ArticleMolecular and cellular biology2008
Ikaros represses the transcriptional response to Notch signaling in T-cell development.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 87 citations in OpenAlex.
- Thymic Bmi-1 hampers γδT17 generation and its derived RORγt-IL-17A signaling to delay cardiac aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- A new pipeline SPICE identifies novel JUN-IKZF1 composite elements.bioRxiv : the preprint server for biology · 2024Article
- Article
- IKAROS Family Transcription Factors in Lymphocyte Differentiation and Function.Advances in experimental medicine and biology · 2024Review
- From Genotype to Phenotype: How Enhancers Control Gene Expression and Cell Identity in Hematopoiesis.HemaSphere · 2023Review
- Ikaros is a principal regulator of AireScience immunology · 2023Article
- TGFCells · 2023Article
- Germline biallelic mutation affecting the transcription factor Helios causes pleiotropic defects of immunity.Science immunology · 2021Article
- IKAROS is required for the measured response of NOTCH target genes upon external NOTCH signaling.PLoS genetics · 2021Article
- Transcriptional Regulation of PIK3CD and PIKFYVE in T-Cell Acute Lymphoblastic Leukemia by IKAROS and Protein Kinase CK2.International journal of molecular sciences · 2021Article
- A Different View for an Old Disease: NEDDylation and Other Ubiquitin-Like Post-Translational Modifications in Chronic Lymphocytic Leukemia.Frontiers in oncology · 2021Review
- Specific Targeting of Notch Ligand-Receptor Interactions to Modulate Immune Responses: A Review of Clinical and Preclinical Findings.Frontiers in immunology · 2020Review
- Ikaros antagonizes DNA binding by STAT5 in pre-B cells.PloS one · 2020Article
- Integration of high-throughput reporter assays identify a critical enhancer of the Ikzf1 gene.PloS one · 2020Article
- Ikaros cooperates with Notch activation and antagonizes TGFβ signaling to promote pDC development.PLoS genetics · 2018Article
- Cytokines, Transcription Factors, and the Initiation of T-Cell Development.Cold Spring Harbor perspectives in biology · 2018Review
- Expression and splicing of Ikaros family members in murine and human thymocytes.Molecular immunology · 2017Article
- The making of a lymphocyte: the choice among disparate cell fates and the IKAROS enigma.Genes & development · 2017Review
- Notch signalling in context.Nature reviews. Molecular cell biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Notch activity is essential for early T-cell differentiation, but aberrant activity induces T-cell transformation. Thus, Notch target genes must be efficiently silenced in cells where Notch activity is no longer required. How these genes are repressed remains poorly understood. We report here that the Ikaros transcription factor plays a crucial role in repressing the transcriptional response to Notch signaling in T-cell development. Using the Notch target gene Hes-1 as a model, we show that Ikaros and RBP-Jkappa, the transcriptional mediator of Notch signaling, compete for binding to two elements in the Hes-1 promoter in immature thymocytes. This antagonistic interaction likely occurs at the CD4(-) CD8(-) CD3(-) double-negative 4 (DN4) stage, where Ikaros levels and binding to the Hes-1 promoter increase sharply and wild-type thymocytes lose their capacity to transcribe Hes-1 upon Notch stimulation. Nonresponsiveness to Notch signaling requires Ikaros, as Ikaros-deficient DN4 and CD4(+) CD8(+) double-positive (DP) cells remain competent to express Hes-1 after Notch activation. Further, Hes-1 promoter sequences from Ikaros-deficient DP cells show reduced trimethylated H3K27, a modification associated with silent chromatin. These results indicate that Ikaros functions as a transcriptional checkpoint to repress Notch target gene expression in T cells.
Indexed as
Identifiers
What OpenQuestion holds
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.