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Endocrine Reviews 18 (3): 281-305
Copyright © 1997 by The Endocrine Society

Molecular Endocrinology of Hydroxysteroid Dehydrogenases1

Trevor M. Penning

Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6084

I. Introduction
II. 3ß-Hydroxysteroid Dehydrogenase/Ketosteroid Isomerase (3ß-HSD/KSI)
A. Physiological and pharmacological significance
B. Cloning and expression of the 3ß-HSD/KSI cDNAs
C. Structure, regulation, and tissue-specific expression of the 3ß-HSD/KSI genes
D. 3ß-HSD deficiencies
III. 17ß-Hydroxysteroid Dehydrogenases
A. Physiological and pharmacological significance
B. Cloning and expression of the 17ß-HSD cDNAs
C. Structure, regulation, and tissue-specific expression of the 17ß-HSD genes
D. 17ß-HSD deficiency
IV. 11ß-Hydroxysteroid Dehydrogenases
A. Physiological and pharmacological significance
B. Cloning and expression of the 11ß-HSD cDNAs
C. Structure, regulation, and tissue-specific expression of the 11ß-HSD genes
D. 11ß-HSD deficiency
V. 3{alpha}-Hydroxysteroid Dehydrogenases
A. Physiological and pharmacological significance
B. Cloning and expression of the 3{alpha}-HSD cDNAs
C. Structure, regulation, and tissue-specific expression of the 3{alpha}-HSD genes
D. 3{alpha}-HSD deficiencies
VI. 20{alpha}-Hydroxysteroid Dehydrogenases
A. Physiological and pharmacological significance
B. Cloning and expression of the 20{alpha}-HSD cDNAs
C. Structure, regulation, and tissue-specific expression of the 20{alpha}-HSD genes
VII. HSDs Belong to Two Protein Families
A. HSDs that belong to the SDR superfamily
B. HSDs that belong to the AKR superfamily
VIII. Structure/Function of HSDs
A. Kinetic mechanism of HSDs
B. Catalytic mechanism of HSDs
C. x-Ray crystal structures of HSDs in the SDR superfamily
D. Site-directed mutagenesis on HSDs that are SDR members
E. x-Ray crystal structures of HSDs in the AKR superfamily
F. Site-directed mutagenesis on HSDs that are AKR members
G. Convergent evolution to a common reaction mechanism
H. Engineering alternate substrate specificity
IX. Conclusions




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