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dc.contributor.authorMin, Irene M.
dc.contributor.authorSchrader, Carol E.
dc.contributor.authorVardo, Joycelyn
dc.contributor.authorLuby, Thomas M.
dc.contributor.authorD'Avirro, Nicole
dc.contributor.authorStavnezer, Janet
dc.contributor.authorSelsing, Erik
dc.date2022-08-11T08:11:04.000
dc.date.accessioned2022-08-23T17:31:06Z
dc.date.available2022-08-23T17:31:06Z
dc.date.issued2003-10-01
dc.date.submitted2007-09-14
dc.identifier.citation<p>Immunity. 2003 Oct;19(4):515-24.</p>
dc.identifier.issn1074-7613 (Print)
dc.identifier.doi10.1016/S1074-7613(03)00262-0
dc.identifier.pmid14563316
dc.identifier.urihttp://hdl.handle.net/20.500.14038/50654
dc.description.abstractDeficiencies of the Msh2 protein or the Smu tandem repeat (SmuTR) sequences each reduce isotype switching in mice by about 2- to 3-fold. We find that switching in mice deficient for both Msh2 and SmuTR is nearly ablated. We propose that the SmuTR provides closely spaced cleavage sites that can undergo switch recombination independent of Msh2, whereas cleavages in sequences flanking the SmuTR require Msh2 processing to allow recombinational joining. We also find that changes in Smu sequences alter the focus of switch junctions within Sgamma sequences, indicating that sequences of switch regions act together in the choice of switch recombination junctions. These findings help to explain the conservation of tandemly repeated switch regions associated with heavy chain constant genes in species capable of switching.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14563316&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/S1074-7613(03)00262-0
dc.subjectAnimals
dc.subject*DNA-Binding Proteins
dc.subjectImmunoglobulin Class Switching
dc.subjectImmunoglobulin Isotypes
dc.subjectIntrons
dc.subjectMembrane Proteins
dc.subjectMice
dc.subjectMutS Homolog 2 Protein
dc.subjectProto-Oncogene Proteins
dc.subject*Tandem Repeat Sequences
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectWomen's Studies
dc.titleThe Smu tandem repeat region is critical for Ig isotype switching in the absence of Msh2
dc.typeJournal Article
dc.source.journaltitleImmunity
dc.source.volume19
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/wfc_pp/180
dc.identifier.contextkey367641
html.description.abstract<p>Deficiencies of the Msh2 protein or the Smu tandem repeat (SmuTR) sequences each reduce isotype switching in mice by about 2- to 3-fold. We find that switching in mice deficient for both Msh2 and SmuTR is nearly ablated. We propose that the SmuTR provides closely spaced cleavage sites that can undergo switch recombination independent of Msh2, whereas cleavages in sequences flanking the SmuTR require Msh2 processing to allow recombinational joining. We also find that changes in Smu sequences alter the focus of switch junctions within Sgamma sequences, indicating that sequences of switch regions act together in the choice of switch recombination junctions. These findings help to explain the conservation of tandemly repeated switch regions associated with heavy chain constant genes in species capable of switching.</p>
dc.identifier.submissionpathwfc_pp/180
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.source.pages515-24


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