Mineralocorticoids: Difference between revisions

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<StructureSection load='' size='300' side='right' caption='Glycosylated human mineralocorticoid receptor ligand-binding domain complex with aldosterone, glycerol and sulfate (PDB entry [[2aa2]])' scene='78/781019/Cv/1'>
<StructureSection load='' size='300' side='right' caption='Glycosylated human mineralocorticoid receptor ligand-binding domain complex with aldosterone, glycerol and sulfate (PDB entry [[2aa2]])' scene='78/781019/Cv/1'>
*[[Mineralocorticoid receptor]] (MR) in epithelial cells is activated by the <scene name='89/896192/Cv/1'>mineralocorticoid hormone aldosterone</scene> promoting renal sodium retention and potassium excretion. It is [[Nuclear receptors|nuclear receptor]]. In non epithelial cells MR is activated by cortisol<ref>PMID:15199296</ref>.  MR is exposed to many steroids including cortisol, cortisone and progesterone, however, aldosterone and deoxycorticosterone are its physiological ligands. MR mutations are the principal cause of renal pseudohypoaldosteronism<ref>PMID:16972228</ref>. MR mutation S810L causes early-onset hypertension<ref>PMID:10884226</ref>. Inhibition of cardia MR prevents doxorubicin-induced cardiotoxicity<ref>PMID:28430882</ref>. MR is an important proadipogenic transcription factor that may mediate aldosterone and glucocorticoid effects on adipose tissue development and hence on obesity and development of metabolic syndrome<ref>PMID:17384139</ref>. The MR ligand aldosterone binds in a <scene name='78/781019/Cv/6'>fully enclosed pocket, contacting residues with six α-helices and a β-turn</scene> ({{Template:ColorKey_Helix}},{{Template:ColorKey_Strand}},{{Template:ColorKey_Loop}},{{Template:ColorKey_Turn}}). <scene name='78/781019/Cv/7'>It forms hydrogen bonds with 4 MR residues</scene><ref>PMID:15967794</ref>. <scene name='78/781019/Cv/8'>Whole binding site</scene>. Water molecules are shown as red spheres.
Mineralocorticoids are a class of corticosteroids. Mineralocorticoids are produced in the adrenal cortex and influence salt and water balances (electrolyte balance and fluid balance). The primary mineralocorticoid is <scene name='89/896192/Cv/1'>aldosterone</scene>.
*[[Mineralocorticoid receptor]] (MR) in epithelial cells is activated by the mineralocorticoid hormone aldosterone promoting renal sodium retention and potassium excretion. It is [[Nuclear receptors|nuclear receptor]]. In non epithelial cells MR is activated by cortisol<ref>PMID:15199296</ref>.  MR is exposed to many steroids including cortisol, cortisone and progesterone, however, aldosterone and deoxycorticosterone are its physiological ligands. MR mutations are the principal cause of renal pseudohypoaldosteronism<ref>PMID:16972228</ref>. MR mutation S810L causes early-onset hypertension<ref>PMID:10884226</ref>. Inhibition of cardia MR prevents doxorubicin-induced cardiotoxicity<ref>PMID:28430882</ref>. MR is an important proadipogenic transcription factor that may mediate aldosterone and glucocorticoid effects on adipose tissue development and hence on obesity and development of metabolic syndrome<ref>PMID:17384139</ref>. The MR ligand aldosterone binds in a <scene name='78/781019/Cv/6'>fully enclosed pocket, contacting residues with six α-helices and a β-turn</scene> ({{Template:ColorKey_Helix}},{{Template:ColorKey_Strand}},{{Template:ColorKey_Loop}},{{Template:ColorKey_Turn}}). <scene name='78/781019/Cv/7'>It forms hydrogen bonds with 4 MR residues</scene><ref>PMID:15967794</ref>. <scene name='78/781019/Cv/8'>Whole binding site</scene>. Water molecules are shown as red spheres.


*[[Angiotensin-Converting Enzyme]], Renin-Angiotensin-Aldosterone System.
*[[Angiotensin-Converting Enzyme]], Renin-Angiotensin-Aldosterone System.
*[[Corticosteroid-binding globulin]]
*[[Hydroxysteroid dehydrogenase]]


</StructureSection>
</StructureSection>
== References ==
== References ==
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