Role of Kenae/CCDC125 in cell motility through the deregulation of RhoGTPase

Int J Mol Med. 2009 Nov;24(5):605-11. doi: 10.3892/ijmm_00000271.

Abstract

Isaac's syndrome is a movement disorder characterized by hyperexcitability of peripheral motor nerves. Patients with Isaac's syndrome often develop auto-antibodies to voltage-gated potassium channels (VGKCs) which block their function. However, anti-VGKC antibodies are not detected in all patients with Isaac's syndrome, suggesting the existence of another etiology. In this study, we performed immunoscreening using the serum from a patient with Isaac's syndrome and identified the novel gene named Kenae/CCDC125. Expression analysis of Kenae/CCDC125 revealed that its transcript was highly expressed in tissues associated with the immune system, such as the thymus, spleen and bone marrow. In cells stably expressing Kenae/CCDC125, delay in cell motility and deregulation of RhoGTPase (RhoA, Rac1 and cdc42) activity to extracellular stimuli were demonstrated. These results suggest that the novel gene, Kenae/CCDC125, acts as a regulator of cell motility through RhoA, Rac1 and cdc42.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Antigens / blood
  • Base Sequence
  • Cell Line, Tumor
  • Cell Movement*
  • Cloning, Molecular
  • GTPase-Activating Proteins / metabolism*
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Humans
  • Isaacs Syndrome / blood
  • Isaacs Syndrome / metabolism
  • Mice
  • Molecular Sequence Data
  • Proteins / chemistry
  • Proteins / genetics
  • Proteins / metabolism*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism

Substances

  • Antigens
  • CCDC125 protein, human
  • CCDC125 protein, mouse
  • GTPase-Activating Proteins
  • Proteins
  • RNA, Messenger

Associated data

  • GENBANK/AB024691