| First Author | Hu ZL | Year | 2010 |
| Journal | Am J Physiol Cell Physiol | Volume | 299 |
| Issue | 6 | Pages | C1355-62 |
| PubMed ID | 20826761 | Mgi Jnum | J:226149 |
| Mgi Id | MGI:5695839 | Doi | 10.1152/ajpcell.00569.2009 |
| Citation | Hu ZL, et al. (2010) Disruption of PICK1 attenuates the function of ASICs and PKC regulation of ASICs. Am J Physiol Cell Physiol 299(6):C1355-62 |
| abstractText | Acid-sensing ion channels (ASICs) extensively exist in both central and peripheral neuronal systems and contribute to many physiological and pathological processes. The protein that interacts with C kinase 1 (PICK1) was cloned as one of the proteins interacting with protein kinase C (PKC) and colocalized with ASIC1 and ASIC2. Here, we used PICK1 knockout (PICK1-KO) C57/BL6 mice together with the whole cell patch clamp, calcium imaging, RT-PCR, Western blot, and immunocytochemistry techniques to explore the possible change in ASICs and the regulatory effects of PKC on ASICs. The results showed that PICK1 played a key role in regulation of ASIC functions. In PICK1-KO mouse cortical neurons, both the amplitude of ASIC currents and elevation of [Ca(2+)](i) mediated by acid were decreased, which were attributable to the decreased expression of ASIC1a and ASIC2a proteins in the plasma membrane. PKC, a partner protein of PICK1, regulated ASIC functions via PICK1. The agonist and antagonist of PKC only altered ASIC currents and acid-induced increase in [Ca(2+)](i) in wild-type, but not in KO mice. In conclusion, our data provided the direct evidence from PICK1-KO mice that a novel target protein, PICK1, would regulate ASIC function and membrane expression in the brain. In addition, PICK1 played the bridge role between PKC and ASICs. |
