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Structure and Catalytic Mechanism of Human Steroid 5-Reductase (AKR1D1)

Journal Article · · Molecular and Cellular Endocrinology
Human steroid 5{beta}-reductase (aldo-keto reductase (AKR) 1D1) catalyzes reduction of {Delta}{sup 4}-ene double bonds in steroid hormones and bile acid precursors. We have reported the structures of an AKR1D1-NADP{sup +} binary complex, and AKR1D1-NADP{sup +}-cortisone, AKR1D1-NADP{sup +}-progesterone and AKR1D1-NADP{sup +}-testosterone ternary complexes at high resolutions. Recently, structures of AKR1D1-NADP{sup +}-5{beta}-dihydroprogesterone complexes showed that the product is bound unproductively. Two quite different mechanisms of steroid double bond reduction have since been proposed. However, site-directed mutagenesis supports only one mechanism. In this mechanism, the 4-pro-R hydride is transferred from the re-face of the nicotinamide ring to C5 of the steroid substrate. E120, a unique substitution in the AKR catalytic tetrad, permits a deeper penetration of the steroid substrate into the active site to promote optimal reactant positioning. It participates with Y58 to create a 'superacidic' oxyanion hole for polarization of the C3 ketone. A role for K87 in the proton relay proposed using the AKR1D1-NADP{sup +}-5{beta}-dihydroprogesterone structure is not supported.
Research Organization:
Brookhaven National Laboratory (BNL) National Synchrotron Light Source
Sponsoring Organization:
DOE - OFFICE OF SCIENCE
DOE Contract Number:
AC02-98CH10886
OSTI ID:
1020212
Report Number(s):
BNL--96062-2011-JA
Journal Information:
Molecular and Cellular Endocrinology, Journal Name: Molecular and Cellular Endocrinology Journal Issue: 1-2 Vol. 301; ISSN MCEND6; ISSN 0303-7207
Country of Publication:
United States
Language:
English