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dc.contributor.authorPoluha, Wojciech
dc.contributor.authorPoluha, Dorota K.
dc.contributor.authorChang, Baochong B.
dc.contributor.authorCrosbie, Nancy E.
dc.contributor.authorSchonhoff, Christopher M.
dc.contributor.authorKilpatrick, Daniel L.
dc.contributor.authorRoss, Alonzo H.
dc.date2022-08-11T08:09:03.000
dc.date.accessioned2022-08-23T16:16:31Z
dc.date.available2022-08-23T16:16:31Z
dc.date.issued1996-04-01
dc.date.submitted2008-11-26
dc.identifier.citation<p>Mol Cell Biol. 1996 Apr;16(4):1335-41.</p>
dc.identifier.issn0270-7306 (Print)
dc.identifier.doi10.1128/MCB.16.4.1335
dc.identifier.pmid8657106
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34350
dc.description.abstractWe are employing recent advances in the understanding of the cell cycle to study the inverse relationship between proliferation and neuronal differentiation. Nerve growth factor and aphidicolin, an inhibitor of DNA polymerases, synergistically induce neuronal differentiation of SH-SY5Y neuroblastoma cells and the expression of p21WAF1, an inhibitor of cyclin-dependent kinases. The differentiated cells continue to express p21WAF1, even after removal of aphidicolin from the culture medium. The p21WAF1 protein coimmunoprecipitates with cyclin E and inhibits cyclin E-associated protein kinase activity. Each of three antisense oligonucleotides complementary to p21WAF1 mRNA partially blocks expression of p21WAF1 and promotes programmed cell death. These data indicate that p21WAF1 expression is required for survival of these differentiating neuroblastoma cells. Thus, the problem of neuronal differentiation can now be understood in the context of negative regulators of the cell cycle.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8657106&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC231117/
dc.subjectAphidicolin; Base Sequence; Blotting, Western; Cell Differentiation; Cell Survival; Cyclin-Dependent Kinase Inhibitor p21; Cyclins; Enzyme Inhibitors; Humans; Molecular Sequence Data; Nerve Growth Factors; Neuroblastoma; Neurons; Oligonucleotides, Antisense; Precipitin Tests; Tumor Cells, Cultured
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleThe cyclin-dependent kinase inhibitor p21 (WAF1) is required for survival of differentiating neuroblastoma cells
dc.typeJournal Article
dc.source.journaltitleMolecular and cellular biology
dc.source.volume16
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/997
dc.identifier.contextkey673213
html.description.abstract<p>We are employing recent advances in the understanding of the cell cycle to study the inverse relationship between proliferation and neuronal differentiation. Nerve growth factor and aphidicolin, an inhibitor of DNA polymerases, synergistically induce neuronal differentiation of SH-SY5Y neuroblastoma cells and the expression of p21WAF1, an inhibitor of cyclin-dependent kinases. The differentiated cells continue to express p21WAF1, even after removal of aphidicolin from the culture medium. The p21WAF1 protein coimmunoprecipitates with cyclin E and inhibits cyclin E-associated protein kinase activity. Each of three antisense oligonucleotides complementary to p21WAF1 mRNA partially blocks expression of p21WAF1 and promotes programmed cell death. These data indicate that p21WAF1 expression is required for survival of these differentiating neuroblastoma cells. Thus, the problem of neuronal differentiation can now be understood in the context of negative regulators of the cell cycle.</p>
dc.identifier.submissionpathgsbs_sp/997
dc.contributor.departmentDepartment of Physiology
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages1335-41


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