Mutations in FL5.12 cells conferring resistance to apoptosis induced by interleukin-3 deprivation.

  • Authors:
    • H Zhang
    • R Brandt
    • J Heim
    • B Meyhack
  • View Affiliations

  • Published online on: Friday, January 1, 1999
  • Pages: 113-133
  • DOI: 10.3892/ijo.14.1.113

Abstract

In an attempt to dissect the signal pathway in which Bax increases cellular responses to apoptotic stimuli and leads to the activation of the caspase cascade, we mutated FL5.12 Bax CL16 cells with a chemical mutagen. In this report we characterize two mutant clones, FL5.12 ms1 and m3. Both clones are resistant to IL-3 deprivation exhibiting no changes in mitochondrial membrane potential, annexin V and propidium iodide binding. FL5.12 ms1 is also resistant to staurosporine and anti-Fas antibody. In cell fusion experiments m3 behaves genetically dominant and ms1 is recessive. The results suggest that m3 has a mutation in a specific function upstream of Bax, while ms1 has a mutational block in the general pathway downstream of the 'Bcl-2 checkpoint'.
Journal Cover

January 1999
Volume 14 Issue 1

Print ISSN: 1019-6439
Online ISSN:1791-2423

2013 Impact Factor: 2.773
Ranked #30/202 Oncology
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APA
Zhang, H., Brandt, R., Heim, J., & Meyhack, B. (1999). Mutations in FL5.12 cells conferring resistance to apoptosis induced by interleukin-3 deprivation.. International Journal of Oncology, 14(1), 113-133.
MLA
Zhang, Brandt, Heim, and B Meyhack. "Mutations in FL5.12 cells conferring resistance to apoptosis induced by interleukin-3 deprivation.." International Journal of Oncology International Journal of Oncology 14.1 (1999): 113-133.
Chicago
Zhang, Brandt, Heim, and B Meyhack. "Mutations in FL5.12 cells conferring resistance to apoptosis induced by interleukin-3 deprivation.." International Journal of Oncology International Journal of Oncology 14 no. 1 (1999): 113-133.