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dc.contributor.advisorDr. Gary L. Johnson
dc.contributor.authorSchiavi, Susan C.
dc.date2022-08-11T08:08:40.000
dc.date.accessioned2022-08-23T16:03:52Z
dc.date.available2022-08-23T16:03:52Z
dc.date.issued1988-08-01
dc.date.submitted2007-03-13
dc.identifier.doi10.13028/3hcw-dw22
dc.identifier.urihttp://hdl.handle.net/20.500.14038/31568
dc.description.abstractPC12 rat pheochromocytoma cells respond to nerve growth factor (NGF) by neuronal differentiation and partial growth arrest. Mouse c-myc and adenovirus E1A genes were introduced into PC12 cells to study the influence of these nuclear oncogenes on neuronal differentiation. Expression of myc and E1A blocked morphological differentiation and caused NGF to stimulate rather than inhibit cell proliferation. NGF binding to cell surface receptors, activation of ribosomal S6 kinase, and ornithine decarboxylase induction were similar in myc and E1A expressing clones compared with wild-type PC12 cells, suggesting that changes in the cellular response to NGF were at a post-receptor level. The ability of myc and E1A expression to block the transcription-dependent induction of microtubule associated proteins by NGF further suggested that these genes may inhibit differentiation by interfering with NGP's ability to regulate transcription. These results illustrate that NGF can promote either growth or differentiation of PC12 cells, and that myc or E1A alter the phenotypic responses to growth factors.
dc.language.isoen_US
dc.rightsCopyright is held by the author, with all rights reserved.
dc.subjectNerve Growth Factor
dc.subjectProto-Oncogene Proteins c-myc
dc.subjectAdenovirus E1A Proteins
dc.subjectPC12 Cells
dc.subjectCell Differentiation
dc.subjectNeurons
dc.subjectTranscription Factors
dc.subjectMice
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectAnimal Experimentation and Research
dc.subjectCells
dc.subjectGenetic Phenomena
dc.subjectNervous System
dc.subjectViruses
dc.titleMYC and E1A Oncogenes Alter the Response of PC12 Cells to Nerve Growth Factor and Block Differentiation: A Thesis
dc.typeDoctoral Dissertation
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1259&context=gsbs_diss&unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_diss/259
dc.legacy.embargo2017-04-24T00:00:00-07:00
dc.identifier.contextkey271876
refterms.dateFOA2022-08-30T03:38:28Z
html.description.abstract<p>PC12 rat pheochromocytoma cells respond to nerve growth factor (NGF) by neuronal differentiation and partial growth arrest. Mouse c-myc and adenovirus E1A genes were introduced into PC12 cells to study the influence of these nuclear oncogenes on neuronal differentiation. Expression of myc and E1A blocked morphological differentiation and caused NGF to stimulate rather than inhibit cell proliferation. NGF binding to cell surface receptors, activation of ribosomal S6 kinase, and ornithine decarboxylase induction were similar in myc and E1A expressing clones compared with wild-type PC12 cells, suggesting that changes in the cellular response to NGF were at a post-receptor level. The ability of myc and E1A expression to block the transcription-dependent induction of microtubule associated proteins by NGF further suggested that these genes may inhibit differentiation by interfering with NGP's ability to regulate transcription. These results illustrate that NGF can promote either growth or differentiation of PC12 cells, and that myc or E1A alter the phenotypic responses to growth factors.</p>
dc.identifier.submissionpathgsbs_diss/259
dc.contributor.departmentBiochemistry
dc.description.thesisprogramBiochemistry and Molecular Pharmacology


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