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Volume 584, Issue 5, Pages 873-877 (5 March 2010)


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Myeloid translocation gene 16b is a dual A-kinase anchoring protein that interacts selectively with plexins in a phospho-regulated manner

Edited by Beat Imhof

Sarah E. Fiedlera, Robynn V. Schillaceab, Crystal J. Danielsa, Sarah F. Andrewsa, Daniel W. CarraCorresponding Author Informationemail address

Received 31 December 2009; accepted 1 February 2010. published online 05 February 2010.

Abstract 

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.

Structured summary

MINT-7556975: PlexinA3 (uniprotkb:P51805) physically interacts (MI:0915) with MTG 16b (uniprotkb:O75081) by anti tag coimmunoprecipitation (MI:0007)

MINT-7557008: RI alpha (uniprotkb:Q9DBC7) physically interacts (MI:0915) with MTG 16b (uniprotkb:O75081) by anti bait coimmunoprecipitation (MI:0006)

MINT-7556989: MTG 16b (uniprotkb:O75081) physically interacts (MI:0915) with PlexinA3 (uniprotkb:P51805) by pull down (MI:0096)

a VA Medical Center and Department of Endocrinology, Oregon Health & Sciences University, Portland, OR, USA

b VA Medical Center and Department of Neurology, Oregon Health & Sciences University, Portland, OR, USA

Corresponding Author InformationCorresponding author. Address: Veterans Affairs Medical Center, Mail Code R&D 8, 3710 SW US Veterans Hospital Road, Portland, OR 97239, USA. Fax: +1 503 721 1082.

PII: S0014-5793(10)00101-8

doi:10.1016/j.febslet.2010.02.007


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