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. 2015 Jun 17;9(4):186–195. doi: 10.1080/19336950.2015.1058454

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

© Jinhong Wie, Byung Joo Kim, Jongyun Myeong, Kotdaji Ha, Seung Joo Jeong, Dongki Yang, Euiyong Kim, Ju-Hong Jeon, and Insuk So

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 4. — Schematic diagram for the signaling pathway involved in dexamethasone-induced TRPC4 channel activity. Rasd1 is classified as a guanine nucleotide exchange factor (GEF) for Gα_i proteins. Dexamethasone enhanced Rasd1 that promotes GDP to GTP exchange in Gα_i proteins and triggers it to be functionally active until the intrinsic GTPase activity of Gα_i proteins turns off the signal by hydrolyzing GTP to GDP. Gα_i-GTP protein activates TRPC4β channel. Leptin binds to its receptor (LRB) to activate Jak2, which phosphorylates IRS proteins and activates PI3 kinase. PI3 kinase activates PLCγ1 to increase TRPC4 channel activity.