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

Yasuhiko Terada, Hiroto Shinomiya, Masayasu Nakano

研究成果: Article

13 引用 (Scopus)

抄録

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.

元の言語English
ページ(範囲)723-729
ページ数7
ジャーナルBiochemical and Biophysical Research Communications
158
発行部数3
DOI
出版物ステータスPublished - 1989 2 15
外部発表Yes

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Calmodulin-Binding Proteins
Inbred C3H Mouse
Macrophages
Interleukin-1
Lipopolysaccharides
Genes
Defects
Calmodulin
Refractory materials
Ionophores
Calcimycin
Peritoneal Macrophages
Protein Kinase C
Assays
Signal Transduction
Chemical activation
Messenger RNA

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

これを引用

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title = "Defect of calmodulin-binding protein in expression of interleukin-1β gene by LPS-nonresponder C3H HeJ mouse macrophages",
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.",
author = "Yasuhiko Terada and Hiroto Shinomiya and Masayasu Nakano",
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T1 - Defect of calmodulin-binding protein in expression of interleukin-1β gene by LPS-nonresponder C3H HeJ mouse macrophages

AU - Terada, Yasuhiko

AU - Shinomiya, Hiroto

AU - Nakano, Masayasu

PY - 1989/2/15

Y1 - 1989/2/15

N2 - 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.

AB - 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.

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