Integrated analysis of genomics and proteomics reveals that CKIP-1 is a novel macrophage migration regulator

Biochem Biophys Res Commun. 2013 Jul 5;436(3):382-7. doi: 10.1016/j.bbrc.2013.05.109. Epub 2013 Jun 4.

Abstract

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.

Keywords: CKIP-1; IP/MS; Macrophage migration; Microarray.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Cell Migration Assays, Macrophage
  • Cell Movement*
  • Chemotactic Factors / pharmacology
  • Fibroblasts / metabolism
  • Gene Knockout Techniques
  • Genomics
  • Macrophages / drug effects
  • Macrophages / metabolism*
  • Mice
  • N-Formylmethionine Leucyl-Phenylalanine / pharmacology
  • Protein Interaction Mapping
  • Proteomics
  • Signal Transduction
  • Transcriptome

Substances

  • CKIP-1 protein, mouse
  • Carrier Proteins
  • Chemotactic Factors
  • N-Formylmethionine Leucyl-Phenylalanine