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Published on: January 17, 2017
Surface expression of TTYH2 is attenuated by direct interaction with β-COP
Jiwon Ryu1, Dong-Gyu Kim2, Young-Sun Lee1
1School of Biosystems and Biomedical Sciences, College of Health Sciences, Korea University, Seoul 02841, Korea.
Abstract:
TTYH2 is a calcium-activated, inwardly rectifying anion channel that has been shown to be related to renal cancer and colon cancer. Based on the topological prediction, TTYH2 protein has five transmembrane domains with the extracellular N-terminus and the cytoplasmic C-terminus. In the present study, we identified a vesicle transport protein, β-COP, as a novel specific binding partner of TTYH2 by yeast two-hybrid screening using a human brain cDNA library with the C-terminal region of TTYH2 (TTYH2-C) as a bait. Using in vitro and in vivo binding assays, we confirmed the protein-protein interactions between TTYH2 and β-COP. We also found that the surface expression and activity of TTYH2 were decreased by co-expression with β-COP in the heterologous expression system. In addition, β-COP associated with TTYH2 in a native condition at a human colon cancer cell line, LoVo cells. The over-expression of β-COP in the LoVo cells led to a dramatic decrease in the surface expression and activity of endogenous TTYH2. Collectively, these data suggested that β-COP plays a critical role in the trafficking of the TTYH2 channel to the plasma membrane. [BMB Reports 2019; 52(7): 445-450].
Insights
Beta-coat protein (β-COP) binds to the TTYH2 channel, reducing its surface expression and activity. This interaction is crucial for regulating TTYH2 channel trafficking to the plasma membrane.
Area of Science:
- Molecular biology
- Cell biology
- Biochemistry
Background:
- TTYH2 is a calcium-activated anion channel implicated in renal and colon cancers.
- TTYH2 possesses five transmembrane domains, with an extracellular N-terminus and cytoplasmic C-terminus.
Discussion:
- Beta-COP, a vesicle transport protein, was identified as a specific binding partner for TTYH2.
- Protein-protein interactions between TTYH2 and beta-COP were confirmed using in vitro and in vivo assays.
- Beta-COP binding reduces TTYH2 surface expression and activity in heterologous systems and colon cancer cells.
Key Insights:
- Beta-COP directly interacts with the TTYH2 channel.
- Beta-COP negatively regulates TTYH2 surface expression and channel activity.
- This interaction is observed in human colon cancer cells (LoVo).
Outlook:
- Beta-COP plays a critical role in the plasma membrane trafficking of TTYH2.
- Further research may explore targeting the TTYH2-beta-COP interaction for cancer therapy.
- This finding provides new insights into the regulation of ion channel localization and function.
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