R. Irannejad

This paper develops spatially restricted antagonists to selectively inhibit β1AR signaling at the plasma membrane versus intracellular compartments, revealing compartment-specific effects on downstream signaling.

This study shows that anionic phospholipids like PI(4,5)P2 enable promiscuous GPCR coupling to both cognate and non-cognate G proteins at the plasma membrane, while restricting coupling to cognate G proteins in other compartments.

This study identifies muscarinic receptor signaling as a key driver of platin-induced enteric neuropathy and shows that its inhibition protects neurons from toxicity.

The paper shows that beta 1 adrenergic receptor-generated cAMP pools at distinct membrane locations regulate cardiac contraction and relaxation through different PKA targets.

This study shows that dopamine D1 receptor signaling occurs at the Golgi apparatus via OCT2-mediated activation, revealing a new mechanism for subcellular GPCR function.

This study shows AC9 traffics from the plasma membrane to endosomes via Gs, unlike AC1, and contributes to cAMP production from endosomes.

The paper identifies SLC22A24 as a transporter for steroid conjugates and bile acids, linking genetic variants to steroid levels and disease.

The paper identifies a pathway where Golgi localized β1-adrenergic receptors stimulate PI4P hydrolysis via PLCε to promote cardiac hypertrophy, distinct from surface receptor signaling.