Glucocorticoid receptors lacking hormone-binding activity are bound in nuclei of ATP-depleted cells.
The glucocorticoid receptor binding capacity of rat thymus cells disappears when the cells are depleted of ATP by anaerobiosis, and rapidly reappears when ATP levels are restored. Loss and recovery of binding capacity occurs even when protein synthesis is suppressed with cycloheximide. In view of this and similar work in other cell systems, we proposed that in cells deprived of ATP the receptor is present in a form--the 'null receptor' form, as we shall call it--that cannot bind hormone. Although many subsequent observations support this idea, no direct evidence has appeared for the existence of the null receptor. We have attempted to detect the null receptor in WEHI-7 mouse thymoma cells with a monoclonal antibody to the glucocorticoid receptor. Here we report that the null receptor is bound in the nuclei of ATP-depleted cells, and is present in amounts comparable to those of receptors in normal cells.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism*; D007700:Kinetics; D051379:Mice; D011965:Receptors, Glucocorticoid / Q000302:isolation & purification / Q000378:metabolism*; D013945:Thymoma / Q000378:metabolism; D013953:Thymus Neoplasms / Q000378:metabolism
D011965:Receptors, Glucocorticoid; D000255:Adenosine Triphosphate