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dc.contributor.authorPark, Seok-Rae
dc.contributor.authorSeo, Goo-Young
dc.contributor.authorChoi, Ae-Jin
dc.contributor.authorStavnezer, Janet
dc.contributor.authorKim, Pyeung-Hyeun
dc.date2022-08-11T08:11:04.000
dc.date.accessioned2022-08-23T17:31:04Z
dc.date.available2022-08-23T17:31:04Z
dc.date.issued2005-03-01
dc.date.submitted2007-09-14
dc.identifier.citationEur J Immunol. 2005 Mar;35(3):946-56. <a href="http://dx.doi.org/10.1002/eji.200425848">Link to article on publisher's site</a>
dc.identifier.issn0014-2980 (Print)
dc.identifier.doi10.1002/eji.200425848
dc.identifier.pmid15688346
dc.identifier.urihttp://hdl.handle.net/20.500.14038/50649
dc.description.abstractTransforming growth factor (TGF)-beta1 directs class switch recombination (CSR) to IgG2b as well as to IgA. Smad3/4, Runx3 and p300 mediate TGF-beta1-induced germ-line (GL) alpha transcription leading to IgA expression. However, the molecular mechanisms by which TGF-beta1 induces IgG2b CSR are unknown. We used luciferase reporter plasmids to investigate how TGF-beta1 regulates the activity of the promoter for GL transcripts of IgG2b constant gene (GLgamma2b promoter). Similarly to the GLalpha promoter, overexpression of Smad3/4 and Runx3 enhances TGF-beta1-induced GLgamma2b promoter activity. Mutation analysis of the promoter identified likely Smad- and Runx3-binding sites. Also similar to the GLalpha promoter, overexpression of p300 enhances Smad3/4-mediated promoter activity, whereas E1A represses promoter activity. Since these regulation mechanisms underlying both GLalpha and GLgamma2b transcription are similar, we explored the possibility that TGF-beta1 induces IgA CSR via transitional IgG2b CSR. TGF-beta1 enhances the expression of both Ialpha-Cmu and Ialpha-Cgamma2b circle transcripts, indicative of direct (Smu-->Salpha) and sequential CSR (Smu-->Sgamma2b-->Salpha).
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15688346&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1002/eji.200425848
dc.subjectAnimals
dc.subjectBase Sequence
dc.subjectCore Binding Factor Alpha 3 Subunit
dc.subjectDNA-Binding Proteins
dc.subjectE1A-Associated p300 Protein
dc.subjectElectrophoretic Mobility Shift Assay
dc.subjectImmunoglobulin A
dc.subjectImmunoglobulin Class Switching
dc.subjectImmunoglobulin G
dc.subjectMice
dc.subjectMice, Inbred BALB C
dc.subjectMolecular Sequence Data
dc.subjectNuclear Proteins
dc.subjectPromoter Regions (Genetics)
dc.subjectReverse Transcriptase Polymerase Chain Reaction
dc.subjectSmad3 Protein
dc.subjectSmad4 Protein
dc.subjectTrans-Activators
dc.subjectTranscription Factors
dc.subject*Transcription, Genetic
dc.subjectTransfection
dc.subjectTransforming Growth Factor beta
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectWomen's Studies
dc.titleAnalysis of transforming growth factor-beta1-induced Ig germ-line gamma2b transcription and its implication for IgA isotype switching
dc.typeJournal Article
dc.source.journaltitleEuropean journal of immunology
dc.source.volume35
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/wfc_pp/175
dc.identifier.contextkey367636
html.description.abstract<p>Transforming growth factor (TGF)-beta1 directs class switch recombination (CSR) to IgG2b as well as to IgA. Smad3/4, Runx3 and p300 mediate TGF-beta1-induced germ-line (GL) alpha transcription leading to IgA expression. However, the molecular mechanisms by which TGF-beta1 induces IgG2b CSR are unknown. We used luciferase reporter plasmids to investigate how TGF-beta1 regulates the activity of the promoter for GL transcripts of IgG2b constant gene (GLgamma2b promoter). Similarly to the GLalpha promoter, overexpression of Smad3/4 and Runx3 enhances TGF-beta1-induced GLgamma2b promoter activity. Mutation analysis of the promoter identified likely Smad- and Runx3-binding sites. Also similar to the GLalpha promoter, overexpression of p300 enhances Smad3/4-mediated promoter activity, whereas E1A represses promoter activity. Since these regulation mechanisms underlying both GLalpha and GLgamma2b transcription are similar, we explored the possibility that TGF-beta1 induces IgA CSR via transitional IgG2b CSR. TGF-beta1 enhances the expression of both Ialpha-Cmu and Ialpha-Cgamma2b circle transcripts, indicative of direct (Smu-->Salpha) and sequential CSR (Smu-->Sgamma2b-->Salpha).</p>
dc.identifier.submissionpathwfc_pp/175
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.source.pages946-56


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