This work was supported by the National Natural Science Foundation of China (No 30400154 and 30400329), Innovation Research Team Program of Ministry of Education (No IRT0560), and the National Program of Basic Research of China (No G2006CB500808). Acknowledgement We thank Prof Yasuo MORI (University of Kyoto) for providing the plasmids of TRPC7 and mutCaM.
Aim: The aim of the present study was to explore the mechanism for the Ca^2+- dependent inactivation of the canonical transient receptor potential (TRPC) 7 channel expressed in human embryonic kidney 293 cells. Me...