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dc.contributor.authorFaulkner, Nicole E.
dc.contributor.authorDujardin, Denis L.
dc.contributor.authorTai, Chin-Yin
dc.contributor.authorVaughan, Kevin T.
dc.contributor.authorO'Connell, Christopher B.
dc.contributor.authorWang, Yu-Li
dc.contributor.authorVallee, Richard B.
dc.date2022-08-11T08:08:57.000
dc.date.accessioned2022-08-23T16:13:22Z
dc.date.available2022-08-23T16:13:22Z
dc.date.issued2000-11-01
dc.date.submitted2008-09-02
dc.identifier.citationNat Cell Biol. 2000 Nov;2(11):784-91. <a href="http://dx.doi.org/10.1038/35041020">Link to article on publisher's site</a>
dc.identifier.issn1465-7392 (Print)
dc.identifier.doi10.1038/35041020
dc.identifier.pmid11056532
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33606
dc.description.abstractMutations in the LIS1 gene cause gross histological disorganization of the developing human brain, resulting in a brain surface that is almost smooth. Here we show that LIS1 protein co-immunoprecipitates with cytoplasmic dynein and dynactin, and localizes to the cell cortex and to mitotic kinetochores, which are known sites for binding of cytoplasmic dynein. Overexpression of LIS1 in cultured mammalian cells interferes with mitotic progression and leads to spindle misorientation. Injection of anti-LIS1 antibody interferes with attachment of chromosomes to the metaphase plate, and leads to chromosome loss. We conclude that LIS1 participates in a subset of dynein functions, and may regulate the division of neuronal progenitor cells in the developing brain.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056532&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1038/35041020
dc.subject1-Alkyl-2-acetylglycerophosphocholine Esterase; Animals; COS Cells; Cell Division; Cell Line; Cercopithecus aethiops; Cytoplasm; Dogs; Dynein ATPase; Gene Expression; Humans; Kinetochores; Microtubule-Associated Proteins; Microtubules; Mitosis; Precipitin Tests; Subcellular Fractions
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleA role for the lissencephaly gene LIS1 in mitosis and cytoplasmic dynein function
dc.typeJournal Article
dc.source.journaltitleNature cell biology
dc.source.volume2
dc.source.issue11
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/277
dc.identifier.contextkey614212
html.description.abstract<p>Mutations in the LIS1 gene cause gross histological disorganization of the developing human brain, resulting in a brain surface that is almost smooth. Here we show that LIS1 protein co-immunoprecipitates with cytoplasmic dynein and dynactin, and localizes to the cell cortex and to mitotic kinetochores, which are known sites for binding of cytoplasmic dynein. Overexpression of LIS1 in cultured mammalian cells interferes with mitotic progression and leads to spindle misorientation. Injection of anti-LIS1 antibody interferes with attachment of chromosomes to the metaphase plate, and leads to chromosome loss. We conclude that LIS1 participates in a subset of dynein functions, and may regulate the division of neuronal progenitor cells in the developing brain.</p>
dc.identifier.submissionpathgsbs_sp/277
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentDepartment of Physiology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages784-91


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