Introduction

Abstract

For three decades it has been known that steroid sex hormones exert their principal biological actions in combination with specific receptor proteins. As first shown with estrogens, the steroid binds to an intracellular receptor and induces hormonal response without itself undergoing chemical change. Studies in many laboratories established that an early event in hormone action is the enhanced expression of genes that are somehow restricted in hormone-dependent cells (for early references see 1,2). Two forms of the receptor were identified, including a native form, with little affinity for nuclei, and an activated or transformed modification, which binds tightly to chromatin and is produced by the action of the hormone on the native receptor. With the demonstration that only the transformed receptor has the ability to influence RNA synthesis in isolated target cell nuclei, there emerged a general concept of steroid hormone action, in which the role of the steroid is to convert the native receptor protein to a modulator of transcription (3).