2. Academic Validation
  3. Role of Kenae/CCDC125 in cell motility through the deregulation of RhoGTPase

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

Affiliation

  • 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.

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