Department of Biomedical Engineering, Chinese PLA 307 Hospital, Beijing 100071, China.
Biochem Biophys Res Commun. 2013 Jul 5;436(3):382-7. doi: 10.1016/j.bbrc.2013.05.109. Epub 2013 Jun 4.
Casein kinase-2 interacting protein-1 (CKIP-1) has been identified to play an important role in cell morphology, differentiation and apoptosis. However, the role of CKIP-1 in other cellular processes is still unknown. Here we investigated transcriptome profiles of WT and CKIP-1-deficient mouse embryonic fibroblasts (MEFs), and found that innate immunity and cell migration related pathways were significantly correlated with CKIP-1 expression. As macrophage is a key cell type in innate immunity, we then used murine macrophage RAW264.7 cells to discover CKIP-1 interacting proteins by immunoprecipitation/mass spectrometry (IP/MS). Analysis of these proteins revealed migration related pathways were enriched. Further experiments indicated that knockdown of CKIP-1 in RAW264.7 cells resulted in impaired cell migration. Our study suggests that CKIP-1 is a novel regulator of macrophage migration.
酪蛋白激酶-2 相互作用蛋白-1（CKIP-1）在细胞形态、分化和凋亡中发挥着重要作用。然而，CKIP-1 在其他细胞过程中的作用尚不清楚。在这里，我们研究了 WT 和 CKIP-1 缺陷型小鼠胚胎成纤维细胞（MEFs）的转录组谱，发现先天免疫和细胞迁移相关途径与 CKIP-1 的表达显著相关。由于巨噬细胞是先天免疫中的关键细胞类型，我们随后使用鼠巨噬细胞 RAW264.7 细胞通过免疫沉淀/质谱（IP/MS）来发现 CKIP-1 的相互作用蛋白。对这些蛋白质的分析表明，迁移相关途径被富集。进一步的实验表明，RAW264.7 细胞中 CKIP-1 的敲低导致细胞迁移受损。我们的研究表明，CKIP-1 是巨噬细胞迁移的一个新的调节因子。
