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.
Natsumi Araya  1 ,  Hitoshi Arimura ,  Ko-ichi Kawahara ,  Naoko Yagishita ,  Junji Ishida ,  Ryoji Fujii ,  Satoko Aratani ,  Hidetoshi Fujita ,  Tomoo Sato ,  Yoshihisa Yamano ,  Itsuro Higuchi ,  Mitsuhiro Osame ,  Kusuki Nishioka ,  Akiyoshi Fukamizu ,  Kimiyoshi Arimura ,  Ikuro Maruyama ,  Toshihiro Nakajima
Affiliations
  • 1. Department of Genome Science, Institute of Medical Science, St. Marianna University School of Medicine, Kanagawa 216-8512, Japan.
PMID: 19787194 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.