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14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels.

Title: 14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels.
Name(s): Liu, Feng, author
Zhou, Qin, author
Zhou, Jie, author
Sun, Hao, author
Wang, Yan, author
Zou, Xiuqun, author
Feng, Lingling, author
Hou, Zhaoyuan, author
Zhou, Aiwu, author
Zhou, Yi, author
Li, Yong, author
Type of Resource: text
Genre: Journal Article
Date Issued: 2015-01-30
Physical Form: computer
online resource
Extent: 1 online resource
Language(s): English
Abstract/Description: Surface expression of voltage-gated Ca(2+) (Cav) channels is important for their function in calcium homeostasis in the physiology of excitable cells, but whether or not and how the α1 pore-forming subunits of Cav channels are trafficked to plasma membrane in the absence of the known Cav auxiliary subunits, β and α2δ, remains mysterious. Here we showed that 14-3-3 proteins promoted functional surface expression of the Cav2.2 α1B channel in transfected tsA-201 cells in the absence of any known Cav auxiliary subunit. Both the surface to total ratio of the expressed α1B protein and the current density of voltage step-evoked Ba(2+) current were markedly suppressed by the coexpression of a 14-3-3 antagonist construct, pSCM138, but not its inactive control, pSCM174, as determined by immunofluorescence assay and whole cell voltage clamp recording, respectively. By contrast, coexpression with 14-3-3τ significantly enhanced the surface expression and current density of the Cav2.2 α1B channel. Importantly, we found that between the two previously identified 14-3-3 binding regions at the α1B C terminus, only the proximal region (amino acids 1706-1940), closer to the end of the last transmembrane domain, was retained by the endoplasmic reticulum and facilitated by 14-3-3 to traffic to plasma membrane. Additionally, we showed that the 14-3-3/Cav β subunit coregulated the surface expression of Cav2.2 channels in transfected tsA-201 cells and neurons. Altogether, our findings reveal a previously unidentified regulatory function of 14-3-3 proteins in promoting the surface expression of Cav2.2 α1B channels.
Identifier: FSU_pmch_25516596 (IID), 10.1074/jbc.M114.567800 (DOI), PMC4317001 (PMCID), 25516596 (RID), 25516596 (EID), M114.567800 (PII)
Keywords: 14-3-3tau, Calcium Channel, Cav 2.2 Channel, Cav Auxiliary Subunits, Electrophysiology, Endoplasmic Reticulum Retention, Membrane Trafficking, Protein-Protein Interaction, Trafficking
Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at
Subject(s): 14-3-3 Proteins/genetics
14-3-3 Proteins/metabolism
Blotting, Western
Calcium Channels, N-Type/genetics
Calcium Channels, N-Type/metabolism
Cell Membrane/metabolism
Cells, Cultured
Endoplasmic Reticulum/metabolism
Protein Binding
Protein Transport/physiology
Rats, Sprague-Dawley
Persistent Link to This Record:
Host Institution: FSU
Is Part Of: The Journal of biological chemistry.
Issue: iss. 5, vol. 290

Choose the citation style.
Liu, F., Zhou, Q., Zhou, J., Sun, H., Wang, Y., Zou, X., … Li, Y. (2015). 14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels. The Journal Of Biological Chemistry. Retrieved from