English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Intracellular signalling by NO/cGMP-dependent protein kinase type I (cGKI) relaxes smooth muscles thereby modulating e.g. vascular tone. An important mediator of this signalling cascade is the inositol 1,4,5,-trisphosphate receptor I (IP3 RI) associated protein cGMP kinase substrate (IRAG). This protein forms a trimeric complex together with the cGMP kinase Iβ and the IP3 RI. Recently, it was shown that the relaxation of hormone-contracted aortic smooth muscle by cGMP was abolished in IRAG Δ12/Δ12 mutant mice with a disrupted IRAG-IP3 RI interaction site [1]. Now we investigated whether IRAG might regulate the vascular tone in small vessels. NO-mediated relaxation of isolated arteria tibialis was nearly absent in the IRAG mutant. Moreover, the relaxing effect of IRAG on NO-mediated dilation of resistance vessels in perfused hind limbs of mutant mice was abolished.

Relaxation of vascular smooth muscle by the cGMP-kinase substrate IRAG