ArticleProceedings of the National Academy of Sciences of the United States of America1994
The E2A and tal-1 helix-loop-helix proteins associate in vivo and are modulated by Id proteins during interleukin 6-induced myeloid differentiation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 104 citations in OpenAlex.
- Multi-hit genetic lesions and a stress-imprinted immune transcriptome define the inflammatory pathology in ALS patients.Research square · 2026Article
- TAL1 cooperates with PI3K/AKT pathway activation in T-cell acute lymphoblastic leukemia.Haematologica · 2022Article
- E47 upregulates ΔNp63α to promote growth of squamous cell carcinoma.Cell death & disease · 2021Article
- Human Cytomegalovirus Immediate-Early 1 Protein Rewires Upstream STAT3 to Downstream STAT1 Signaling Switching an IL6-Type to an IFNγ-Like Response.PLoS pathogens · 2016Article
- Article
- Diversity, function, and transcriptional regulation of gut innate lymphocytes.Frontiers in immunology · 2013Article
- NKX3.1 is a direct TAL1 target gene that mediates proliferation of TAL1-expressing human T cell acute lymphoblastic leukemia.The Journal of experimental medicine · 2010Article
- Article
- The TAL1/SCL transcription factor regulates cell cycle progression and proliferation in differentiating murine bone marrow monocyte precursors.Molecular and cellular biology · 2010Article
- Inhibitor of differentiation 4 (Id4) is a potential tumor suppressor in prostate cancer.BMC cancer · 2009Article
- Article
- Efficient retroviral transduction of human B-lymphoid and myeloid progenitors: marked inhibition of their growth by the Pax5 transgene.International journal of hematology · 2008Article
- Transcriptional regulatory networks downstream of TAL1/SCL in T-cell acute lymphoblastic leukemia.Blood · 2006Article
- Expression of GCIP in transgenic mice decreases susceptibility to chemical hepatocarcinogenesis.Oncogene · 2006Article
- Article
- OLIG2 (BHLHB1), a bHLH transcription factor, contributes to leukemogenesis in concert with LMO1.Cancer research · 2005Article
- ID1 and ID2 are retinoic acid responsive genes and induce a G0/G1 accumulation in acute promyelocytic leukemia cells.Leukemia · 2005Article
- Disruption of pre-TCR expression accelerates lymphomagenesis in E2A-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- The DNA binding activity of TAL-1 is not required to induce leukemia/lymphoma in mice.Oncogene · 2001Article
- Development and characterization of T cell leukemia cell lines established from SCL/LMO1 double transgenic mice.Leukemia · 2001Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immunoglobulin enhancer-binding proteins, E12 and E47, encoded by the E2A gene belong to the basic helix-loop-helix (bHLH) family of regulatory proteins and act as transcriptional activators. In addition to their critical role in B-lymphocyte development, the E12 and E47 proteins have been implicated in the induction of myogenesis as heterodimeric partners of myogenic bHLH proteins, MyoD and myogenin. Here we demonstrate that the E2A proteins form heterodimers with the bHLH oncoprotein tal-1 in myeloid and erythroid cells and that these heterodimers specifically bind to the CANNTG DNA motif. Heterodimerization with tal-1 represses transactivation by E47 and could function to prevent the expression of immunoglobulin genes in cells other than B lymphocytes. DNA binding by E2A-tal-1 heterodimers in the M1 mouse myeloid cell line is abrogated upon terminal macrophage differentiation induced by the cytokine interleukin 6. The loss of E2A-tal-1 DNA binding is correlated with elevated expression of mRNA encoding the dominant negative HLH proteins, Id1 and particularly Id2. Moreover, recombinant Id proteins inhibit the E2A-tal-1-specific DNA binding activity from undifferentiated M1 cells. These results suggest that E2A-tal-1 heterodimers may play a role in preventing terminal differentiation in the myeloid lineage and provide a possible explanation for oncogenic transformation induced by ectopic tal-1 expression in acute T-cell lymphoblastic leukemias.
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