Clnk plays a role in TNF-alpha-induced cell death in murine fibrosarcoma cell line L929

Biochem Biophys Res Commun. 2015 Jul 31;463(3):275-9. doi: 10.1016/j.bbrc.2015.05.046. Epub 2015 May 22.

Abstract

Clnk, as a third member of the Blnk/SLP-76 adapter family, is involved in the positive regulation of immunoreceptor signaling. Here we provide findings that Clnk may be is required for TNF induced cell death, it functions downstream of RIP3 and promotes TNF- induced ROS generation and MLKL tetramer formation and subsequent necrosis of L929 cells. Therefore, Clnk, as an adaptor protein, may take part in the other cellular processes.

Keywords: Clnk; MLKL; Necrosis; RIP3; ROS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Carrier Proteins / immunology*
  • Cell Death
  • Cell Line, Tumor
  • Fibrosarcoma / immunology*
  • Fibrosarcoma / pathology
  • HeLa Cells
  • Humans
  • Mice
  • Necrosis / immunology
  • Protein Kinases / chemistry
  • Protein Kinases / immunology
  • Protein Multimerization
  • Reactive Oxygen Species / immunology*
  • Receptor-Interacting Protein Serine-Threonine Kinases / immunology
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / immunology*

Substances

  • Adaptor Proteins, Signal Transducing
  • Carrier Proteins
  • Clnk protein, mouse
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • MLKL protein, mouse
  • Protein Kinases
  • Receptor-Interacting Protein Serine-Threonine Kinases
  • Ripk3 protein, mouse