Abstract
Pretreatment of cells with 0.5 mM sodium arsenite (but not other activators of stress-activated MAP kinase cascades) prevents the activation of p21Ras and strongly suppresses the activation of c-Raf and the MAP kinase cascade by a variety of growth factors. Arsenite appears to exert its effect by preventing the guanine nucleotide exchange factor mSos from converting Ras to its active GTP-bound state. Exposure to arsenite may be a simple way of assessing whether Ras plays an essential role in mediating activation of the MAP kinase cascade by extracellular signals.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 50 print issues and online access
$259.00 per year
only $5.18 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Doza, Y., Hall-Jackson, C. & Cohen, P. Arsenite blocks growth factor induced activation of the MAP kinase cascade, upstream of Ras and downstream of Grb2-Sos. Oncogene 17, 19–24 (1998). https://doi.org/10.1038/sj.onc.1202168
Received:
Revised:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1038/sj.onc.1202168
Keywords
This article is cited by
-
Sodium arsenite-induced inhibition of cell proliferation is related to inhibition of IL-2 mRNA expression in mouse activated T cells
Archives of Toxicology (2007)
-
Arsenic trioxide (As2O3) induces apoptosis through activation of Bax in hematopoietic cells
Oncogene (2005)
-
mCICR is required for As2O3-induced permeability transition pore opening and cytochrome c release from mitochondria
Molecular and Cellular Biochemistry (2005)
-
Effect of SB 203580 on the activity of c-Raf in vitro and in vivo
Oncogene (1999)