Insulin potentiates the transactivation potency of the glucocorticoid receptor.

Abstract:

:A single copy of a glucocorticoid-responsive element (GRE) is sufficient in mediating the combinatorial response of a promoter to both glucocorticoids and insulin in HepG2 cells. This requires the presence of active glucocorticoid receptor (GR) since the response is significantly inhibited by the anti-glucocorticoid RU30406. The N'- and C'-terminal parts of the GR protein are not involved in mediating the response. Insulin had no effect on GR binding to GRE but it affected both the level and the phosphorylation state of nuclear-bound GR. Thus, insulin alters the GR transactivation potency while, concomitantly, modifies the molecule at the posttranslational level.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Georgakopoulos A,Tsawdaroglou N

doi

10.1016/0014-5793(96)00115-9

subject

Has Abstract

pub_date

1996-03-04 00:00:00

pages

177-82

issue

3

eissn

0014-5793

issn

1873-3468

pii

0014-5793(96)00115-9

journal_volume

381

pub_type

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