| First Author | Wang L | Year | 2018 |
| Journal | Cell Rep | Volume | 24 |
| Issue | 11 | Pages | 2894-2907 |
| PubMed ID | 30208315 | Mgi Jnum | J:270995 |
| Mgi Id | MGI:6278362 | Doi | 10.1016/j.celrep.2018.05.075 |
| Citation | Wang L, et al. (2018) The Atypical Kinesin KIF26A Facilitates Termination of Nociceptive Responses by Sequestering Focal Adhesion Kinase. Cell Rep 24(11):2894-2907 |
| abstractText | Kinesin superfamily proteins (KIFs) are molecular motors that typically alter the subcellular localization of their cargos. However, the atypical kinesin KIF26A does not serve as a motor but can bind microtubules and affect cellular signaling cascades. Here, we show that KIF26A maintains intracellular calcium homeostasis and negatively regulates nociceptive sensation. Kif26a(-/-) mice exhibit intense and prolonged nociceptive responses. In their primary sensory neurons, excessive inhibitory phosphorylation of plasma membrane Ca(2+) ATPase (PMCA) mediated by focal adhesion kinase (FAK) rendered the Ca transients resistant to termination, and the peripheral axonal outgrowth was significantly enhanced. Upstream, KIF26A is directly associated with a FERM domain of FAK and antagonizes FAK function in integrin-Src family kinase (SFK)-FAK signaling, possibly through steric hindrance and localization to cytoplasmic microtubules. |
