Ishikawa H, Asano M, Kanda T, Kumar S, Gélinas C, Ito Y
Department of Viral Oncology, Kyoto University, Japan.
Oncogene. 1993 Nov;8(11):2889-96.
The v-Rel oncoprotein and its cellular homolog c-Rel belong to the Rel/kappa B family of transcription factors. Members of this family share extensive sequence similarity in their N-terminal halves, a region referred to as the Rel Homology Region (RHR), bind to NF-kappa B DNA motifs and form heterodimers with one another. Whereas c-Rel activates transcription of kappa B-linked genes, v-Rel behaves as a dominant-interfering mutant of c-Rel- and kappa B-mediated transcription activation. Here we describe two novel activities of the Rel oncoproteins. One induces kappa B-site dependent stimulation of polyomavirus (Py) DNA replication and maps to the N-terminus of the RHR, a region where no transcription activation function was detected. This activity is common to v-Rel, c-Rel, p52 (p49/lyt10), RelA (p65) and the p50 subunit of NF-kappa B. The second promotes transcriptional activation in undifferentiated F9 cells and maps 3' to the RHR, a region essential for the transforming activity of v-Rel.
v-Rel癌蛋白及其细胞同源物c-Rel属于Rel/κB转录因子家族。该家族成员在其N端的一半区域具有广泛的序列相似性，该区域被称为Rel同源区域（RHR），可与NF-κB DNA基序结合并相互形成异二聚体。虽然c-Rel可激活与κB相关基因的转录，但v-Rel表现为c-Rel和κB介导的转录激活的显性干扰突变体。在此，我们描述了Rel癌蛋白的两种新活性。一种诱导多瘤病毒（Py）DNA复制的κB位点依赖性刺激，并定位于RHR的N端，在该区域未检测到转录激活功能。这种活性在v-Rel、c-Rel、p52（p49/lyt10）、RelA（p65）和NF-κB的p50亚基中是常见的。第二种促进未分化F9细胞中的转录激活，并定位于RHR的3'端，该区域是v-Rel转化活性所必需的。
