Progesterone-induced inactivation of nuclear estrogen receptor in the hamster uterus is mediated by acid phosphatase

Richard G MacDonald, William C. Okulicz, Wendell W. Leavitt

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)570-576
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume104
Issue number2
DOIs
StatePublished - Jan 29 1982

Fingerprint

Acid Phosphatase
Cricetinae
Estrogen Receptors
Uterus
Progesterone
Vanadates
Electrophoresis
Phosphoric Monoester Hydrolases
Alkaline Phosphatase
Estrogens
Gels
Acids

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Progesterone-induced inactivation of nuclear estrogen receptor in the hamster uterus is mediated by acid phosphatase. / MacDonald, Richard G; Okulicz, William C.; Leavitt, Wendell W.

In: Biochemical and Biophysical Research Communications, Vol. 104, No. 2, 29.01.1982, p. 570-576.

Research output: Contribution to journalArticle

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