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Literature summary for 1.3.1.3 extracted from

  • Appanna, N.; Gibson, H.; Gangitano, E.; Dempster, N.J.; Morris, K.; George, S.; Arvaniti, A.; Gathercole, L.L.; Keevil, B.; Penning, T.M.; Storbeck, K.H.; Tomlinson, J.W.; Nikolaou, N.
    Differential activity and expression of human 5beta-reductase (AKR1D1) splice variants (2021), J. Mol. Endocrinol., 66, 181-194 .
    View publication on PubMed
Search for more literature for 1.3.1.3

Cloned(Commentary)

Cloned (Comment) Organism
expression of splice variant AKR1D1 in HEK-293 cell Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P51857
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Source Tissue

Source Tissue Comment Organism Textmining
liver splice variants AKR1D1-002 and AKR1D1-001 are expressed in liver Homo sapiens
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testis only splice variant AKR1D1-006 is expressed in testis Homo sapiens
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
dexamethasone + NADPH + H+ substrate of splice variant AKR1D1-002 Homo sapiens ? + NADP+
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 ?
additional information splice variant AKR1D1-002 efficiently metabolizes glucocorticoids and androgens and decreases receptor activation. Variants AKR1D1-001 and AKR1D1-006 poorly metabolize dexamethasone, but do not metabolize cortisol, prednisolone, testosterone or androstenedione Homo sapiens ?
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prednisolone + NADPH + H+ substrate of splice variant AKR1D1-002 Homo sapiens ? + NADP+
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 ?
testosterone + NADPH + H+ substrate of splice variant AKR1D1-002 Homo sapiens (5beta,17beta)-17-hydroxyandrostan-3-one + NADP+
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 ?

Expression

Organism Comment Expression
Homo sapiens treatment of cells with proteasomal inhibitor, MG-132 increases expression of splice variants AKR1D1-001 and AKR1D1-006 up