Signaling of NO/cGMP via IRAG

Jens Schlossmann

doi:10.1186/1471-2210-7-s1-s49

Abstract

Signaling by NO/cGMP/cGMP-dependent kinase I (cGKI) is important for a variety of physiological functions comprising relaxation of smooth muscle and inhibition of platelet aggregation. An important pathway of this signaling cascade includes the inositol 1,4,5-trisphosphate receptor I (IP3RI) associated protein cGMP kinase substrate (IRAG). This protein interacts in a trimeric macrocomplex with cGKIβ and the IP3RI. To get insight into the physiological function of IRAG two different mice strains were generated by targeted deletion: (1) IRAGΔ12/Δ12 with an exon 12 deletion disrupting the IRAG/IP3RI interaction. (2) IRAG-/with an exon 3 deletion generating an IRAG knockout mutant.

Highlights

3rd International Conference on cGMP Generators, Effectors and Therapeutic Implications Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here.
Analysis of IRAGΔ12/Δ12 platelet aggregation in vitro using collagen and thrombin as agonists and Fura2 calcium measurements revealed that IP3RI/IRAG interaction is essential for NO/cGMP signaling mediating inhibition of platelet aggregation
It was shown that IP3RI/IRAG interaction is essential for the NO-dependent prevention of thrombus formation

Summary

Introduction

3rd International Conference on cGMP Generators, Effectors and Therapeutic Implications Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here. . Signaling of NO/cGMP via IRAG Jens Schlossmann* Address: Institut für Pharmakologie und Toxikologie, Universität Regensburg, D-93040 Regensburg, Germany Email: Jens Schlossmann* - jens.schlossmann@chemie.uni-regensburg.de * Corresponding author from 3rd International Conference on cGMP Generators, Effectors and Therapeutic Implications Dresden, Germany.

Results

Conclusion