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dc.contributor.authorVallee, Richard B.
dc.contributor.authorTai, Chin-Yin
dc.contributor.authorFaulkner, Nicole E.
dc.date2022-08-11T08:08:50.000
dc.date.accessioned2022-08-23T16:09:32Z
dc.date.available2022-08-23T16:09:32Z
dc.date.issued2001-04-18
dc.date.submitted2009-01-13
dc.identifier.citation<p>Trends Cell Biol. 2001 Apr;11(4):155-60.</p>
dc.identifier.issn0962-8924 (Print)
dc.identifier.doi10.1016/S0962-8924(01)01956-0
dc.identifier.pmid11306294
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32720
dc.description.abstractBrain development is severely defective in children with lissencephaly. The highly organized distribution of neurons within the cerebral cortex is disrupted, a condition that might arise from improper migration of neuronal progenitors to their cortical destinations. Type I lissencephaly results from mutations in the LIS1 gene, which has been implicated in the cytoplasmic dynein and platelet-activating factor pathways. Recent studies have identified roles for the product of LIS1 in nuclear migration, mitotic spindle orientation and chromosome alignment, where it appears to act in concert with cytoplasmic dynein. A unifying hypothesis for the subcellular function of LIS1 is presented.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=11306294&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/S0962-8924(01)01956-0
dc.subject1-Alkyl-2-acetylglycerophosphocholine Esterase; Brain; Brain Diseases, Metabolic, Inborn; Child; Developmental Disabilities; Humans; Microtubule-Associated Proteins
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleLIS1: cellular function of a disease-causing gene
dc.typeJournal Article
dc.source.journaltitleTrends in cell biology
dc.source.volume11
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1276
dc.identifier.contextkey693204
html.description.abstract<p>Brain development is severely defective in children with lissencephaly. The highly organized distribution of neurons within the cerebral cortex is disrupted, a condition that might arise from improper migration of neuronal progenitors to their cortical destinations. Type I lissencephaly results from mutations in the LIS1 gene, which has been implicated in the cytoplasmic dynein and platelet-activating factor pathways. Recent studies have identified roles for the product of LIS1 in nuclear migration, mitotic spindle orientation and chromosome alignment, where it appears to act in concert with cytoplasmic dynein. A unifying hypothesis for the subcellular function of LIS1 is presented.</p>
dc.identifier.submissionpathgsbs_sp/1276
dc.contributor.departmentDept of Cell Biology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages155-60


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