Chung J, Deutsch H H, Kalthoff F S
Department of Immunodermatology, Sandoz Research Institute, Vienna, Austria.
J Leukoc Biol. 1996 Apr;59(4):586-90. doi: 10.1002/jlb.59.4.586.
We have studied the regulation of growth and apoptosis in murine BA/F3 cells stably expressing cytoplasmic deletion mutants of the human interleukin-4 receptor (hIL-4R). Previously, we showed that BA/F3 cell transfectants expressing a cytoplasmic deletion mutant of the hIL-4R that lacks the region between Thr(462) and Ala(580), referred to as delta R3, fails to proliferate in the presence of hIL-4. Here we report that supertransfection of delta R3-expressing cells with a constitutively active murine bcl-2 gene results in prolonged survival of the delta R3/bel-2 double transfectants in the absence of cytokines. More importantly, however, the constitutive expression of Bcl-2 restored their capacity to grow permanently with hIL-4. This may provide an explanation for the discrepancy with previous reports showing growth mediation by hIL-4R truncated at position 367.
我们研究了稳定表达人白细胞介素-4受体（hIL-4R）胞质缺失突变体的小鼠BA/F3细胞中生长和凋亡的调控。此前，我们发现，表达hIL-4R胞质缺失突变体（缺失Thr(462)和Ala(580)之间区域，称为δR3）的BA/F3细胞转染子在hIL-4存在的情况下无法增殖。在此我们报告，用组成型活性小鼠bcl-2基因对表达δR3的细胞进行超转染，可使δR3/bcl-2双转染子在无细胞因子的情况下延长存活时间。然而，更重要的是，Bcl-2的组成型表达恢复了它们在hIL-4存在下永久生长的能力。这可能解释了与之前报道的在367位截断的hIL-4R介导生长之间的差异。
