| First Author | Moriwaki Y | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 11996 |
| PubMed ID | 32686737 | Mgi Jnum | J:299826 |
| Mgi Id | MGI:6490712 | Doi | 10.1038/s41598-020-68947-7 |
| Citation | Moriwaki Y, et al. (2020) Endogenous neurotoxin-like protein Ly6H inhibits alpha7 nicotinic acetylcholine receptor currents at the plasma membrane. Sci Rep 10(1):11996 |
| abstractText | alpha7 nicotinic acetylcholine receptors (nAChRs) are widely expressed in the central nervous system and regarded as potential therapeutic targets for neurodegenerative conditions, such as Alzheimer's disease and schizophrenia. Yet, despite the assumed pathophysiological importance of the alpha7 nAChR, molecular physiological characterization remains poorly advanced because alpha7 nAChR cannot be properly folded and sorted to the plasma membranes in most mammalian cell lines, thus preventing the analyses in heterologous expression system. Recently, ER-resident membrane protein NACHO was discovered as a strong chaperone for the functional expression of alpha7 nAChR in non-permissive cells. Ly6H, a brain-enriched GPI-anchored neurotoxin-like protein, was reported as a novel modulator regulating intracellular trafficking of alpha7 nAChR. In this study, we established cell lines that stably and robustly express surface alpha7 nAChR by introducing alpha7 nAChR, Ric-3, and NACHO cDNA into HEK293 cells (Triple alpha7 nAChR/RIC-3/NACHO cells; TARO cells), and re-evaluated the function of Ly6H. We report here that Ly6H binds with alpha7 nAChRs on the cell membrane and modulates the channel activity without affecting intracellular trafficking of alpha7 nAChR. |
