Nomura T, Sakai N, Sarai A, Sudo T, Kanei-Ishii C, Ramsay R G, Favier D, Gonda T J, Ishii S
Tsukuba Life Science Center, Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan.
J Biol Chem. 1993 Oct 15;268(29):21914-23.
The trans-activating and transforming capacities of the c-myb proto-oncogene product (c-Myb) are negatively regulated through a leucine zipper structure in its negative regulatory domain. We show here tht in cotransfection assays, maximal Myb-induced trans-activation occurs with relatively low amounts of wild-type c-Myb, while higher levels of c-Myb result in reduced Myb-induced trans-activation. By contrast, this apparent negative autoregulation is not observed with a c-Myb mutant containing an impaired leucine zipper. Data presented here suggest that this negative autoregulation of trans-activation by wild-type c-Myb is a consequence of homodimer formation by c-Myb through its leucine zipper and of the inability of c-Myb dimers to bind DNA. These findings point to a novel mechanism of regulation of a transcription factor.
c-myb原癌基因产物(c-Myb)的反式激活和转化能力通过其负调控域中的亮氨酸拉链结构受到负调控。我们在此表明,在共转染实验中,相对少量的野生型c-Myb就能实现最大程度的Myb诱导的反式激活,而较高水平的c-Myb则会导致Myb诱导的反式激活减少。相比之下,含有受损亮氨酸拉链的c-Myb突变体未观察到这种明显的负自调节。此处呈现的数据表明,野生型c-Myb对反式激活的这种负自调节是c-Myb通过其亮氨酸拉链形成同二聚体以及c-Myb二聚体无法结合DNA的结果。这些发现指出了一种转录因子调控的新机制。