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Corticosteroid 11-beta-dehydrogenase isozyme 2

Corticosteroid 11-β-dehydrogenase isozyme 2 also known as 11-β-hydroxysteroid dehydrogenase 2 is an enzyme that in humans is encoded by the HSD11B2 gene.[5][6][7]

AliasesHSD11B2, AME, AME1, HSD11K, HSD2, SDR9C3, hydroxysteroid (11-beta) dehydrogenase 2, hydroxysteroid 11-beta dehydrogenase 2
External IDsOMIM: 614232 MGI: 104720 HomoloGene: 20088 GeneCards: HSD11B2
Gene location (Human)
Chromosome 16 (human)
Chr.Chromosome 16 (human)[1]
Chromosome 16 (human)
Genomic location for HSD11B2
Genomic location for HSD11B2
Band16q22.1Start67,430,652 bp[1]
End67,437,553 bp[1]
RNA expression pattern
PBB GE HSD11B2 204130 at fs.png
More reference expression data
RefSeq (mRNA)



RefSeq (protein)



Location (UCSC)Chr 16: 67.43 – 67.44 MbChr 8: 105.52 – 105.52 Mb
PubMed search[3][4]
View/Edit HumanView/Edit Mouse



Corticosteroid 11-β-dehydrogenase isozyme 2 is an NAD+-dependent enzyme expressed in aldosterone-selective epithelial tissues such as the kidney, colon, salivary and sweat glands. HSD211B2 expression is also found in the brainstem in a small, aldosterone-sensitive subset of neurons located in the nucleus of the solitary tract referred to as HSD2 neurons.[8]

In these tissues, HSD11B2 oxidizes the glucocorticoid cortisol to the inactive metabolite cortisone, thus preventing illicit activation of the mineralocorticoid receptor. This protective mechanism is necessary because cortisol circulates at 100- to 1000-fold higher concentrations than aldosterone, and binds with equal affinity to the mineralocorticoid receptor, thereby out-competing aldosterone in cells that do not produce HSD11B2.

This glucocorticoid-inactivating enzyme is also expressed in tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, as well as parts of the developing brain, including the rhombencephalic progenitor cells that proliferate into cerebellar granule cells. In these tissues, HSD11B2 protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development.

Clinical significanceEdit

Inhibition of this enzyme, for example by a compound in liquorice, results in a condition known as pseudohyperaldosteronism. A genetically inherited deficiency of HSD11B2 is the underlying cause of the syndrome of apparent mineralocorticoid excess.


  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000176387 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000031891 - Ensembl, May 2017
  3. ^ "Human PubMed Reference:".
  4. ^ "Mouse PubMed Reference:".
  5. ^ Albiston AL, Obeyesekere VR, Smith RE, Krozowski ZS (November 1994). "Cloning and tissue distribution of the human 11 beta-hydroxysteroid dehydrogenase type 2 enzyme". Mol. Cell. Endocrinol. 105 (2): R11–7. doi:10.1016/0303-7207(94)90176-7. PMID 7859916.
  6. ^ Brown RW, Chapman KE, Kotelevtsev Y, Yau JL, Lindsay RS, Brett L, Leckie C, Murad P, Lyons V, Mullins JJ, Edwards CR, Seckl JR (February 1996). "Cloning and production of antisera to human placental 11 beta-hydroxysteroid dehydrogenase type 2". Biochem. J. 313 (Pt 3): 1007–17. doi:10.1042/bj3131007. PMC 1216963. PMID 8611140.
  7. ^ "Entrez Gene: HSD11B2 hydroxysteroid (11-beta) dehydrogenase 2".
  8. ^ Geerling, Joel C.; Arthur D. Loewy (September 2009). "Aldosterone in the brain". American Journal of Physiology. Renal Physiology. 297 (3): F559–76. doi:10.1152/ajprenal.90399.2008. PMC 2739715. PMID 19261742.

Further readingEdit