These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Co-induction of cell death and survival pathways by phosphoinositide 3-kinase.
    Author: Lee SB, Hong SH, Kim H, Um HD.
    Journal: Life Sci; 2005 Nov 19; 78(1):91-8. PubMed ID: 16154597.
    Abstract:
    A single stimulus can induce both the cell death and survival pathway, suggesting that these pathways share common upstream signaling components. In order to define these components, human U937 cells grown in 10% serum were exposed to serum-free media. This treatment resulted in apoptosis, which was found to be mediated by SAPK/JNK. It was previously reported that the serum withdrawal (SW)-induced SAPK activation is mediated by a positive mutual interaction between the reactive oxygen species (ROS) and phosphoinositide 3-kinase (PI3K). This study shows that the ROS/PI3K interaction also induces a NF-kappaB-dependent survival pathway. Despite the role of PI3K, Akt was found to be irrelevant to the activation of SAPK and NF-kappaB. Comparative analyses of SAPK and NF-kappaB for their responses to exogenous H(2)O(2) revealed that SAPK activation requires much higher H(2)O(2) concentrations than those required for NF-kappaB activation. Moreover, high lethal concentrations of H(2)O(2) were found to activate NF-kappaB and SAPK in a PI3K-independent manner. These results suggest that ROS induce both the SAPK-dependent apoptotic and NF-kappaB-mediated survival pathways, and these inducer signals are amplified by PI3K in the SW-triggered pathway. Cell death appears to be favored as this amplification proceeds.
    [Abstract] [Full Text] [Related] [New Search]