Role of protein kinase A in LPS-induced activation of NF-kappa B proteins of a mouse macrophage-like cell line, J774

Cell Signal. 1993 May;5(3):289-98. doi: 10.1016/0898-6568(93)90019-i.


The electrophoretic mobility shift assays (EMSA) with the use of the synthetic HIV-1 NF-kappa B motif as a probe, showed that LPS-treatment of J774 cells (a mouse macrophage cell line) leads to the activation of the fast-moving (denoted as B1) and the slow-moving NF-kappa B (denoted as B2). The binding of both B1 and B2 to the NF-kappa B probe was inhibited specifically by either unlabelled NF-kappa B, or competitor probes, but not by unrelated probes. LPS-induced activation of NF-kappa B was inhibited by a protein kinase A (PKA) inhibitor (H-89), but not by a protein kinase C (PKC) inhibitor (H-7). PMA itself failed to activate NF-kappa B and the depletion of PKC did not prevent LPS-induced activation of NF-kappa B. The pre-treatment of J774 cells with dibutyric cAMP, forskolin, prostaglandin E2 or cholera toxin resulted in NF-kappa B activation. Thus, these data suggested a probable involvement of PKA in LPS-induced NF-kappa B activation in macrophages.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Bucladesine / pharmacology
  • Cholera Toxin / pharmacology
  • Colforsin / pharmacology
  • Consensus Sequence
  • Cyclic AMP / physiology*
  • Dinoprostone / pharmacology
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Isoquinolines / pharmacology
  • Lipopolysaccharides / antagonists & inhibitors
  • Lipopolysaccharides / pharmacology*
  • Macrophage Activation / drug effects*
  • Macrophages / drug effects*
  • Macrophages / enzymology
  • Mice
  • Mice, Inbred BALB C
  • Molecular Sequence Data
  • NF-kappa B / metabolism*
  • Neoplasm Proteins / metabolism
  • Phosphorylation
  • Piperazines / pharmacology
  • Protein Kinases / physiology*
  • Protein Processing, Post-Translational
  • Proto-Oncogene Proteins / metabolism
  • Signal Transduction* / drug effects
  • Sulfonamides*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription Factor RelB
  • Transcription Factors*
  • Transcription, Genetic* / drug effects
  • Tumor Cells, Cultured


  • Isoquinolines
  • Lipopolysaccharides
  • NF-kappa B
  • Neoplasm Proteins
  • Piperazines
  • Proto-Oncogene Proteins
  • Relb protein, mouse
  • Sulfonamides
  • Transcription Factors
  • Transcription Factor RelB
  • Colforsin
  • Bucladesine
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • Cholera Toxin
  • Cyclic AMP
  • Protein Kinases
  • Dinoprostone
  • N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide
  • Tetradecanoylphorbol Acetate