Nuclear factor I interferes with transformation induced by nuclear oncogenes.

摘要: The four nuclear factor I genes (NFI-A, NFI-B, NFI-C, and NFI-X) give rise to multiple isoforms by alternative splicing in many tissues. These NFI proteins cooperate with AP-1, Myc, other transcription factors regulating of numerous cellular viral genes. We have investigated the growth-regulatory potential overexpressing cDNAs from chicken -A, -B, -C, -X embryo fibroblasts (CEF). None induced oncogenic transformation CEF. However, overexpression each caused similar morphological alteration cells, inducing them become flattened polygonal show increased adherence. growth properties these cells were normal When morphologically altered CEF challenged superinfection retroviruses, they resistant oncogenes jun, fos, junD, myc, qin but readily transformed cytoplasmic src, mil/raf, ras, fps. NFI-A1 protein was able alter transactivation Jun a promoter-dependent manner. changes cell morphology reduced susceptibility not seen carboxy-terminal truncation domain NFI, suggesting that this region is essential for observed effects. dichotomy between activities system discussed.