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个人简介
My research spans the spectrum from clinical research in pulmonary vascular disease, to translational research in cardiovascular disease, to the basic science of receptor signaling.
Our basic science resesarch focuses on understanding and untapping the signaling potential of G protein-coupled receptors (GPCRs) to regulate inflammation in vascular disease. GPCRs are the most common transmembrane receptors in the human genome (over 800 members) and are some of the most successful targets for drug therapies. While it has been known for some time that these receptors signal through multiple downstream effectors (such as heterotrimeric G proteins and multifunctional beta arrestin adapter proteins), over the past decade it has been better appreciated that these receptors are capable of signaling with different efficacies to these effectors, a phenomenon referred to as “biased agonism”. Ligands can be biased, by activating different pathways from one another, and receptors can be biased, by signaling to a limited number of pathways that are normally available to them. Moreover, this phenomenon also appears to be common to other transmembrane and nuclear receptors. While a growing number of biased agonists acting at multiple receptors have been identified, there is still little known regarding the mechanisms underlying biased signaling and its physiologic impact.
Our basic science resesarch focuses on understanding and untapping the signaling potential of G protein-coupled receptors (GPCRs) to regulate inflammation in vascular disease. GPCRs are the most common transmembrane receptors in the human genome (over 800 members) and are some of the most successful targets for drug therapies. While it has been known for some time that these receptors signal through multiple downstream effectors (such as heterotrimeric G proteins and multifunctional beta arrestin adapter proteins), over the past decade it has been better appreciated that these receptors are capable of signaling with different efficacies to these effectors, a phenomenon referred to as “biased agonism”. Ligands can be biased, by activating different pathways from one another, and receptors can be biased, by signaling to a limited number of pathways that are normally available to them. Moreover, this phenomenon also appears to be common to other transmembrane and nuclear receptors. While a growing number of biased agonists acting at multiple receptors have been identified, there is still little known regarding the mechanisms underlying biased signaling and its physiologic impact.
研究兴趣
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American journal of respiratory and critical care medicineno. 2 (2024): 131-133
CURRENT RESPIRATORY MEDICINE REVIEWS (2024)
Chloe Hicks,Julia Gardner, Dylan Scott Eiger, Nicholas D Camarda,Uyen Pham, Saisha Dhar, Hailey Rodriguez,Anand Chundi,Sudarshan Rajagopal
bioRxiv : the preprint server for biology (2024)
Julia Gardner,Dylan Scott Eiger,Chloe Hicks,Issac Choi,Uyen Pham, Anand Chundi, Ojas Namjoshi,Sudarshan Rajagopal
SCIENCE SIGNALINGno. 823 (2024): eadd9139-eadd9139
CIRCULATIONno. 17 (2023): 1316-1329
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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS (2023)
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Circulation (2023)
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Kidney360no. 5 (2023): 631-640
European Heart Journalno. 14 (2023): 1280-1282
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Biochimica et biophysica acta. General subjectsno. 10 (2023): 130428-130428
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