Bcl-x(L) inhibits different apoptotic pathways in rat PC12 cells

Liora Lindenboim, Ronit Haviv, Reuven Stein*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Bcl-x(L), a member of the bcl-2 family of proteins is required for the survival of neurons early in development. To study the mechanism of action of Bcl-x(L) in a neuronal context, we generated rat PC12 cells overexpressing Bcl-x(L) and examined their susceptibility to apoptotic stimuli that induce apoptosis through different pathways involving trophic-factor deprivation, staurosporine, tumor necrosis factor alpha or cisplatin. Overexpression of Bcl-x(L) in both naive and neuronal PC12 cells inhibited apoptosis induced by the different pathways. However, the extent of this protective effect varied, suggesting that the contribution of the Bcl-x(L)-controlled step to apoptosis differs in the different pathways. Our findings also showed that TNFα- induced activation of caspase-3 is inhibited by overexpression of Bcl-x(L), suggesting that Bcl-x(L) acts upstream of caspase activation.

Original languageEnglish
Pages (from-to)37-40
Number of pages4
JournalNeuroscience Letters
Volume253
Issue number1
DOIs
StatePublished - 28 Aug 1998

Funding

FundersFunder number
German-Israeli Foundation for Scientific Research and Development
Israel Science Foundation

    Keywords

    • Apoptosis
    • Bcl-x(L)
    • Caspases
    • PC12 cells
    • TNFα

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