| First Author | Wallace SW | Year | 2011 |
| Journal | Mol Cell Biol | Volume | 31 |
| Issue | 1 | Pages | 81-91 |
| PubMed ID | 20974804 | Mgi Jnum | J:169711 |
| Mgi Id | MGI:4941685 | Doi | 10.1128/MCB.01001-10 |
| Citation | Wallace SW, et al. (2011) The Rho target PRK2 regulates apical junction formation in human bronchial epithelial cells. Mol Cell Biol 31(1):81-91 |
| abstractText | Rho GTPases regulate multiple signaling pathways to control a number of cellular processes during epithelial morphogenesis. To investigate the downstream pathways through which Rho regulates epithelial apical junction formation, we screened a small interfering RNA (siRNA) library targeting 28 known Rho target proteins in 16HBE human bronchial epithelial cells. This led to the identification of the serine-threonine kinase PRK2 (protein kinase C-related kinase 2, also called PKN2). Depletion of PRK2 does not block the initial formation of primordial junctions at nascent cell-cell contacts but does prevent their maturation into apical junctions. PRK2 is recruited to primordial junctions, and this localization depends on its C2-like domain. Rho binding is essential for PRK2 function and also facilitates PRK2 recruitment to junctions. Kinase-dead PRK2 acts as a dominant-negative mutant and prevents apical junction formation. We conclude that PRK2 is recruited to nascent cell-cell contacts through its C2-like and Rho-binding domains and promotes junctional maturation through a kinase-dependent pathway. |
