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Vitamin B6 and Other Inhibitors of Glucocorticoid Receptor Function and Cell Death of B16 Melanoma Cells
Book chapter

Vitamin B6 and Other Inhibitors of Glucocorticoid Receptor Function and Cell Death of B16 Melanoma Cells

Gerald Litwack, Noreen M. Robertson, Andrew B. Maksymowych and Mahmut Celiker
Vitamins and Minerals in the Prevention and Treatment of Cancer
1991

Abstract

Melanoma Cells Melanoma Cell Proliferation Pigmented Melanoma Cells Pyridoxal Phosphate Concentration Indirect Immunofluorescence B16 Melanoma Cells Glucocorticoid Responsive Element DEAE Cellulose Chromatography DNA Binding Dietary Vitamin B6 Pyridoxal Schiff Base Ion Exchange Chromatography Activated Receptor Complex Glucocorticoid Receptor Complexes Glucocorticoid Receptor Side Chain Amino Pyridoxal Phosphate Activated Glucocorticoid Receptor Intact Cells Nuclear Translocation Lysine Residue Glucocorticoid Receptor Function Steroid Binding Mouse B16 Melanoma Cells
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.

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