Showing papers by "Robert J. Lefkowitz published in 1970"
TL;DR: This study demonstrates directly the binding of ACTH to its biologically significant site in direct proportion to their biological activity.
Abstract: Pure monoiodo ACTH-(125)I was prepared that was biologically active and free of unlabeled ACTH. Extracts of adrenal cortex that contained ACTH-sensitive adenyl cyclase, bound ACTH-(125)I; extracts that lacked the ACTH-sensitive cyclase did not bind ACTH-(125)I. Unlabeled ACTH inhibited the binding of ACTH-(125)I. Five ACTH derivatives which varied widely in biological activity were tested. All inhibited the binding of ACTH-(125)I in direct proportion to their biological activity. Albumin, insulin, and four unrelated iodinated hormones were inert. The addition of excess hormone or acetic acid produced rapid dissociation of bound ACTH-(125)I. This study demonstrates directly the binding of ACTH to its biologically significant site.
280 citations
TL;DR: This system, which appears to be applicable to all polypeptide hormones, provides a rapid and sensitive method for measurements of biologically active ACTH in dilute whole plasma.
Abstract: Biologically active iodine-125-labeled adrenocorticotropic hormone (ACTH) binds specifically to ACTH receptors extracted from adrenals. Unlabeled ACTH at 1 picogram per milliliter significantly displaces labeled ACTH from these receptors. This system, which appears to be applicable to all polypeptide hormones, provides a rapid and sensitive method for measurements of biologically active ACTH in dilute whole plasma.
150 citations
TL;DR: Calcium is thought to be required for the binding of adrenal corticotrophic hormone (ACTH) to its cellular receptor and inhibit the activation of adenyl cyclase by ACTH in subcellular particles from adipose and adrenal tissue.
Abstract: CALCIUM is thought to be required for the binding of adrenal corticotrophic hormone (ACTH) to its cellular receptor1–5: in its absence, ACTH fails to stimulate steroidogenesis in the adrenal or lipolysis in adipose tissue1,2,6,7. The actions of other lipolytic hormones such as adrenaline and glucagon do not require calcium1–3. On the other hand, high calcium concentrations (>1 mM) inhibit the activation of adenyl cyclase by ACTH in subcellular particles from adipose and adrenal tissue8,9. The sites of these effects of calcium have not been unequivocally located.
149 citations