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Induction of a prenylated 65‐kd protein in macrophages by interferon or lipopolysaccharide
Author(s) -
Vestal Deborah J.,
Maki Richard A.,
Buss Janice E.
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.58.5.607
Subject(s) - prenylation , lipopolysaccharide , biology , interferon , macrophage , immunology , microbiology and biotechnology , virology , biochemistry , in vitro , enzyme
Treatment of murine bone marrow‐derived macrophages with interferon‐γ (IFN‐γ) and/or lipopolysaccharide (LPS) resulted in changes in the abundance of a number of prenylated proteins. The most significant change involved a protein of 65 kd (p65) that became one of the most abundant prenylated proteins following treatment. The 65‐kd protein was induced by agents that stimulate macrophage activation (IFNs or LPS) but not by cytokines that promote macrophage proliferation, such as granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), M‐CSF, or interleukin‐3. The majority of p65 was localized to subcellular fractions containing internal and plasma membranes but was not detected in nuclear membranes. The farnesyltransferase inhibitor BZA‐5B caused a dramatic decrease in p65 prenylation, suggesting that this protein may be modified by the C 15 isoprenoid farnesyl. These observations provide the first direct evidence that interferons and LPS cause changes in the abundance of specific isoprenoid‐modified proteins in macrophages.