Chen U
Basel Institute for Immunology, Switzerland.
Gene. 1988 Dec 10;72(1-2):209-17. doi: 10.1016/0378-1119(88)90146-1.
Activation of resting mouse B-cells with anti-immunoglobulin M (IgM) antibodies and a mitogen such as bacterial lipopolysaccharide leads to a specific inhibition of IgM expression. [3H]Uridine pulse-chase experiments show that the inhibition of RNA metabolism by anti-IgM antibody treatment occurs in the nucleus at the mu-RNA processing level and results in low levels of mature mu-mRNA expression. By applying the RNA synthesis inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole, the half lives of various forms of Ig-mRNA are estimated to be 8-12 h. The fact that the residual mu-mRNA left in B-cells after anti-IgM antibody treatment can still be translated into polypeptides indicates that the mu-mRNA in these cells is still functional.