Title
Modulation of steroid receptor-mediated gene expression by vitamin B6. 70 REFS
AUTHOR
Tully DB; Allgood VE; Cidlowski JA
ORGANISATION
Department of Physiology, University of North Carolina at Chapel Hill 27599-7545.
SOURCE
FASEB J 1994 Mar 1; 8 (3): 343-9
LANGUAGE OF ORIGIN
English
ABSTRACT
Gene transcription mediated by steroid hormones has become one of the most extensively
characterized model systems for studying the regulation of gene expression in eukaryotic
cells. However, specific details of gene regulation by steroid hormones are often complex
and may be unique in specific cell types. Diverse regulatory mechanisms leading to either
activation or repression of particular genes frequently involve interactions between
steroid hormone receptors and other ubiquitous and/or cell-specific transcription factors
that act on the complex promoter of the regulated gene. Interplay between steroid
receptor-mediated and other signal transduction pathways may also be involved. In
addition, recent novel results indicate that moderate variations in the intracellular
concentration of pyridoxal 5'-phosphate (PLP), the biologically active form of vitamin B6,
can have pronounced modulatory effects on steroid-induced gene expression. Specifically,
elevation of intracellular PLP levels leads to decreased transcriptional responses to
glucocorticoid, progesterone, androgen, or estrogen hormones. Conversely, cells in a
vitamin B6-deficient state exhibit enhanced responsiveness to steroid hormones. One aspect
of the mechanism by which these transcriptional modulatory effects of PLP occur has
recently been shown to involve interruption of functional interactions between steroid
hormone receptors and the nuclear transcription factor NF1. These findings -- that the
vitamin B6 nutritional status of cells modulates their capacity to respond to steroid
hormones -- impose an additional level of cell-specific control over steroid hormone
regulation of gene expression and will serve as the focal point for this review.
MJTR: Gene Expression DE. Pyridoxine PD. Receptors, Steroid PH.
MNTR: Animal. Human. In Vitro. Pyridoxal Phosphate PD. Receptors, Glucocorticoid
DE. Receptors, Glucocorticoid PH. Receptors, Steroid DE. Support, Non-U.S. Gov't.
Support, U.S. Gov't, P.H.S.. Transcription, Genetic DE. JOURNAL ARTICLE. REVIEW.
REVIEW, TUTORIAL
RNUM: 0 (Receptors, Glucocorticoid); 0 (Receptors, Steroid); 54-47-7 (Pyridoxal
Phosphate); 65-23-6 (Pyridoxine)
GEOT: UNITED STATES
IDEN: ISSN: 0892-6638. JOURNAL-CODE: FAS. ENTRY-DATE: 940504.
NIH-GRANT-NUMBER: DK 32459DKNIDDK. JOURNAL-SUBSET: M X. IM-DATE: 9407.
ACCE: 94192903