Department of Cellular and Molecular Research, National Cancer Centre Singapore, Singapore, Singapore.
PLoS One. 2010 Oct 26;5(10):e13597. doi: 10.1371/journal.pone.0013597.
Accumulated literature suggests that the acidic nuclear phosphoprotein 32 kilodalton (Anp32) proteins control multiple cellular activities through different molecular mechanisms. Like other Anp32 family members, Anp32e (a.k.a. Cpd1, PhapIII) has been conserved throughout vertebrate evolution, suggesting that it has an important function in organismal survival.
Here, we demonstrate that the Anp32e gene can be deleted in mice without any apparent effect on their wellbeing. No defects in thymocyte apoptosis in response to various stresses, fibroblast growth, gross behaviour, physical ability, or pathogenesis were defined. Furthermore, combined deletion of Anp32a and Anp32e also resulted in a viable and apparently healthy mouse.
These results provide evidence that significant functional redundancy exists among Anp32 family members.
积累的文献表明，酸性核磷蛋白 32 千道尔顿（Anp32）蛋白通过不同的分子机制控制多种细胞活动。与其他 Anp32 家族成员一样，Anp32e（又名 Cpd1、PhapIII）在整个脊椎动物进化过程中都得到了保守，这表明它在生物生存中具有重要功能。
在这里，我们证明了在没有明显影响其健康的情况下，小鼠可以删除 Anp32e 基因。未发现对各种应激、成纤维细胞生长、大体行为、身体能力或发病机制的胸腺细胞凋亡有缺陷。此外，Anp32a 和 Anp32e 的联合缺失也导致了一种存活且明显健康的小鼠。
这些结果提供了证据，表明 Anp32 家族成员之间存在显著的功能冗余。
