Dominant Negative Actions of Human Prostacyclin Receptor Variant Through Dimerization: Implications for Cardiovascular Disease | Zendy

Salam A. Ibrahim | Zendy; Mazell M. Tetruashvily | Zendy; Alex J. Frey | Zendy; Stephen J. Wilson | Zendy; Jeremiah Stitham | Zendy; John Hwa | Zendy; Emer M. Smyth | Zendy

Open Access

Dominant Negative Actions of Human Prostacyclin Receptor Variant Through Dimerization: Implications for Cardiovascular Disease

Author(s) -

Salam A. Ibrahim,

Mazell M. Tetruashvily,

Alex J. Frey,

Stephen J. Wilson,

Jeremiah Stitham,

John Hwa,

Emer M. Smyth

Publication year - 2010

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.110.208900

Subject(s) - prostacyclin , endoplasmic reticulum , thromboxane , receptor , agonist , transfection , thromboxane receptor , hek 293 cells , endocrinology , medicine , thromboxane a2 , microbiology and biotechnology , biology , chemistry , platelet , biochemistry , gene

Prostacyclin and thromboxane mediate opposing cardiovascular effects through their receptors, the prostacyclin receptor (IP) and thromboxane receptor (TP). Individuals heterozygous for an IP variant, IP(R212C), displayed exaggerated loss of platelet IP responsiveness and accelerated cardiovascular disease. We examined association of IP(R212C) into homo- and heterodimeric receptor complexes and the impact on prostacyclin and thromboxane biology.

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