{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T19:52:30Z","timestamp":1787687550980,"version":"build-2784847793"},"reference-count":41,"publisher":"National Academy of Sciences","issue":"35","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2008,9,2]]},"abstract":"<jats:p>\n                    E-proteins are a class of helix-loop-helix (HLH) proteins, which play multiple roles throughout lymphoid development. The DNA binding activities of the E-proteins are regulated by a distinct class of antagonistic HLH proteins, named Id1\u20134. Here we demonstrate that Id2 deficient mice in a C57BL\/6 genetic background exhibit increased cellularity in the granulocyte\/myeloid progenitor compartment and show significantly higher numbers of maturing neutrophils. Within 6 months of age, Id2 deficient mice succumbed from overwhelming granulocytosis. The disease closely mimicked the distinctive features of human chronic myeloid leukemia: leukocytosis with maturing neutrophils, splenomegaly, hepatomegaly, and myeloid infiltration into peripheral tissues, including spleen, liver, and lungs. Strikingly, forced Id2 expression in murine bone marrow cells substantially delayed the onset of myeloproliferative disease (MPD). Collectively, these studies show that suppression of E-protein activity interferes with the development of\n                    <jats:italic>BCR-ABL<\/jats:italic>\n                    -mediated MPD.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0805073105","type":"journal-article","created":{"date-parts":[[2008,8,25]],"date-time":"2008-08-25T21:09:32Z","timestamp":1219698572000},"page":"12967-12972","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":13,"title":["Suppression of E-protein activity interferes with the development of\n                    <i>BCR-ABL<\/i>\n                    -mediated myeloproliferative disease"],"prefix":"10.1073","volume":"105","author":[{"given":"Jinkyung","family":"Ko","sequence":"first","affiliation":[{"name":"*Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nihal","family":"Patel","sequence":"additional","affiliation":[{"name":"Tufts Medical Center, 800 Washington Street, Boston, MA 02111;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomokatsu","family":"Ikawa","sequence":"additional","affiliation":[{"name":"Laboratory for Lymphocyte Development, RIKEN Research Center for Allergy and Immunology, Yokohama 230-0045, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroshi","family":"Kawamoto","sequence":"additional","affiliation":[{"name":"Laboratory for Lymphocyte Development, RIKEN Research Center for Allergy and Immunology, Yokohama 230-0045, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oliver","family":"Frank","sequence":"additional","affiliation":[{"name":"III Medizinische Klinik, Medizinische Fakult\u00e4t Mannheim der Universit\u00e4t Heidelberg, Wiesbadener Strasse 7-11, 68305 Mannheim, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard R.","family":"Rivera","sequence":"additional","affiliation":[{"name":"*Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard A.","family":"Van Etten","sequence":"additional","affiliation":[{"name":"Tufts Medical Center, 800 Washington Street, Boston, MA 02111;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cornelis","family":"Murre","sequence":"additional","affiliation":[{"name":"*Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2008,9,2]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccr.2004.12.004"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199907153410306"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1210758"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/300765a0"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.2406902"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm0596-561"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-09-2896"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1260"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.20.2.429-440.2000"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/84273"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90077-9"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90076-0"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.186.9.1597"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.194.6.733"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.20.18.6677-6685.2000"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20060268"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20061959"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90214-Y"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80155-7"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.17.12.7317"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-12-4883"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1038\/17812"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni903"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1403"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1206620"},{"key":"e_1_3_3_26_2","first-page":"45","article-title":"E2A-HLF chimeric transcription factors in pro-B cell acute lymphoblastic leukemia","volume":"220","author":"Look AT","year":"1997","unstructured":"AT Look, E2A-HLF chimeric transcription factors in pro-B cell acute lymphoblastic leukemia. 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