R. Irannejad

Selective activation of intracellular β1AR using a spatially restricted antagonist

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.

Anionic phospholipids determine G protein coupling selectivity at distinct subcellular membrane compartments

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.

Inhibition of muscarinic receptor signaling protects human enteric inhibitory neurons against platin chemotherapy toxicity

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

Cardiac contraction and relaxation are regulated by beta 1 adrenergic receptor generated cAMP pools at distinct membrane locations

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

The OCT2 Transporter Regulates Dopamine D1 Receptor Signaling at the GolgiApparatus

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.

G protein-regulated endocytic trafficking of adenylyl cyclase type 9

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

Unraveling the functional role of the orphan solute carrier, SLC22A24 in the transport of steroid conjugates through metabolomic and genome-wide association studies

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

Golgi localized β1-adrenergic receptors stimulate Golgi PI4P hydrolysis by PLCε to regulate cardiac hypertrophy

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.