Kwon M, Oshima R G
Cancer Research Center, La Jolla Cancer Research Foundation, California 92037.
Dev Dyn. 1992 Feb;193(2):193-8. doi: 10.1002/aja.1001930211.
JunB, a member of the jun gene family of transcription factors, is distinguished from c-Jun by its differential activity on certain arrangements of promoter regulatory elements and the ability of JunB to inhibit the action of cJun in both transforming and trans-activating assays. We have tested the potential negative regulatory role of JunB during the retinoic acid induced differentiation of F9 murine embryonal carcinoma cells. Constitutive expression of high levels of JunB in F9 cells failed to inhibit the differentiation dependent induction of c-Jun or the coincident expression of differentiation markers keratin 8 and 18, tissue plasminogen activator, and laminin B1. Among these marker genes, keratin 18, has been shown to contain an AP-1 binding site, TGA(C/G)TCA, which is essential for high level, differentiation dependent expression and which is transactivated by Jun and Fos proteins. These results suggest that JunB does not play a major negative or positive regulatory role during the retinoic acid induced differentiation of F9 cells.
JunB是转录因子jun基因家族的成员之一,它与c-Jun的区别在于对某些启动子调控元件排列的不同活性,以及在转化和反式激活试验中JunB抑制c-Jun作用的能力。我们测试了JunB在视黄酸诱导的F9小鼠胚胎癌细胞分化过程中的潜在负调控作用。F9细胞中高水平的JunB组成型表达未能抑制c-Jun的分化依赖性诱导,也未能抑制分化标志物角蛋白8和18、组织纤溶酶原激活剂和层粘连蛋白B1的同时表达。在这些标志物基因中,角蛋白18已被证明含有一个AP-1结合位点TGA(C/G)TCA,它对于高水平的、分化依赖性表达至关重要,并且可被Jun和Fos蛋白反式激活。这些结果表明,JunB在视黄酸诱导的F9细胞分化过程中不发挥主要的负调控或正调控作用。