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Oligospecificity of the cellular adhesion receptor mac-1 encompasses an inducible recognition specificity for fibrinogen

Academic Article
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Overview

authors

  • Altieri, D. C.
  • Bader, R.
  • Mannucci, P. M.
  • Edgington, Thomas

publication date

  • November 1988

journal

  • Journal of Cell Biology  Journal

abstract

  • Mitogenesis, cellular aggregation, and motility follow upon the interaction of fibrinogen with certain defined cell surface receptors. In addition to circulating platelets and vascular endothelium, monocytes express what appears to be a receptor for fibrinogen. Evidence is presented here that the leukocyte adhesion receptor Mac-1 can be specifically induced to bind fibrinogen with characteristics immunochemically and functionally distinct from the established Arg-Gly-Asp-directed fibrinogen receptors. The competence of Mac-1 as a fibrinogen receptor is a general property of cells of monocyte and myeloid lineage acquired after maturational changes of some regions of the alpha subunit of Mac-1 during the process of cell differentiation. This ligand recognition specificity of Mac-1 is lacking for the resting cell. Rather, induction of fibrinogen binding capacity of Mac-1 is due to a cellular response to selected agonists characterized by inducing rapid transients of cytosolic Ca2+. Although different in activation pathways and recognition specificity, Mac-1 exhibits an oligospecific ligand versatility characteristic of other homologous Arg-Gly-Asp-directed adhesion receptors.

subject areas

  • Amino Acid Sequence
  • Antigens, Differentiation
  • Cell Adhesion
  • Cell Line
  • Fibrinogen
  • Fluorescent Antibody Technique
  • Humans
  • Macrophage-1 Antigen
  • Molecular Sequence Data
  • Monocytes
  • Platelet Membrane Glycoproteins
  • Precipitin Tests
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Identity

International Standard Serial Number (ISSN)

  • 0021-9525

Digital Object Identifier (DOI)

  • 10.1083/jcb.107.5.1893

PubMed ID

  • 3053736
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Additional Document Info

start page

  • 1893

end page

  • 1900

volume

  • 107

issue

  • 5

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