Open AccessTranscriptional activation of a ras-like gene (kir) by oncogenic tyrosine kinases.
Author(s) -
Lucie Cohen,
Randolph N. Mohr,
Y Y Chen,
Mary Huang,
Roberta M. Kato,
Dominique Dorin,
Fuyuhiko Tamanoi,
Andrei Goga,
Daniel Afar,
Naomi Rosenberg
Publication year - 1994
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.91.26.12448
Subject(s) - biology , gene , tyrosine kinase , abl , gtpase , receptor tyrosine kinase , transcription factor , microbiology and biotechnology , guanine nucleotide exchange factor , kinase , cancer research , signal transduction , genetics
We report the characterization of a member of the ras gene family that is overexpressed in cells transformed by abl tyrosine kinase oncogenes. The gene, named kir (for kinase-inducible ras-like), is induced at the transcriptional level. kir mRNA has a rapid turnover and encodes a protein of 33 kDa with guanine nucleotide-binding activity but undetectable intrinsic GTPase activity. kir was cloned by differential screening of genes present in fully malignant versus growth factor-independent cell lines expressing wild-type or mutant forms of BCR/ABL. BCR/ABL and v-Abl induce transcription of the kir gene via specific signaling pathway(s), but kir overexpression alone is not sufficient to mediate transformation.