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. 2011 Dec 22;44(3):225–235. doi: 10.3858/emm.2012.44.3.017

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Copyright © 2012 by the Korean Society for Biochemistry and Molecular Biology

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Model for the molecular processes underlying hemorrhage phenotype in AKAP12 morphant. AKAP12 depletion in endothelial cells decreases PAK2 and AF6 expression. PAK2 depletion induces stress fiber formation, while AF6 depletion decreases cortical actin assembly in AKAP12-depleted endothelial cells. These changes in AKAP12-depleted endothelial cells lead to the disruption of endothelial junctions and the loss of vascular integrity, thereby causing hemorrhages in akap12 morphants. This model conversely indicates the role for AKAP12 in the maintenance of both PAK2 and AF6 expression.