Gangwani Laxman
Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
J Biol Chem. 2006 Dec 29;281(52):40330-40. doi: 10.1074/jbc.M608165200. Epub 2006 Oct 26.
The zinc finger protein ZPR1 is present in both the cytoplasm and nucleoplasm. Cell cycle analysis demonstrates that ZPR1 undergoes major changes in subcellular distribution during proliferation. ZPR1 is diffusely localized throughout the cell during the G(1) and G(2)/M phases of the cell cycle. In contrast, ZPR1 redistributes to the nucleus during S phase and ZPR1 exhibits prominent co-localization with the survival motor neurons protein and the histone gene-specific transcription factor NPAT in subnuclear foci, including Cajal bodies that associate with histone gene clusters. ZPR1 deficiency causes disruption of survival motor neurons and NPAT localization within the nucleus, blocks S phase progression, and arrests cells in both the G(1) and G(2) phases of the cell cycle. These changes in subnuclear architecture and cell cycle progression may be caused by transcriptional defects in ZPR1-deficient cells, including decreased histone gene expression.
锌指蛋白ZPR1存在于细胞质和核质中。细胞周期分析表明，ZPR1在增殖过程中经历亚细胞分布的重大变化。在细胞周期的G(1)期和G(2)/M期，ZPR1分散地定位于整个细胞中。相比之下，ZPR1在S期重新分布到细胞核，并且ZPR1在亚核灶中与存活运动神经元蛋白和组蛋白基因特异性转录因子NPAT表现出显著的共定位，包括与组蛋白基因簇相关的卡哈尔体。ZPR1缺乏会导致存活运动神经元和NPAT在细胞核内的定位破坏，阻断S期进程，并使细胞停滞在细胞周期的G(1)期和G(2)期。亚核结构和细胞周期进程的这些变化可能是由ZPR1缺陷细胞中的转录缺陷引起的，包括组蛋白基因表达降低。
