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PHLPP1 counter-regulates STAT1-mediated inflammatory signaling.

Ksenya Cohen Katsenelson1, Joshua D Stender2, Agnieszka T Kawashima1,3

  • 1Department of Pharmacology, University of California, San Diego, San Diego, United States.

Elife
|August 14, 2019
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Summary

PH domain Leucine-rich repeat Protein Phosphatase 1 (PHLPP1) deletion protects mice from infection. Nuclear PHLPP1 dephosphorylates STAT1, controlling inflammatory signaling duration and magnitude in macrophages.

Keywords:
PHLPP1STAT1biochemistrychemical biologyimmunologyinflammationmousephosphatasetranscription factors

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Inflammation is crucial for innate immunity but implicated in various diseases.
  • Kinases controlling inflammatory signaling are well-studied, but opposing phosphatases are less understood.

Purpose of the Study:

  • To investigate the role of PH domain Leucine-rich repeat Protein Phosphatase 1 (PHLPP1) in inflammatory responses.
  • To elucidate the mechanism by which PHLPP1 regulates inflammatory signaling pathways.

Main Methods:

  • Mice lacking the PHLPP1 gene were challenged with lipopolysaccharide (LPS) and live *Escherichia coli*.
  • PHLPP1 function was analyzed in macrophages, focusing on its interaction with STAT1.
  • Nuclear localization and dephosphorylation activity of PHLPP1 were assessed.

Main Results:

  • PHLPP1 gene deletion conferred protection against lethal LPS and *E. coli* infection in mice.
  • PHLPP1 dephosphorylates STAT1 at Ser727 in macrophages, inhibiting its activity and promoter residency.
  • This dephosphorylation reduces the expression of innate immunity and cytokine signaling target genes.

Conclusions:

  • PHLPP1 acts as a negative regulator of inflammatory signaling in macrophages.
  • Nuclear PHLPP1 dephosphorylation of STAT1 controls the magnitude and duration of inflammatory responses.
  • PHLPP1 represents a potential therapeutic target for inflammatory diseases.