ArticleOncogene2002
Overexpression of the Notch target genes Hes in vivo induces lymphoid and myeloid alterations.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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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Who cites it
38 citing papers in PubMed, 115 citations in OpenAlex.
- Prenatal SEB Exposure Triggers Biphasic Notch Signaling Modulation in Offspring Thymus From Neonatal Suppression to Adult Activation.Journal of applied toxicology : JAT · 2026Article
- Neuronal Cell Adhesion Molecules May Mediate Neuroinflammation in Autism Spectrum Disorder.Frontiers in psychiatry · 2022Review
- Homodimeric and Heterodimeric Interactions among Vertebrate Basic Helix-Loop-Helix Transcription Factors.International journal of molecular sciences · 2021Review
- Review
- The NOTCH-HES-1 axis is involved in promoting Th22 cell differentiation.Cellular & molecular biology letters · 2021Article
- FANCD2 and HES1 suppress inflammation-induced PPARɣ to prevent haematopoietic stem cell exhaustion.British journal of haematology · 2021Article
- Targeting the Notch Signaling Pathway in Chronic Inflammatory Diseases.Frontiers in immunology · 2021Review
- Hes1 deficiency causes hematopoietic stem cell exhaustion.Stem cells (Dayton, Ohio) · 2020Article
- Review
- T cell development requires constraint of the myeloid regulator C/EBP-α by the Notch target and transcriptional repressor Hes1.Nature immunology · 2013Article
- Early T-cell progenitors are the major granulocyte precursors in the adult mouse thymus.Blood · 2013Article
- GATA-1 utilizes Ikaros and polycomb repressive complex 2 to suppress Hes1 and to promote erythropoiesis.Molecular and cellular biology · 2012Article
- Notch Signaling during Oogenesis in Drosophila melanogaster.Genetics research international · 2012Article
- Hematopoietic cytokine-induced transcriptional regulation and Notch signaling as modulators of MDSC expansion.International immunopharmacology · 2011Review
- MT1-MMP cleaves Dll1 to negatively regulate Notch signalling to maintain normal B-cell development.The EMBO journal · 2011Article
- ADAM10 overexpression shifts lympho- and myelopoiesis by dysregulating site 2/site 3 cleavage products of Notch.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Notch/HES1-mediated PARP1 activation: a cell type-specific mechanism for tumor suppression.Blood · 2011Article
- T-cell lineage determination.Immunological reviews · 2010Review
- Eliciting the T cell fate with Notch.Seminars in immunology · 2010Review
- Hes1 potentiates T cell lymphomagenesis by up-regulating a subset of notch target genes.PloS one · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To examine the effects of Notch signaling on hematopoiesis, we transplanted mice with progenitors transduced with a constitutively active form of Notch1 (Notch1IC) or the Notch1 target genes Hes. Notch1IC-transduced cells induce T cell tumors and cannot generate B lymphocytes in vivo. Hes-transplanted mice remained healthy but cells transduced with Hes1 or Hes5 were partially impaired in their ability to differentiate into B cells. Both Hes1 and Hes5 were upregulated in the BM of Notch1IC mice and their ability to interfere with the transcriptional activity of E2A in a reporter assay was comparable to that of Notch1IC. This suggests that the inhibition of B cell development in the Notch1IC-transduced cells could be mediated by the interference of HES1/HES5 proteins with E2A. Hes1-, Hes5- and Notch1IC-transduced bone marrow cells cultured ex vivo in a colony forming assay in the presence of cytokines that promote myeloid differentiation remained very immature, indicating that the myeloid potential of these bone marrow cells was altered. Thymocytes overexpressing Hes1, Hes5 or Notch1IC matured normally into CD4 and CD8 single positive cells in vivo. Altogether our data suggest that Notch1IC induces T cell tumors independently of Hes genes but that its interference with lymphoid B and myeloid maturation is partly mediated by Hes1 and Hes5. DOI:
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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.