Nakabeppu Y, Nathans D
Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Cell. 1991 Feb 22;64(4):751-9. doi: 10.1016/0092-8674(91)90504-r.
Fos and Jun transcription factors are induced by a variety of extracellular signaling agents. We describe here an unusual member of the Fos family that is also induced, namely, a truncated form of FosB (delta FosB) missing the C-terminal 101 amino acids of FosB. delta FosB retains the dimerization and DNA-binding activities of FosB but has lost the ability in transfection assays to activate a promoter with an AP-1 site and to repress the c-fos promoter. Rather, delta FosB inhibits gene activation by Jun or Jun + Fos and inhibits repression of the c-fos promoter by FosB or c-Fos, presumably by competing with full-length Fos proteins at the steps of dimerization with Jun and binding to DNA. In stimulated cells delta FosB may act to limit the transcriptional effects of Fos and Jun proteins.
Fos和Jun转录因子可被多种细胞外信号因子诱导产生。我们在此描述了Fos家族中一个不同寻常的成员，它同样也能被诱导产生，即一种截短形式的FosB（δFosB），缺失了FosB的C末端101个氨基酸。δFosB保留了FosB的二聚化和DNA结合活性，但在转染实验中失去了激活含有AP-1位点的启动子以及抑制c-fos启动子的能力。相反，δFosB抑制Jun或Jun + Fos介导的基因激活，并抑制FosB或c-Fos对c-fos启动子的抑制作用，推测这是通过在与Jun二聚化以及结合DNA的步骤中与全长Fos蛋白竞争来实现的。在受刺激的细胞中，δFosB可能起到限制Fos和Jun蛋白转录效应的作用。
