Receptor-like Protein-tyrosine Phosphatase alpha  Specifically Inhibits Insulin-increased Prolactin Gene Expression

doi:10.1074/jbc.273.8.4800

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Receptor-like Protein-tyrosine Phosphatase $alpha$ Specifically Inhibits Insulin-increased Prolactin Gene Expression

Kirsten K. Jacob, Jan Sap^§^¶, and Frederick M. Stanley^§^¶

From the Department of Medicine, ^§ Department of Pharmacology, and ^¶ Kaplan Cancer Center, New York University Medical Center, New York, New York 10016

A physiologically relevant response to insulin, stimulation of prolactin promoter activity in GH4 pituitary cells, was usedas an assay to study the specificity of protein-tyrosine phosphatasefunction. Receptor-like protein-tyrosine phosphatase $alpha$ (RPTP $alpha$ )blocks the effect of insulin to increase prolactin gene expressionbut potentiates the effects of epidermal growth factor and cAMPon prolactin promoter activity. RPTP $alpha$ was the only protein-tyrosinephosphatase tested that did this. Thus, the effect of RPTP $alpha$ onprolactin-chloramphenicol acetyltransferase (CAT) promoter activityis specific by two criteria.

A number of potential RPTP $alpha$ targets were ruled out by finding (a) that they are not affected or (b) that they are not on thepathway to insulin-increased prolactin-CAT activity. The negativeeffect of RPTP $alpha$ on insulin activation of the prolactin promoteris not due to reduced phosphorylation or kinase activity of theinsulin receptor or to reduced phosphorylation of insulin receptorsubstrate-1 or Shc. Inhibitor studies suggest that insulin-increasedprolactin gene expression is mediated by a Ras-like GTPase butis not mitogen-activated protein kinase dependent. Experimentswith inhibitors of phosphatidylinositol 3-kinase suggest thatinsulin-increased prolactin-CAT expression is phosphatidylinositol3-kinase-independent. These results suggest that RPTP $alpha$ may bea physiological regulator of insulin action.

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