ArticleProceedings of the National Academy of Sciences of the United States of America2008
Suppression of E-protein activity interferes with the development of BCR-ABL-mediated myeloproliferative disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- ID2 secures cDC1 specification by antagonizing E proteins at a pleiotropic Zeb2 enhancer.Nature immunology · 2026Article
- ID2 secures cDC1 specification by antagonizing E proteins at a pleiotropicResearch square · 2025Article
- ID2 and HIF-1α collaborate to protect quiescent hematopoietic stem cells from activation, differentiation, and exhaustion.The Journal of clinical investigation · 2022Article
- Inhibitor of DNA binding proteins revealed as orchestrators of steady state, stress and malignant hematopoiesis.Frontiers in immunology · 2022Review
- Inhibitor of Differentiation-2 Protein Ameliorates DSS-Induced Ulcerative Colitis by Inhibiting NF-κB Activation in Neutrophils.Frontiers in immunology · 2021Article
- Inhibitor of DNA binding in heart development and cardiovascular diseases.Cell communication and signaling : CCS · 2019Review
- Regulation of p21 by TWIST2 contributes to its tumor-suppressor function in human acute myeloid leukemia.Oncogene · 2015Article
- The E-Id protein axis modulates the activities of the PI3K-AKT-mTORC1-Hif1a and c-myc/p19Arf pathways to suppress innate variant TFH cell development, thymocyte expansion, and lymphomagenesis.Genes & development · 2015Article
- A requirement for SOCS-1 and SOCS-3 phosphorylation in Bcr-Abl-induced tumorigenesis.Neoplasia (New York, N.Y.) · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 Id1-4. 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 BCR-ABL-mediated MPD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.