Defect of calmodulin-binding protein in expression of interleukin-1β gene by LPS-nonresponder C3H HeJ mouse macrophages

Yasuhiko Terada, Hiroto Shinomiya, Masayasu Nakano

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Peritoneal macrophages of Lipopolysaccharide (LPS)-refractory C3H HeJ mouse failed to express the mRNA coding interleukin 1 (IL-1)β when stimulated by the Ca2+ ionophore A23187 or LPS, though macrophages of LPS-responsive C3H He responded to these stimulants. These results suggest that the defect of the response in C3H HeJ macrophages toward LPS stimulation may be related to the Ca2+-dependent signal pathway. The extracts from the C3H HeJ macrophages showed normal activities of both protein kinase C (PKC) and calmodulin (CaM) in comparison with those from LPS-responsive C3H He macrophages. However, one species of CaM-binding proteins could hardly be detected by the cross-linking assay with 125I-CaM in C3H HeJ macrophages stimulated by LPS. These results suggest that the LPS-refractory site in C3H HeJ macrophages is related to the lack of this CaM-binding protein, and the Ca2+-dependent CaM system may play an important role in the activation of cells by LPS.

Original languageEnglish
Pages (from-to)723-729
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume158
Issue number3
DOIs
Publication statusPublished - 1989 Feb 15
Externally publishedYes

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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