Aquaporin‐2 trafficking is regulated by PDZ‐domain containing protein SPA‐1

FEBS Letters - Tập 568 - Trang 139-145 - 2004
Yumi Noda1,2, Saburo Horikawa3, Tetsushi Furukawa4, Keiji Hirai2, Yoshifumi Katayama2, Tomoki Asai1, Michio Kuwahara1, Koko Katagiri5, Tatsuo Kinashi5, Masakazu Hattori6, Nagahiro Minato6, Sei Sasaki1
1Department of Homeostasis Medicine and Nephrology, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
2Autonomic Physiology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
3Pathological Biochemistry, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
4Bio-informational Pharmacology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
5Departments of Molecular Immunology and Allergy, Kyoto University, Kyoto 606-8501, Japan
6Immunology and Cell Biology, Kyoto University, Kyoto 606-8501, Japan

Tóm tắt

Targeted positioning of water channel aquaporin‐2 (AQP2) strictly regulates body water homeostasis. Trafficking of AQP2 to the apical membrane is critical to the reabsorption of water in renal collecting ducts. Controlled apical positioning of AQP2 suggests the existence of proteins that interact with AQP2. A biochemical search for AQP2‐interacting proteins led to the identification of PDZ‐domain containing protein, signal‐induced proliferation‐associated gene‐1 (SPA‐1) which is a GTPase‐activating protein (GAP) for Rap1. The distribution of SPA‐1 coincided with that of AQP2 in renal collecting ducts. The site of colocalization was concomitantly relocated by hydration status. AQP2 trafficking to the apical membrane was inhibited by the SPA‐1 mutant lacking Rap1GAP activity and by the constitutively active mutant of Rap1. AQP2 trafficking was impaired in SPA‐1‐deficient mice. Our results show that SPA‐1 directly binds to AQP2 and regulates at least in part AQP2 trafficking.

Tài liệu tham khảo

10.1152/physrev.00024.2001 10.1038/361549a0 10.1074/jbc.M008216200 10.1093/emboj/18.9.2394 10.1086/323643 10.1093/hmg/11.7.779 10.1242/jcs.114.18.3219 10.1083/jcb.139.1.169 10.1152/ajprenal.2000.278.3.F395 10.1096/fj.01-0845fje J Sambrook E.F Fritsch T Maniatis 1989 Cold Spring Harbor Laboratory Press Cold Spring Harbor NY 10.1074/jbc.272.44.28081 10.1073/pnas.1834525100 10.1016/S1535-6108(03)00163-6 10.1083/jcb.148.6.1151 10.1016/S0968-0004(98)01224-9 10.1046/j.1523-1755.2003.00049.x 10.1083/jcb.200301133 10.1074/jbc.M207525200 10.1038/35073073 10.1046/j.1365-2443.2002.00546.x 10.1074/jbc.274.26.18463 10.1038/ncb728 10.1074/jbc.M010270200 10.1152/ajprenal.0091.2001 10.1146/annurev.neuro.24.1.1
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FEBS Letters

Tập 568

139-145

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