ArticleMolecular and cellular biology2006
Notch activation is an early and critical event during T-Cell leukemogenesis in Ikaros-deficient mice.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 156 citations in OpenAlex.
- SUMOylation is destined for regulatory T cell-related immune dysregulation.Cell death discovery · 2026Review
- Article
- IKAROS: from chromatin organization to transcriptional elongation control.Cell death and differentiation · 2025Review
- Evaluating the Role of Methylated Circulating Tumor DNA in Combination With Pathological Prognostic Factors for Predicting Recurrence of Colorectal Cancer.Biomarker insights · 2024Article
- IKAROS Family Transcription Factors in Lymphocyte Differentiation and Function.Advances in experimental medicine and biology · 2024Review
- IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?International journal of molecular sciences · 2023Review
- T-ALL can evolve to oncogene independence.Leukemia · 2021Article
- IKAROS is required for the measured response of NOTCH target genes upon external NOTCH signaling.PLoS genetics · 2021Article
- Ikaros Proteins in Tumor: Current Perspectives and New Developments.Frontiers in molecular biosciences · 2021Review
- Specific Targeting of Notch Ligand-Receptor Interactions to Modulate Immune Responses: A Review of Clinical and Preclinical Findings.Frontiers in immunology · 2020Review
- Assessing the Functional Relevance of Variants in theFrontiers in immunology · 2019Article
- Sources of Type I Interferons in Infectious Immunity: Plasmacytoid Dendritic Cells Not Always in the Driver's Seat.Frontiers in immunology · 2019Review
- Ikaros cooperates with Notch activation and antagonizes TGFβ signaling to promote pDC development.PLoS genetics · 2018Article
- Article
- The many faces of IKZF1 in B-cell precursor acute lymphoblastic leukemia.Haematologica · 2018Review
- Germline IKAROS mutation associated with primary immunodeficiency that progressed to T-cell acute lymphoblastic leukemia.Leukemia · 2017Article
- Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1The Journal of experimental medicine · 2017Article
- Conserved IKAROS-regulated genes associated with B-progenitor acute lymphoblastic leukemia outcome.The Journal of experimental medicine · 2017Article
- Tumor suppressors BTG1 and IKZF1 cooperate during mouse leukemia development and increase relapse risk in B-cell precursor acute lymphoblastic leukemia patients.Haematologica · 2017Article
- The making of a lymphocyte: the choice among disparate cell fates and the IKAROS enigma.Genes & development · 2017Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ikaros transcription factor is both a key regulator of lymphocyte differentiation and a tumor suppressor in T lymphocytes. Mice carrying a hypomorphic mutation (Ik(L/L)) in the Ikaros gene all develop thymic lymphomas. Ik(L/L) tumors always exhibit strong activation of the Notch pathway, which is required for tumor cell proliferation in vitro. Notch activation occurs early in tumorigenesis and may precede transformation, as ectopic expression of the Notch targets Hes-1 and Deltex-1 is detected in thymocytes from young Ik(L/L) mice with no overt signs of transformation. Notch activation is further amplified by secondary mutations that lead to C-terminal truncations of Notch 1. Strikingly, restoration of Ikaros activity in tumor cells leads to a rapid and specific downregulation of Notch target gene expression and proliferation arrest. Furthermore, Ikaros binds to the Notch-responsive element in the Hes-1 promoter and represses Notch-dependent transcription from this promoter. Thus, Ikaros-mediated repression of Notch target gene expression may play a critical role in defining the tumor suppressor function of this factor.
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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.