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Literature summary for 1.1.1.146 extracted from

  • Kim, J.; Temple, K.A.; Jones, S.A.; Meredith, K.N.; Basko, J.L.; Brady, M.J.
    Differential modulation of 3T3-L1 adipogenesis mediated by 11beta-hydroxysteroid dehydrogenase-1 levels (2007), J. Biol. Chem., 282, 11038-11046.
    View publication on PubMed

Application

Application Comment Organism
medicine differentiation of cells causes a strong increase in 11beta-hydroxysteroid dehydrogenase protein levels, occuring late in the differentiation protocol. Reduction of 11beta-hydroxysteroid dehydrogenase activity in 3T3-L1 fibroblasts, achieved by pharmacological inhibition or adenovirally mediated delivery of short hairpin RNA constructs, specifically blocks the ability of inactive glucocorticoids to drive 3T3-L1 differentiation. Even modest increases in exogenous 11beta-hydroxysteroid dehydrogenase expression in 3T3-L1 fibroblasts, to levels comparable with endogenous 1 11beta-hydroxysteroid dehydrogenase in differentiated 3T3-L1 adipocytes, are sufficient to block adipogenesis Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining
3T3-L1 cell differentiation of cells causes a strong increase in 11beta-hydroxysteroid dehydrogenase protein levels, occuring late in the differentiation protocol. Reduction of 11beta-hydroxysteroid dehydrogenase activity in 3T3-L1 fibroblasts, achieved by pharmacological inhibition or adenovirally mediated delivery of short hairpin RNA constructs, specifically blocks the ability of inactive glucocorticoids to drive 3T3-L1 differentiation. Even modest increases in exogenous 11beta-hydroxysteroid dehydrogenase expression in 3T3-L1 fibroblasts, to levels comparable with endogenous 1 11beta-hydroxysteroid dehydrogenase in differentiated 3T3-L1 adipocytes, are sufficient to block adipogenesis Mus musculus
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