The regulation of mammary prolactin receptor metabolism by a retroviral envelope protein

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Updated: Jul 28, 2026

Evaluation of Mammary Gland Development and Function in Mouse Models
08:51

Evaluation of Mammary Gland Development and Function in Mouse Models

Published on: July 21, 2011

F F Bolander1, E Ginsburg, B K Vonderhaar

  • 1Department of Biological Sciences, University of South Carolina, Columbia 29208, USA.

Journal of Molecular Endocrinology
|October 29, 1997
PubMed

Insights

Mouse mammary tumor virus (MMTV) infection enhances mammary epithelial sensitivity to prolactin (PRL). This occurs because the MMTV envelope protein (gp52) increases prolactin receptors (PRLR) via synthesis and internal pool redistribution.

Area of Science:

  • * Molecular biology
  • * Virology
  • * Endocrinology

Background:

  • * Previous studies indicated that mouse mammary tumor virus (MMTV) infection increases mammary epithelial sensitivity to prolactin (PRL).
  • * This effect was reproducible by the MMTV envelope protein (gp52) binding to its receptor.

Purpose of the Study:

  • * To investigate if gp52-induced alterations in prolactin receptors (PRLR) mediate the increased PRL sensitivity in mammary epithelium.
  • * To elucidate the mechanisms behind gp52-mediated changes in PRLR levels.

Main Methods:

  • * In vitro experiments using mammary epithelial cells.
  • * Quantification of PRLR concentration and mRNA levels.
  • * Assessment of PRLR redistribution and degradation rates.

Main Results:

  • * gp52 treatment doubled the plasma membrane PRLR concentration in mammary epithelium without altering binding affinity.
  • * gp52 significantly stimulated PRLR mRNA levels (nearly fivefold), indicating increased receptor synthesis.
  • * A rapid redistribution of PRLRs from an internal cellular pool to the plasma membrane was observed within 30 minutes; PRLR degradation rates remained unaffected.

Conclusions:

  • * The MMTV envelope protein gp52 enhances mammary epithelial PRL sensitivity by increasing PRLR levels.
  • * This elevation is achieved through a dual mechanism: stimulating new PRLR synthesis and recruiting existing receptors from intracellular stores.
  • * The findings provide a molecular explanation for how MMTV infection influences mammary gland function and PRL signaling.

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