Stuart E T, Haffner R, Oren M, Gruss P
Department of Molecular Cell Biology, Max-Planck Institute for Biophysical Chemistry, Göttingen, Germany.
EMBO J. 1995 Nov 15;14(22):5638-45. doi: 10.1002/j.1460-2075.1995.tb00251.x.
Direct interactions between the genes that regulate development and those which regulate the cell cycle would provide a mechanism by which numerous biological events could be better understood. We have identified a direct role for PAX5 in the control of p53 transcription. In primary human diffuse astrocytomas, PAX5 expression inversely correlated with p53 expression. The human p53 gene harbours a PAX binding site within its untranslated first exon that is conserved throughout evolution. PAX5 and its paralogues PAX2 and PAX8 are capable of inhibiting both the p53 promoter and transactivation of a p53-responsive reporter in cell culture. Mutation of the identified binding site eliminates PAX protein binding in vitro and renders the promoter inactive in cells. These data suggest that PAX proteins might regulate p53 expression during development and propose a novel alternative mechanism for tumour initiation or progression, by which loss of p53 function occurs at the transcriptional level.
调控发育的基因与调控细胞周期的基因之间的直接相互作用,将提供一种机制,通过该机制可以更好地理解众多生物学事件。我们已经确定PAX5在控制p53转录中具有直接作用。在原发性人类弥漫性星形细胞瘤中,PAX5表达与p53表达呈负相关。人类p53基因在其未翻译的第一个外显子内有一个PAX结合位点,该位点在整个进化过程中都是保守的。PAX5及其旁系同源物PAX2和PAX8能够在细胞培养中抑制p53启动子以及p53反应性报告基因的反式激活。所鉴定的结合位点的突变消除了PAX蛋白在体外的结合,并使启动子在细胞中失活。这些数据表明,PAX蛋白可能在发育过程中调节p53表达,并提出了一种肿瘤起始或进展的新的替代机制,即p53功能的丧失发生在转录水平。