Platelet protein synthesis, regulation, and post-translational modifications: mechanics and function.

Dogma had been firmly entrenched in the minds of the scientific community that the anucleate mammalian platelet was incapable of protein biosynthesis since their identification in the late 1880s. These beliefs were not challenged until the 1960s when several reports demonstrated that platelets possessed the capacity to biosynthesize proteins. Even then, many still dismissed the synthesis as trivial and unimportant for at least another two decades.

Superagonist, Full Agonist, Partial Agonist, and Antagonist Actions of Arylguanidines at 5-Hydroxytryptamine-3 (5-HT) Subunit A Receptors.

Introduction of minor variations to the substitution pattern of arylguanidine 5-hydroxytryptamine-3 (5-HT) receptor ligands resulted in a broad spectrum of functionally-active ligands from antagonist to superagonist. For example, (i) introduction of an additional Cl-substituent(s) to our lead full agonist N-(3-chlorophenyl)guanidine (mCPG, 2; efficacy % = 106) yielded superagonists 7-9 (efficacy % = 186, 139, and 129, respectively), (ii) a positional isomer of 2, p-Cl analog 11, displayed partial agonist actions (efficacy % = 12), and (iii) replacing the halogen atom at the meta or para position with an electron donating OCH group or a stronger electron withdrawing (i.e.