Pathway candidateNCBI-verifiedprotein-coding

HSD11B2

hydroxysteroid 11-beta dehydrogenase 2

NCBI Gene: 3291 Ensembl GeneCards UniProt: P80365

Pathway candidate — not linked to PFS or PSSD by any record here

HSD11B2 is in the library because it belongs to the steroid synthesis family. No study, report or commentary in the corpus names it, so a variant in HSD11B2 is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 16 (steroid hormone synthesis). There are at least two isozymes of the corticosteroid 11-beta-dehydrogenase, a microsomal enzyme complex responsible for the interconversion of cortisol and cortisone. The type I isozyme has both 11-beta-dehydrogenase (cortisol to cortisone) and 11-oxoreductase (cortisone to cortisol) activities.

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: 11-beta-hydroxysteroid dehydrogenase type 2
Function (excerpt): Catalyzes the conversion of biologically active 11beta-hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD(+). Functions as a dehydrogenase (oxidase), thereby decreasing the concentration of active glucocorticoids, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids. Plays an important role in maintaining glucocorticoids balance during preimplantation and protects the fetus from excessive maternal corticosterone exposure (By similarity). Catalyzes the oxidation of 11beta-hydroxytestosterone (11beta,17beta-dihydroxyandrost-4-ene-3-one) to 11-ketotestosterone (17beta-hydroxyandrost-4-ene-3,11-dione), a major bioactive androgen. Catalyzes the conversion of 11beta-hydroxyandrostenedione (11beta-hydroxyandrost-4-ene-3,17-dione) to 11-ketoandrostenedione (androst-4-ene-3,11,17-trione), which can be further metabolized to 11-ketotestosterone.
Pathway: Steroid metabolism.
Subcellular location: Microsome; Endoplasmic reticulum.
Tissue specificity: Expressed in kidney, placenta, pancreas, prostate, ovary, small intestine and colon, and in lower levels in the spleen and testis. At midgestation, expressed at high levels in placenta and in fetal kidney and, at much lower levels, in fetal lung and testis.
Associated conditions: Apparent mineralocorticoid excess (AME).

Source: UniProtKB/Swiss-Prot P80365, release 2026_03, licensed CC BY 4.0. This is the protein’s normal biology, not evidence about post-drug syndromes; associated conditions are inherited disorders of the gene, not PFS, PSSD or PRSD.

Why its pathway is in the library

Steroid-synthesis enzymes sit directly on the pathways perturbed by 5-alpha-reductase inhibitors and SSRIs; inherited variation here is a candidate susceptibility factor for persistent post-drug phenotypes.

Written for the whole steroid synthesis family, not for HSD11B2 specifically.

Mentioned in 0 corpus records

No corpus record names HSD11B2 directly yet. It is in the library because it sits in a pathway the corpus tracks (Steroid synthesis).

Also in steroid hormone synthesis

All 38 genes

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Gene summary

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: 11-beta-hydroxysteroid dehydrogenase type 2
Function (excerpt): Catalyzes the conversion of biologically active 11beta-hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD(+). Functions as a dehydrogenase (oxidase), thereby decreasing the concentration of active glucocorticoids, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids. Plays an important role in maintaining glucocorticoids balance during preimplantation and protects the fetus from excessive maternal corticosterone exposure (By similarity). Catalyzes the oxidation of 11beta-hydroxytestosterone (11beta,17beta-dihydroxyandrost-4-ene-3-one) to 11-ketotestosterone (17beta-hydroxyandrost-4-ene-3,11-dione), a major bioactive androgen. Catalyzes the conversion of 11beta-hydroxyandrostenedione (11beta-hydroxyandrost-4-ene-3,17-dione) to 11-ketoandrostenedione (androst-4-ene-3,11,17-trione), which can be further metabolized to 11-ketotestosterone.
Pathway: Steroid metabolism.
Subcellular location: Microsome; Endoplasmic reticulum.
Tissue specificity: Expressed in kidney, placenta, pancreas, prostate, ovary, small intestine and colon, and in lower levels in the spleen and testis. At midgestation, expressed at high levels in placenta and in fetal kidney and, at much lower levels, in fetal lung and testis.
Associated conditions: Apparent mineralocorticoid excess (AME).