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The Second Intron of the K-ras Gene Contains Regulatory Elements Associated with Mouse Lung Tumor Susceptibility
Bin Chen, Lisa Johanson, Jonathan S. Wiest, Marshall W. Anderson and Ming You
Proceedings of the National Academy of Sciences of the United States of America
Vol. 91, No. 4 (Feb. 15, 1994), pp. 1589-1593
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/2364147
Page Count: 5
You can always find the topics here!Topics: Alleles, Lungs, Tumors, ras genes, Introns, Inbred strains, Hybridity, Adenoma, Cell lines, Tumor cell line
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We have previously demonstrated the preferential activation of the K-ras gene from the susceptible A/J parent in lung tumors from F1 mouse hybrids. In the present study, the mechanism of this observation is further investigated. Higher levels of expression of A/J K-ras allele were detected in lung adenomas (30 of 30) from the C3A mouse. In addition, three K-ras alleles, designated as susceptible (Ks), intermediate (Ki), or resistant (Kr), were identified by sequence analysis of the second intron of the K-ras gene from 32 strains of mice. These K-ras alleles are associated with differences in mouse lung tumor susceptibility. All Kr alleles have a tandem 37-bp direct repeat (nt 282-355) in the second intron of the K-ras gene. Ks and Ki alleles have only one copy of the 37-bp sequence (nt 282-318). Ks strains have three base variations at nt 288, 296, and 494, and Ki strains have two base variations at nt 288 and 494 in the second intron of the K-ras gene. Differential protein-binding patterns were observed in gel-mobility-shift experiments between the duplicated 37-bp sequence of the Kr allele and the single 37-bp sequence of the Ks and Ki alleles. DNase I footprinting assay revealed protein binding sites in the second intron of the K-ras gene that correspond to the tandem repeat sequences. Our data suggest that higher expression of the A/J allele relative to C3H allele may be responsible for the allele-specific activation of the K-ras gene in lung tumors from F1 hybrid mice.
Proceedings of the National Academy of Sciences of the United States of America © 1994 National Academy of Sciences