| First Author | Andersson T | Year | 2000 |
| Journal | Mol Immunol | Volume | 37 |
| Issue | 15 | Pages | 889-99 |
| PubMed ID | 11282393 | Mgi Jnum | J:68456 |
| Mgi Id | MGI:1932720 | Doi | 10.1016/s0161-5890(01)00005-0 |
| Citation | Andersson T, et al. (2000) The lymphoid-specific cofactor OBF-1 is essential for the expression of a V(H) promoter/HS1,2 enhancer-linked transgene in late B cell development. Mol Immunol 37(15):889-99 |
| abstractText | Mice deficient for the lymphoid-specific cofactor OBF-1 display reduced levels of IgG, IgA and IgE. To examine whether the lowered immunoglobulin expression is linked to reduced activity of IgH cis-regulatory elements, OBF-1(-/-) mice were crossed with mice expressing transgenes driven by a V(H) or beta-globin promoter linked to the HS1,2 enhancer. Here we show that OBF-1 is essential for the induced expression of a V(H) promoter-linked transgene, in contrast to a beta-globin promoter-dependent transgene, in LPS/IL-4 or CD40-stimulated splenic B cells. Furthermore, impaired transgene expression is observed in OBF-1(-/-) peritoneal B cells. This deficiency may be linked to OBF-1, as peritoneal cells from normal mice express OBF-1 protein constitutively. Our data link OBF-1 to IgH gene expression in late B lymphoid development. |
