TY - JOUR
T1 - Tctex-1 augments G protein-coupled receptor-mediated Gs signaling by activating adenylyl cyclase
AU - Saito, Masaki
AU - Chiba, Ayano
AU - Sato, Takeya
AU - Moriya, Takahiro
AU - Sukegawa, Jun
AU - Nakahata, Norimichi
N1 - Funding Information:
We greatly thank Dr. Ching-Hwa Sung (Weill Cornell Medical College, NY) for providing mTctex-1-shRNA plasmid. We would also like to acknowledge Biomedical Research Core (Tohoku University Graduate School of Medicine) for technical support. We would also like to thank Editage ( www.editage.jp/ ) for English language editing. This work was supported by the Grant-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (Nos. 15K20856 and 18K06125 to M.S.; No. 18K06885 to T. S.; and Nos. 21200007 , 21590267 , and 26460331 to J.S.), Takeda Science Foundation , Nishinomiya Basic Research Fund (to M.S.), and Shokei Gakuin University (to J.S.).
Publisher Copyright:
© 2020 The Authors
PY - 2021/1
Y1 - 2021/1
N2 - Proteins interacting with G protein-coupled receptors (GPCRs) can modulate signal transduction of these receptors. However, the regulatory mechanisms of the interacting proteins are diverse and largely unknown. We have previously shown that Tctex-1 (or DYNLT1) can interact with the parathyroid hormone receptor (PTHR). In the present study, we investigated the role of Tctex-1 in the PTHR signaling and found that Tctex-1 augmented the PTHR-mediated Gs/adenylyl cyclase (AC) pathway by activating AC regardless of the binding to PTHR. Furthermore, Tctex-1 directly bound to AC type 6. These data demonstrate a novel mechanism underlying GPCR/Gs signaling regulated by Tctex-1.
AB - Proteins interacting with G protein-coupled receptors (GPCRs) can modulate signal transduction of these receptors. However, the regulatory mechanisms of the interacting proteins are diverse and largely unknown. We have previously shown that Tctex-1 (or DYNLT1) can interact with the parathyroid hormone receptor (PTHR). In the present study, we investigated the role of Tctex-1 in the PTHR signaling and found that Tctex-1 augmented the PTHR-mediated Gs/adenylyl cyclase (AC) pathway by activating AC regardless of the binding to PTHR. Furthermore, Tctex-1 directly bound to AC type 6. These data demonstrate a novel mechanism underlying GPCR/Gs signaling regulated by Tctex-1.
KW - Adenylyl cyclase
KW - Cytoplasmic dynein light chain Tctex-1
KW - Parathyroid hormone receptor
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U2 - 10.1016/j.jphs.2020.11.011
DO - 10.1016/j.jphs.2020.11.011
M3 - Article
C2 - 33357773
AN - SCOPUS:85097749978
SN - 1347-8613
VL - 145
SP - 150
EP - 154
JO - Journal of Pharmacological Sciences
JF - Journal of Pharmacological Sciences
IS - 1
ER -