinct abnormalities in microtubule organization and similar defects in the distribution of beta-COP-positive vesicles (to assess dynein function) between Ndel1 or Lis1-null MEFs, as well as similar neuronal migration defects in Ndel1- or Lis1-null granule cells. Rescue of these defects in mouse embryonic fibroblasts and granule cells by overexpressing LIS1, NDEL1, or NDE1 suggest that NDEL1, LIS1, and NDE1 act in a common pathway to regulate dynein but each has distinct roles in the regulation of microtubule organization and neuronal migration. | lld:pubmed |
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| pubmed-article:16107726 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16107726 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16107726 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16107726 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:16107726 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:MuramatsuMasa... | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:SasakiShinjiS | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:HiraiwaNoriko... | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:YoshikiAtsush... | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:MiyagawaShuji... | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:Wynshaw-Boris... | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:ChenAmyA | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:MoriDaisukeD | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:HirotsuneShin... | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:Toyo-okaKazuh... | lld:pubmed |
| pubmed-article:16107726 | pubmed:author | pubmed-author:Garrett-BealL... | lld:pubmed |
| pubmed-article:16107726 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16107726 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:16107726 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16107726 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16107726 | pubmed:pagination | 7812-27 | lld:pubmed |
| pubmed-article:16107726 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:16107726 | pubmed:year | 2005 | lld:pubmed |
