| pubmed-article:12461083 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12461083 | lifeskim:mentions | umls-concept:C0206071 | lld:lifeskim |
| pubmed-article:12461083 | lifeskim:mentions | umls-concept:C1150566 | lld:lifeskim |
| pubmed-article:12461083 | lifeskim:mentions | umls-concept:C1611645 | lld:lifeskim |
| pubmed-article:12461083 | pubmed:dateCreated | 2002-12-3 | lld:pubmed |
| pubmed-article:12461083 | pubmed:abstractText | Class switch recombination (CSR), similar to V(D)J recombination, is thought to involve DNA double strand breaks and repair by the nonhomologous end-joining pathway. A key component of this pathway is DNA-dependent protein kinase (DNA-PK), consisting of a catalytic subunit (DNA-PKcs) and a DNA-binding heterodimer (Ku70/80). To test whether DNA-PKcs activity is essential for CSR, we examined whether IgM(+) B cells from scid mice with site-directed H and L chain transgenes were able to undergo CSR. Although B cells from these mice were shown to lack DNA-PKcs activity, they were able to switch from IgM to IgG or IgA with close to the same efficiency as B cells from control transgenic and nontransgenic scid/+ mice, heterozygous for the scid mutation. We conclude that CSR, unlike V(D)J recombination, can readily occur in the absence of DNA-PKcs activity. We suggest nonhomologous end joining may not be the (primary or only) mechanism used to repair DNA breaks during CSR. | lld:pubmed |
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| pubmed-article:12461083 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12461083 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12461083 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12461083 | pubmed:author | pubmed-author:KimJiyoonJ | lld:pubmed |
| pubmed-article:12461083 | pubmed:author | pubmed-author:RadicMarko... | lld:pubmed |
| pubmed-article:12461083 | pubmed:author | pubmed-author:BosmaMelvin... | lld:pubmed |
