Inhibition of receptor internalization attenuates the TNFα-induced ROS generation in non-phagocytic cells

Chang Hoon Woo, Tae Hee Kim, Jung A. Choi, Ho Cheol Ryu, Jung Eun Lee, Hye Jin You, Yun Soo Bae, Jae Hong Kim

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


Reactive oxygen species (ROS) are important regulatory molecules implicated in the signaling cascade triggered by tumor necrosis factor (TNF)α, although the events through which TNFα induces ROS generation are not well characterized. Here, we report that TNFα-induced ROS production was blocked by pretreatment with internalization inhibitor monodansyl cadaverine (MDC). Similarly, a transient expression of a GTP-binding and hydrolysis-defective dynamin mutant (dynaminK44A) that had been shown to be defective in internalization significantly attenuated the TNFα-induced intracellular ROS production. Importantly, the inhibition of receptor internalization suppressed TNFα signaling to mitogen-activated protein kinases (MAPKs) stimulation. Together, our results suggest that receptor internalization is somehow necessary for the TNFα-induced ROS generation and subsequent intracellular downstream signaling in non-phagocytes.

Original languageEnglish
Pages (from-to)972-978
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - 29 Dec 2006

Bibliographical note

Funding Information:
This work was supported by the Frontier 21 Programs (Proteomics), the BioDiscovery Research Program of the Korea Ministry of Science and Technology, and the SRC program (Aging and Apoptosis Research Center) (2002) of the Korea Science and Engineering Foundation (KOSEF).


  • Non-phagocytes
  • Nox
  • ROS
  • Receptor internalization
  • Signal transduction
  • TNFα


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