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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Annexin II modulates volume-activated chloride currents in vascular endothelial cells.

The membrane-associated, microfilament-binding protein annexin II is abundantly expressed in endothelial cells from calf pulmonary artery (CPAE cells). We have analyzed its role in the regulation of volume-activated chloride currents (ICl, vol) by loading the cells via the patch pipette with a peptide comprising the N-terminal 14 residues of annexin II. This sequence harbors the binding site for the intracellular annexin II ligand, p11, and the peptide interferes with the annexin II-p11 complex formation. Loading of a CPAE cell with this peptide caused a gradual decrease in the amplitude of ICl, vol during repetitive stimulations with a 28% hypotonic extracellular solution. This run down of the current was virtually absent in untreated cells and in cells that were loaded with a mutated 14-amino acid peptide, which has a single amino acid replacement known to result in a more than 1000 times reduced affinity for binding to p11. We conclude that annexin II-p11 complex formation is either directly or indirectly involved in the activation of ICl, vol in endothelial cells.[1]

References

  1. Annexin II modulates volume-activated chloride currents in vascular endothelial cells. Nilius, B., Gerke, V., Prenen, J., Szücs, G., Heinke, S., Weber, K., Droogmans, G. J. Biol. Chem. (1996) [Pubmed]
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