ABSTRACT
In 1977 and 1978, authors provided the first evidence that pyridoxal phosphate, the biologically active form of vitamin B6, interfered with the ability of the activated (DNA-binding form) glucocorticoid receptor to interact with DNA. Thus opening the possibility that the cellular level of pyridoxal phosphate might regulate the functioning of the receptor mechanism. The precursor or pyridoxal phosphate is dietary vitamin B6, pyridoxine. Pyridoxal phosphate in the micromolar to millimolar range inhibits the specific binding of glucocorticoid to the unactivated receptor complex. If pyridoxal phosphate is added before steroid, the inhibition of steroid binding is substantially more intense so that a preferred target is the unactivated steroid hormone receptor in the absence of steroid. An important aspect of the inhibition by pyridoxal phosphate was to determine whether the vitamer interacts directly with the receptor molecule or with another molecule in the system that regulates receptor function.
