| First Author | Tiwari-Woodruff S | Year | 2006 |
| Journal | Am J Physiol Cell Physiol | Volume | 291 |
| Issue | 4 | Pages | C687-98 |
| PubMed ID | 16624990 | Mgi Jnum | J:119873 |
| Mgi Id | MGI:3703402 | Doi | 10.1152/ajpcell.00510.2005 |
| Citation | Tiwari-Woodruff S, et al. (2006) K+ channel KV3.1 associates with OSP/claudin-11 and regulates oligodendrocyte development. Am J Physiol Cell Physiol 291(4):C687-98 |
| abstractText | K(+) channels are differentially expressed throughout oligodendrocyte (Olg) development. K(V)1 family voltage-sensitive K(+) channels have been implicated in proliferation and migration of Olg progenitor cell (OPC) stage, and inward rectifier K+ channels (K(IR))4.1 are required for OPC differentiation to myelin-forming Olg. In this report we have identified a Shaw family K(+) channel, K(V)3.1, that is involved in proliferation and migration of OPC and axon myelination. Application of anti-K(V)3.1 antibody or knockout of Kv3.1 gene decreased the sustained K(+) current component of OPC by 50% and 75%, respectively. In functional assays block of K(V)3.1-specific currents or knockout of Kv3.1 gene inhibited proliferation and migration of OPC. Adult Kv3.1 gene-knockout mice had decreased diameter of axons and decreased thickness of myelin in optic nerves compared with age-matched wild-type littermates. Additionally, K(V)3.1 was identified as an associated protein of Olg-specific protein (OSP)/claudin-11 via yeast two-hybrid analysis, which was confirmed by coimmunoprecipitation and coimmunohistochemistry. In summary, the K(V)3.1 K(+) current accounts for a significant component of the total K(+) current in cells of the Olg lineage and, in association with OSP/claudin-11, plays a significant role in OPC proliferation and migration and myelination of axons. |
