| Role of Kenae/CCDC125 in cell motility through the deregulation of RhoGTPase |
Authors: Natsumi Araya, 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:
Department of Genome Science, Institute of Medical Science, St. Marianna University School of Medicine, Kanagawa 216-8512, Japan
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Doi: 10.3892/ijmm_00000271 |
Pages: 605-611 |
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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