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Papers In Press, published online ahead of print February 11, 2002
Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455
Corresponding Author: larga002{at}tc.umn.edu
Retroviruses induce leukemia in inbred strains of mice by activating cellular proto-oncogenes and/or inactivating tumor suppressors. The proviral integration sites in these leukemias provide powerful genetic tags for disease gene identification. Here we show that Evi24, a common site of retroviral integration in AKXD B cell and BXH-2 myeloid leukemias, contains a novel member of the Dbl family guanine nucleotide exchange factor (GEF) genes. We have designated this gene Clg (common-site lymphoma/leukemia GEF). Proviral integrations on chromosome 7 at Evi24 are located 7.6 to 10.3 kb upstream of Clg and increase Clg expression two- to five-fold compared with leukemias lacking proviral integrations at Evi24. Clg contains DH/PH domains with substantial sequence homology to many Rho family activators, including the transforming Dbl and Dbs/Ost oncogenes. Nucleotide exchange assays indicate that Clg specifically activates nucleotide exchange on Cdc42, but not RhoA or Rac1 in vitro. NIH 3T3 transfection studies show overexpression of full-length and carboxyl-terminally truncated forms of Clg morphologically transforms NIH 3T3 cells. These and studies showing that the human homolog of EVI24 is located in a region of 19q13 frequently amplified in B cell lymphoma and pancreatic and breast cancer, implicate Clg and Cdc42 activation in mouse and human cancer.
J. Biol. Chem, 10.1074/jbc.M110981200
Submitted on November 15, 2001
Revised on January 17, 2002
Accepted on February 11, 2002
Activation of Clg, a novel Dbl family guanine nucleotide exchange factor gene, by proviral insertion at Evi24, a common integration site in B cell and myeloid Leukemia
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