Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

Mechanism of Activation of an N-ras Oncogene of SW-1271 Human Lung Carcinoma Cells

Yasuhito Yuasa, Rose A. Gol, Audrey Chang, Ing-Ming Chiu, E. Premkumar Reddy, Steven R. Tronick and Stuart A. Aaronson
Proceedings of the National Academy of Sciences of the United States of America
Vol. 81, No. 12, [Part 1: Biological Sciences] (Jun. 15, 1984), pp. 3670-3674
Stable URL: http://www.jstor.org/stable/24334
Page Count: 5
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Mechanism of Activation of an N-ras Oncogene of SW-1271 Human Lung Carcinoma Cells
Preview not available

Abstract

An N-ras-related transforming gene was detected in the human lung carcinoma cell line SW-1271 and molecularly cloned. The lesion responsible for its acquisition of transforming activity was localized to a single nucleotide transition from A to G in codon 61 of the predicted protein. This lesion in the second exon results in the substitution of arginine for glutamine at this position. These findings, together with previous studies, indicate that the activation of ras oncogenes in human tumors is most commonly due to point mutations at one of two major ``hot spots'' in the ras coding sequence.

Page Thumbnails

  • Thumbnail: Page 
3670
    3670
  • Thumbnail: Page 
3671
    3671
  • Thumbnail: Page 
3672
    3672
  • Thumbnail: Page 
3673
    3673
  • Thumbnail: Page 
3674
    3674