Tumor necrosis factor α stimulates sphingomyelinase through the 55 kDa receptor in HL-60 cells

Fumi Yanaga, Steve P. Watson

研究成果: Contribution to journalArticle査読

56 被引用数 (Scopus)

抄録

Tumor necrosis factor α (TNFα) stimulated rapid (seconds) hydrolysis of sphingomyelin in HL-60 cells, formation of phosphocholine (PCho) and a decrease in choline. The response to TNFα was concentration dependent with a maximal effect at 3-10 nM. The monoclonal antibody (mAb). htr-9, which behaves as an agonist at the 55 kDa subtype of the TNF receptor, also stimulated sphingomyelin hydrolysis in intact cells. In contrast, the mAb, utr-1, which behaves as an antagonist at the 75 kDa receptor subtype, had no effect on sphingomyelin hydrolysis either on its own or in the presence of TNFα. In addition, htr-9 or TNFα stimulated hydrolysis of sphingomyelin in a membrane fraction of HL-60 cells. These results are consistent with a role of sphinpomyelin hydrolysis as an early event in the signalling mechanism or TNFα, and suggest that this pathway is activated through the 55 kDa subtype of the TNF receptor.

本文言語英語
ページ(範囲)297-300
ページ数4
ジャーナルFEBS Letters
314
3
DOI
出版ステータス出版済み - 12 21 1992

All Science Journal Classification (ASJC) codes

  • 生物理学
  • 構造生物学
  • 生化学
  • 分子生物学
  • 遺伝学
  • 細胞生物学

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