{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,7]],"date-time":"2026-02-07T22:36:38Z","timestamp":1770503798227,"version":"3.49.0"},"reference-count":27,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"4497","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[1981,5,22]]},"abstract":"<jats:p>\n            The molecularly cloned, long terminal repeat (LTR) of the Moloney sarcoma virus (M-MSV) provirus has been covalently linked to c-\n            <jats:italic>mos<\/jats:italic>\n            , the cellular homolog of the M-MSV-specific sequence, v-\n            <jats:italic>mos<\/jats:italic>\n            . These newly constructed clones lack any M-MSV-derived sequences other than the LTR, but in DNA transfection assays they transform cells as efficiently as cloned subgenomic M-MSV fragments containing both v-\n            <jats:italic>mos<\/jats:italic>\n            and LTR. Cells transformed by LTR:c-\n            <jats:italic>mos<\/jats:italic>\n            hybrid molecules contain additional copies of\n            <jats:italic>mos<\/jats:italic>\n            DNA, and several size classes of polyadenylated RNA's with sequence homology to\n            <jats:italic>mos<\/jats:italic>\n            . The activation of the transforming potential of c-\n            <jats:italic>mos<\/jats:italic>\n            by the proviral LTR suggests a model whereby LTR-like elements could activate other normal cell sequences with oncogenic potential.\n          <\/jats:p>","DOI":"10.1126\/science.7233190","type":"journal-article","created":{"date-parts":[[2006,10,5]],"date-time":"2006-10-05T17:45:58Z","timestamp":1160070358000},"page":"941-943","source":"Crossref","is-referenced-by-count":169,"title":["Activation of the Transforming Potential of a Normal Cell Sequence: A Molecular Model for Oncogenesis"],"prefix":"10.1126","volume":"212","author":[{"given":"D. G.","family":"Blair","sequence":"first","affiliation":[{"name":"Laboratory of Viral Carcinogenesis, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21701"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Oskarsson","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Virology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20205"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T. G.","family":"Wood","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Virology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20205"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W. L.","family":"McClements","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Virology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20205"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. J.","family":"Fischinger","sequence":"additional","affiliation":[{"name":"Laboratory of Viral Carcinogenesis, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21701"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. 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