Julie Y. Crider
Papers
2
Total Citations
48
H-Index
2
About
Julie Y. Crider has made foundational contributions to ocular pharmacology, particularly in understanding how prostaglandins regulate cellular signaling in the eye. Her research focuses on the molecular mechanisms of prostanoid receptors—specifically EP₂, DP, and IP subtypes—and their role in modulating adenylyl cyclase activity and cyclic AMP production. In her highly cited 1998 study, Crider characterized a pharmacologically defined EP₂ receptor in human nonpigmented ciliary epithelial (NPE) cells, demonstrating how prostaglandin-stimulated adenylyl cyclase activity influences intraocular pressure regulation—a key pathway in glaucoma research. That same year, she advanced the field by developing a semi-automated, robotic radioimmunoassay to measure cAMP generated by DP-, EP₂-, and IP-prostaglandin receptor activation across human ocular and other cell types. This methodological innovation enabled high-throughput, precise quantification of receptor signaling, accelerating studies in ocular physiology and drug development. With over 48 citations across these two landmark papers, Crider’s work remains essential for researchers exploring prostaglandin receptor pharmacology, ocular hypertension, and targeted therapies for glaucoma. Her contributions exemplify how careful receptor characterization and innovative assay design can illuminate fundamental signaling pathways with direct clinical relevance.
Research Focus
Key Achievements
Top Papers
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- 2