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Related Experiment Videos

PRAM-1 is required for optimal integrin-dependent neutrophil function.

Regina A Clemens1, Sally A Newbrough, Elaine Y Chung

  • 1Dept. of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6160, USA.

Molecular and Cellular Biology
|December 2, 2004
PubMed
Summary
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PML-retinoic acid receptor alpha (RARalpha) regulated adaptor molecule 1 (PRAM-1) is crucial for select neutrophil functions. PRAM-1 deficiency impairs adhesion-dependent responses like oxygen intermediate production and degranulation, but not differentiation or Fcgamma receptor function.

Area of Science:

  • Immunology
  • Cell Biology
  • Hematology

Background:

  • PML-retinoic acid receptor alpha (RARalpha) regulated adaptor molecule 1 (PRAM-1) is an intracellular adaptor molecule.
  • PRAM-1 is upregulated during granulocytic differentiation and normal human myelopoiesis.

Purpose of the Study:

  • To generate PRAM-1-deficient mice.
  • To analyze PRAM-1's function in neutrophil differentiation and mature neutrophil function.

Main Methods:

  • Generation of PRAM-1-deficient mice.
  • Analysis of neutrophil differentiation and function in PRAM-1-deficient mice.
  • Assessment of Fcgamma receptor and integrin-dependent responses.

Main Results:

  • Neutrophil differentiation is not impaired in PRAM-1-deficient mice.

Related Experiment Videos

  • PRAM-1-deficient neutrophils exhibit normal function following Fcgamma receptor engagement.
  • Mature PRAM-1-null neutrophils show defects in adhesion-dependent reactive oxygen intermediate production and degranulation.
  • Integrin-dependent cell spreading and signaling pathways remain normal in PRAM-1-null neutrophils.

    • Conclusions:

    • PRAM-1 is critical for select integrin-dependent functions in neutrophils.
    • The absence of PRAM-1 uncouples key integrin-dependent responses, highlighting its specific role.