ArticleThe Journal of biological chemistry2008
Ikaros directly represses the notch target gene Hes1 in a leukemia T cell line: implications for CD4 regulation.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 57 citations in OpenAlex.
- Lenalidomide boosts CD1d-Vδ2 bispecific antibody-engaged Vγ9Vδ2-T cell effector functions via CD28, Notch signaling and IL-2 release.Journal for immunotherapy of cancer · 2026Article
- Systematic functional validation of IKAROS variants from patients and laboratory-generated mutations.Blood advances · 2026Article
- Notch signaling in the tumor microenvironment: recent advances and targeted therapeutics.Molecular cancer · 2026Review
- TGFCells · 2023Article
- 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
- NKAP Must Associate with HDAC3 to Regulate Hematopoietic Stem Cell Maintenance and Survival.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Article
- Variations in mRNA and protein levels of Ikaros family members in pediatric T cell acute lymphoblastic leukemia.Annals of translational medicine · 2016Article
- Forging T-Lymphocyte Identity: Intersecting Networks of Transcriptional Control.Advances in immunology · 2016Review
- Activated Notch counteracts Ikaros tumor suppression in mouse and human T-cell acute lymphoblastic leukemia.Leukemia · 2015Article
- Murine pancreatic adenocarcinoma reduces Ikaros expression and disrupts T cell homeostasis.PloS one · 2015Article
- The evolution of thymic lymphomas in p53 knockout mice.Genes & development · 2014Article
- Inhibitory effects of transcription factor Ikaros on the expression of liver cancer stem cell marker CD133 in hepatocellular carcinoma.Oncotarget · 2014Article
- Epstein-Barr virus utilizes Ikaros in regulating its latent-lytic switch in B cells.Journal of virology · 2014Article
- Adult T-cell leukemia cells are characterized by abnormalities of Helios expression that promote T cell growth.Cancer science · 2013Article
- miR-146a and miR-150 promote the differentiation of CD133+ cells into T-lymphoid lineage.Molecular biology reports · 2013Article
- Ikaros inhibits megakaryopoiesis through functional interaction with GATA-1 and NOTCH signaling.Blood · 2013Article
- Notch signalling inhibits CD4 expression during initiation and differentiation of human T cell lineage.PloS one · 2012Article
- Ikaros-Notch axis in host hematopoietic cells regulates experimental graft-versus-host disease.Blood · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Ikaros and Notch1, two regulators of gene transcription, are critically important at many stages of T cell development. Deregulation of Ikaros and Notch activities cooperate to promote T cell leukemogenesis, providing evidence that they function in converging pathways in developing T cells. In this report, a mechanism for Ikaros:Notch cooperativity is described, revealing a non-redundant role for Ikaros in regulating expression of the Notch target gene Hes1 in a leukemia T cell line. We provide evidence that Ikaros directly represses Hes1 in concert with the transcriptional repressor, RBP-Jkappa, allowing for cross-talk between Notch and Ikaros that impacts regulation of CD4 expression. Taken together, these data describe a potential mechanism for Ikaros' function during T cell development and define Ikaros as an obligate repressor of Hes1.
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.