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Glucocorticoid receptor phosphorylation in v-mos-transformed cells
K C Borror1, M J Garabedian, D B DeFranco
1Department of Biological Sciences, University of Pittsburgh, Pennsylvania 15260, USA.
Steroids
|May 1, 1995
Summary
Glucocorticoid receptors (GRs) are hyperphosphorylated in v-mos-transformed cells, disrupting their movement between the nucleus and cytoplasm. This hyperphosphorylation stems from increased GR phosphorylation, not reduced dephosphorylation.
Area of Science:
- Cell Biology
- Molecular Endocrinology
- Oncogenic Transformation
Background:
- Nucleocytoplasmic shuttling of glucocorticoid receptors (GRs) is crucial for cellular response to glucocorticoids.
- Disruption of GR shuttling is observed in v-mos-transformed cells, leading to cytoplasmic mislocalization.
Purpose of the Study:
- To investigate the mechanism behind GR hyperphosphorylation and disrupted nucleocytoplasmic shuttling in v-mos-transformed cells.
- To determine if hyperphosphorylation results from inhibited dephosphorylation or stimulated phosphorylation.
Main Methods:
- Analysis of GR phosphorylation status in v-mos-transformed and nontransformed cells.
- In vitro protein phosphatase activity assays.
- In vivo pulse-chase analysis of GR phosphate turnover.
Main Results:
- GRs in v-mos-transformed cells exhibit hyperphosphorylation and sustained hormone-induced phosphorylation.
- Protein phosphatase activity was similar in both cell types.
- No significant difference in GR dephosphorylation rates was observed in vivo.
Conclusions:
- GR hyperphosphorylation in v-mos-transformed cells is caused by increased GR phosphorylation, not decreased dephosphorylation.
- This altered phosphorylation state contributes to the disruption of GR nucleocytoplasmic shuttling.