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Identification of a Ser/Thr cluster in the C-terminal domain of the human prostaglandin EP4-R essential for agonist-induced beta-arrestin1 recruitment that differs from the apparent principal phosphorylation site.

hEP4-R (human prostaglandin E2 receptor, subtype EP4) is a Gs-linked heterotrimeric GPCR (G-protein-coupled receptor). It undergoes agonist-induced desensitization and internalization that depend on the presence of its C-terminal domain. Desensitization and internalization of GPCRs are often linked to agonist-induced b-arrestin complex formation, which is stabilized by phosphorylation. Subsequentl

Unusual CO adsorption sites on vanadium oxide-Pd(111) "inverse model catalyst" surfaces

The morphology, structure, and reactivity of vanadium oxide-decorated Pd(111) surfaces, which have been subjected to oxidation and reduction treatments, have been investigated by scanning tunneling microscopy (STM), high-resolution electron energy loss spectroscopy (HREELS), and high-resolution X-ray photoelectron spectroscopy (HR-XPS) with synchrotron radiation combined with ab initio density fun

Accurate Predictions of Nonpolar Solvation Free Energies Require Explicit Consideration of Binding-Site Hydration

Continuum solvation methods are frequently used to increase the efficiency of computational methods to estimate free energies. In this paper, we have evaluated how well such methods estimate the nonpolar solvation free-energy change when a ligand binds to a protein. Three different continuum methods at various levels of approximation were considered, viz., the polarized continuum model (PCM), a me

Localization of functional sites in the viral complement inhibitor KCP

Kaposi's sarcoma-associated herpes virus (KSHV) encodes a complement inhibitor named KSHV complement control protein (KCP). We have previously shown that KCP inhibits the human complement system by disrupting the C3 convertase of complement. KCP can accelerate the decay of the classical C3 convertase and it can act as a cofactor for factor I (R), which then cleaves and inactivates C4b or C3b (in t