TY - JOUR
T1 - Progesterone-induced inactivation of nuclear estrogen receptor in the hamster uterus is mediated by acid phosphatase
AU - MacDonald, Richard G.
AU - Okulicz, William C.
AU - Leavitt, Wendell W.
N1 - Funding Information:
* To whom correspondence should be addressed. by grants HD 15452 and HD 13152 from the NIH.
Funding Information:
work was supported
PY - 1982/1/29
Y1 - 1982/1/29
N2 - Inactivation of hamster uterine estrogen receptor was assayed in nuclear KCl extracts (30 min, 37°C, pH 7.5) after progesterone treatment invivo for 2h. At very low concentrations (>0.05 mM), molybdate and vanadate blocked the progesterone-induced increase in receptor inactivation. In contrast, only high concentrations (>10 mM) of the inhibitors blocked receptor inactivation in extracts from untreated hamsters. Gel electrophoresis and inhibition curves for phosphatases in nuclear extract demonstrated that acid, rather than alkaline, phosphatase activity is most likely responsible for these effects. These data suggest that progesterone antagonizes estrogen action in the hamster uterus by promoting estrogen receptor dephosphorylation leading to inactivation.
AB - Inactivation of hamster uterine estrogen receptor was assayed in nuclear KCl extracts (30 min, 37°C, pH 7.5) after progesterone treatment invivo for 2h. At very low concentrations (>0.05 mM), molybdate and vanadate blocked the progesterone-induced increase in receptor inactivation. In contrast, only high concentrations (>10 mM) of the inhibitors blocked receptor inactivation in extracts from untreated hamsters. Gel electrophoresis and inhibition curves for phosphatases in nuclear extract demonstrated that acid, rather than alkaline, phosphatase activity is most likely responsible for these effects. These data suggest that progesterone antagonizes estrogen action in the hamster uterus by promoting estrogen receptor dephosphorylation leading to inactivation.
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U2 - 10.1016/0006-291X(82)90675-1
DO - 10.1016/0006-291X(82)90675-1
M3 - Article
C2 - 6918219
AN - SCOPUS:0020029230
SN - 0006-291X
VL - 104
SP - 570
EP - 576
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -