First Author | Fiedler SE | Year | 2010 |
Journal | FEBS Lett | Volume | 584 |
Issue | 5 | Pages | 873-7 |
PubMed ID | 20138877 | Mgi Jnum | J:157523 |
Mgi Id | MGI:4431088 | Doi | 10.1016/j.febslet.2010.02.007 |
Citation | Fiedler SE, et al. (2010) Myeloid translocation gene 16b is a dual A-kinase anchoring protein that interacts selectively with plexins in a phospho-regulated manner. FEBS Lett 584(5):873-7 |
abstractText | The myeloid translocation gene (MTG) homologue Nervy associates with PlexinA on the plasma membrane, where it functions as an A-kinase anchoring protein (AKAP) to modulate plexin-mediated semaphorin signaling in Drosophila. Mammalian MTG16b is an AKAP found in immune cells where plexin-mediated semaphorin signaling regulates immune responses. This study provides the first evidence that MTG16b is a dual AKAP capable of binding plexins. These interactions are selective (PlexinA1 and A3 bind MTG, while PlexinB1 does not) and can be regulated by PKA-phosphorylation. Collectively, these data suggest a possible mechanism for the targeting and integration of adenosine 3',5'-cyclic monophosphate (cAMP) and semaphorin signaling in immune cells. |