| First Author | Rolink A | Year | 1996 |
| Journal | Immunity | Volume | 5 |
| Issue | 4 | Pages | 319-30 |
| PubMed ID | 8885865 | Mgi Jnum | J:36026 |
| Mgi Id | MGI:83468 | Doi | 10.1016/s1074-7613(00)80258-7 |
| Citation | Rolink A, et al. (1996) The SCID but not the RAG-2 gene product is required for S mu-S epsilon heavy chain class switching. Immunity 5(4):319-30 |
| abstractText | We have investigated the capacity of precursor B cells from normal (BDF1) and V(D)J recombinase-deficient (RAG-27) or defective (SCID) mice to be induced by a CD40-specific monoclonal antibody and IL-4 to epsilon H chain gene transcription and to S mu-S epsilon switch recombination. In differentiating precursor B cells from all three strains of mice, the development of similar numbers of CD19+, CD23+, CD40+, and MHC class II+ expressing B lineage cells and similar levels of epsilon H chain gene transcription were induced. Efficient S mu-S epsilon switching occurred in normal and RAG-2-deficient, but not in SCID, precursor B cells. Thus, the transcription of the epsilon H chain is independent of the RAG-2 and the SCID gene product, while the S mu-S epsilon switch recombination requires the SCID gene-encoded DNA-dependent protein kinase, but not the RAG-2 protein. |
