ArticleMolecular and cellular biology1998
The notch pathway intermediate HES-1 silences CD4 gene expression.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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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.
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Who cites it
19 citing papers in PubMed, 82 citations in OpenAlex.
- Repression of Ccr9 transcription in mouse T lymphocyte progenitors by the Notch signaling pathway.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Runx transcription factors repress human and murine c-Myc expression in a DNA-binding and C-terminally dependent manner.PloS one · 2013Article
- Ikaros represses the transcriptional response to Notch signaling in T-cell development.Molecular and cellular biology · 2008Article
- Lineage fate and intense debate: myths, models and mechanisms of CD4- versus CD8-lineage choice.Nature reviews. Immunology · 2008Review
- Repression of chondrogenesis through binding of notch signaling proteins HES-1 and HEY-1 to N-box domains in the COL2A1 enhancer site.Arthritis and rheumatism · 2008Article
- Ikaros directly represses the notch target gene Hes1 in a leukemia T cell line: implications for CD4 regulation.The Journal of biological chemistry · 2008Article
- bHLH-Orange Transcription Factors in Development and Cancer.Translational oncogenomics · 2007Article
- Delta-Notch--and then? Protein interactions and proposed modes of repression by Hes and Hey bHLH factors.Nucleic acids research · 2007Review
- Overexpression of the Notch target genes Hes in vivo induces lymphoid and myeloid alterations.Oncogene · 2002Article
- Notch signaling induces rapid degradation of achaete-scute homolog 1.Molecular and cellular biology · 2002Article
- Combined expression of pTalpha and Notch3 in T cell leukemia identifies the requirement of preTCR for leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Review
- Negative regulation of CD4 gene expression by a HES-1-c-Myb complex.Molecular and cellular biology · 2001Article
- Precise arrangement of factor-binding sites is required for murine CD4 promoter function.Nucleic acids research · 2000Article
- Article
- Subclass-specific nuclear localization of a novel CD4 silencer binding factor.The Journal of experimental medicine · 1999Article
- Rel/NF-kappaB can trigger the Notch signaling pathway by inducing the expression of Jagged1, a ligand for Notch receptors.The EMBO journal · 1999Article
- The bHLH gene Hes1 is essential for expansion of early T cell precursors.Genes & development · 1999Article
- c-Myb is essential for early T cell development.Genes & development · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
We have previously identified a transcriptional silencer that is critical for proper expression of the CD4 gene during T-cell development. Here we report that the Hairy/Enhancer of Split homologue HES-1, a transcription factor in the lin12/Notch signaling pathway, binds to an important functional site in the CD4 silencer. Overexpression of HES-1 leads to the silencer site-dependent repression of CD4 promoter and enhancer function as well as the downregulation of endogenous CD4 expression in CD4(+) CD8(-) TH cells. Interestingly, overexpression of an activated form of Notch1 (NotchIC) leads to the repression of CD4 promoter and enhancer function both in the presence and absence of the silencer. NotchIC-mediated CD4 silencer function is not affected by the deletion of the HES-1-binding site, indicating that multiple factors binding to CD4 transcriptional control elements are responsive to signaling from this pathway, including other silencer-binding factors. Taken together, these data are consistent with the hypothesis that the lin12/Notch signaling pathway is important in thymic development and provide a molecular mechanism via the control of CD4 gene expression in which the lin12/Notch pathway affects T-cell developmental fate.
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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.