GO reference used by source annotation pipeline
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Source annotation pipeline provenance for Hsd11b2 annotations including 7-beta-hydroxysteroid dehydrogenase (NADP+) activity.
"GO_REF entry used only to trace source annotation method; biological support was assessed from UniProt and cached literature where available."
GO reference used by source annotation pipeline
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Source annotation pipeline provenance for Hsd11b2 annotations including 11-beta-hydroxysteroid dehydrogenase (NAD+) activity; glucocorticoid metabolic process.
"GO_REF entry used only to trace source annotation method; biological support was assessed from UniProt and cached literature where available."
GO reference used by source annotation pipeline
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Source annotation pipeline provenance for Hsd11b2 annotations including endoplasmic reticulum.
"GO_REF entry used only to trace source annotation method; biological support was assessed from UniProt and cached literature where available."
GO reference used by source annotation pipeline
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Source annotation pipeline provenance for Hsd11b2 annotations including cortisol metabolic process; positive regulation of smoothened signaling pathway.
"GO_REF entry used only to trace source annotation method; biological support was assessed from UniProt and cached literature where available."
GO reference used by source annotation pipeline
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Source annotation pipeline provenance for Hsd11b2 annotations including 11-beta-hydroxysteroid dehydrogenase (NAD+) activity; 7-beta-hydroxysteroid dehydrogenase (NADP+) activity.
"GO_REF entry used only to trace source annotation method; biological support was assessed from UniProt and cached literature where available."
GO reference used by source annotation pipeline
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Source annotation pipeline provenance for Hsd11b2 annotations including 11-beta-hydroxysteroid dehydrogenase (NAD+) activity; 7-beta-hydroxysteroid dehydrogenase (NADP+) activity; cortisol metabolic process; female pregnancy; positive regulation of smoothened signaling pathway.
"GO_REF entry used only to trace source annotation method; biological support was assessed from UniProt and cached literature where available."
Gene expression of 11beta-hydroxysteroid dehydrogenase type 1 and type 2 in the kidneys of insulin-dependent diabetic rats.
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For Hsd11b2, this publication was assessed for annotations including response to insulin.
"The renal 11beta-HSD2 activity and level of mRNA expression were significantly decreased in diabetic rats."
Effects of spironolactone on systolic blood pressure in experimental diabetic rats.
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For Hsd11b2, this publication was assessed for annotations including response to xenobiotic stimulus.
"Four weeks after an injection of STZ, the renal 11beta-HSD2 and mRNA levels were significantly lower in diabetic rats than in control rats, and the mean systolic blood pressure was 14.8% higher in diabetic rats than in controls."
Effect of cellular differentiation on 11beta-hydroxysteroid dehydrogenase activity in the intestine.
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For Hsd11b2, this publication was assessed for annotations including glucocorticoid metabolic process.
"Type 2 11betaHSD has only oxidase activity converting corticosterone to 11-dehydrocorticosterone."
Interactions between 11beta-hydroxysteroid dehydrogenase and COX-2 in kidney.
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For Hsd11b2, this publication was assessed for annotations including regulation of blood volume by renal aldosterone.
"These data indicate that COX-2 plays a modulating role in the development of hypertension due to 11betaHSD2 deficiency and that 11betaHSD2 regulates renal COX-2 expression by preventing glucocorticoid access to MRs during postnatal development."
11{beta}-Hydroxysteroid dehydrogenase 2 in rat leydig cells: its role in blunting glucocorticoid action at physiological levels of substrate.
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For Hsd11b2, this publication was assessed for annotations including NAD binding; steroid binding.
"We showed that 11beta HSD2 is present in rat Leydig cells by PCR amplification, immunohistochemical staining, enzyme histochemistry, immunoprecipitation, and Western blotting."
Expression and functional state of the corticosteroid receptors and 11 beta-hydroxysteroid dehydrogenase type 2 in Schwann cells.
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For Hsd11b2, this publication was assessed for annotations including glucocorticoid metabolic process.
"11 beta-Hydroxysteroid-dehydrogenase type 2 (HSD2), an enzyme that inactivates glucocorticoids, was strongly expressed and active in quiescent SC."
DHEA induces 11 -HSD2 by acting on CCAAT/enhancer-binding proteins.
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For Hsd11b2, this publication was assessed for annotations including response to steroid hormone.
"DHEA treatment markedly increased mRNA expression and activity of 11beta-HSD2 in a rat cortical collecting duct cell line and in kidneys of C57BL/6J mice and Sprague-Dawley rats."
Tissue-specific programming expression of glucocorticoid receptors and 11 beta-HSDs by maternal perinatal undernutrition in the HPA axis of adult male rats.
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For Hsd11b2, this publication was assessed for annotations including response to food.
"This study demonstrated that maternal food restriction has both long-term and tissue-specific effects on gene expression of factors involved in glucocorticoid sensitivity."
Reciprocal changes in maternal and fetal metabolism of corticosterone in rat during gestation.
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For Hsd11b2, this publication was assessed for annotations including female pregnancy.
"The final third of gestation is accompanied by reciprocal changes in placental and fetal metabolism of corticosterone due to changes in 11HSD1 and 11HSD2."
Chronic intermittent hypoxia induces 11beta-hydroxysteroid dehydrogenase in rat heart.
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For Hsd11b2, this publication was assessed for annotations including response to hypoxia.
"We first demonstrated that adaptation to CIH led to a significant increase in 11HSD2 transcript levels and activity in the myocardium."
Dexamethasone and betamethasone administration during pregnancy affects expression and function of 11 beta-hydroxysteroid dehydrogenase type 2 in the rat placenta.
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For Hsd11b2, this publication was assessed for annotations including response to glucocorticoid.
"Placental 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) is the key enzyme which protects the fetus from overexposure to glucocorticoids (GCs) by their oxidation into inactive derivates."
Falcon (Edison Scientific) deep research report: rat Hsd11b2 (11-beta-hydroxysteroid dehydrogenase type 2, UniProt P50233)
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11beta-HSD2 is the inactivating (oxidative) member of the 11beta-HSD pair, distinct from the reductive 11beta-HSD1.
"11β‑HSD2 is the inactivating dehydrogenase"
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The catalyzed reaction is the oxidation/inactivation of active glucocorticoids to their inert 11-keto forms.
"11β‑HSD2 catalyzes oxidation/inactivation of glucocorticoids: **cortisol→cortisone** and **corticosterone→11‑dehydrocorticosterone**."
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The enzyme uses NAD(+) as cofactor, consistent with SDR-family oxidative directionality in epithelia.
"11β‑HSD2 is described as **NAD-dependent/NAD+-dependent**, consistent with SDR-family dehydrogenase directionality in epithelia."
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By locally removing active glucocorticoids the enzyme confers aldosterone specificity on the otherwise non-selective mineralocorticoid receptor.
"11β‑HSD2 enables aldosterone-specific MR signaling** in target cells by locally removing active glucocorticoids."
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Glucocorticoids circulate far in excess of aldosterone; the enzyme prevents them occupying MR while aldosterone, not a substrate, signals through MR.
"aldosterone is not a substrate and can therefore signal through MR."
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Canonical sites of action are the classic aldosterone-sensitive epithelia.
"Canonical sites include **distal nephron/kidney**, **colon**, **salivary glands**, and **sweat glands**"
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The enzyme acts as a placental/fetal barrier limiting fetal exposure to maternal glucocorticoids.
"11β‑HSD2 is highly expressed in **placenta and fetal tissues** where it **minimizes fetal exposure to maternal glucocorticoids**"
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In adult rodent CNS the enzyme is restricted to discrete hindbrain regions supporting aldosterone-specific control of salt appetite and blood pressure.
"nucleus of the solitary tract** and **subcommissural organ**, where 11β-HSD2 supports aldosterone-specific control of **salt appetite** and influences **blood pressure**."
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Loss of enzyme function causes apparent mineralocorticoid excess (AME), underscoring its physiological role.
"Loss of 11β‑HSD2 function causes **AME**"