ArticleMolecular and cellular biology2000
Essential roles for ankyrin repeat and transactivation domains in induction of T-cell leukemia by notch1.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
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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.
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Who cites it
132 citing papers in PubMed, 285 citations in OpenAlex.
- Trial
- Pre-TCR-targeted immunotherapy for T cell acute lymphoblastic leukemia.Nature immunology · 2025Article
- Functional and molecular single-cell analyses implicate PRDM14 in the initiation of B cell leukemia in mice.Scientific reports · 2025Article
- Essential and dual effects of Notch activity on a natural transdifferentiation event.Nature communications · 2025Article
- Structural requirements for activity of Mind bomb1 in Notch signaling.Structure (London, England : 1993) · 2024Article
- Structural Requirements for Activity of Mind bomb1 in Notch Signaling.bioRxiv : the preprint server for biology · 2024Article
- Cdc73 protects Notch-induced T-cell leukemia cells from DNA damage and mitochondrial stress.Blood · 2023Article
- A spatiotemporal Notch interaction map from plasma membrane to nucleus.Science signaling · 2023Article
- Gamma-secretase inhibitor does not induce cytotoxicity in adult T-cell leukemia cell lines despite NOTCH1 expression.BMC cancer · 2022Article
- Interleukin-7 receptor signaling is crucial for enhancer-dependent TCRδ germline transcription mediated through STAT5 recruitment.Frontiers in immunology · 2022Article
- Sirtuin1 meditated modification of Notch1 intracellular domain regulates nucleolar localization and activation of distinct signaling cascades.Frontiers in cell and developmental biology · 2022Article
- Biophysics of Notch Signaling.Annual review of biophysics · 2021Review
- The Earliest T-Precursors in the Mouse Embryo Are Susceptible to Leukemic Transformation.Frontiers in cell and developmental biology · 2021Article
- A Regulatory Loop Involving Notch and Wnt Signaling Maintains Leukemia Stem Cells in T-Cell Acute Lymphoblastic Leukemia.Frontiers in cell and developmental biology · 2021Article
- Review
- Review
- Combinatorial ETS1-dependent control of oncogenic NOTCH1 enhancers in T-cell leukemia.Blood cancer discovery · 2020Article
- The SWI/SNF complex in cancer - biology, biomarkers and therapy.Nature reviews. Clinical oncology · 2020Review
- MAML1-Dependent Notch-Responsive Genes Exhibit Differing Cofactor Requirements for Transcriptional Activation.Molecular and cellular biology · 2020Article
- The effect of co-occurring lesions on leukaemogenesis and drug response in T-ALL and ETP-ALL.British journal of cancer · 2020Review
72 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Notch receptors participate in a conserved signaling pathway that controls the development of diverse tissues and cell types, including lymphoid cells. Signaling is normally initiated through one or more ligand-mediated proteolytic cleavages that permit nuclear translocation of the intracellular portion of the Notch receptor (ICN), which then binds and activates transcription factors of the Su(H)/CBF1 family. Several mammalian Notch receptors are oncogenic when constitutively active, including Notch1, a gene initially identified based on its involvement in a (7;9) chromosomal translocation found in sporadic T-cell lymphoblastic leukemias and lymphomas (T-ALL). To investigate which portions of ICN1 contribute to transformation, we performed a structure-transformation analysis using a robust murine bone marrow reconstitution assay. Both the ankyrin repeat and C-terminal transactivation domains were required for T-cell leukemogenesis, whereas the N-terminal RAM domain and a C-terminal domain that includes a PEST sequence were nonessential. Induction of T-ALL correlated with the transactivation activity of each Notch1 polypeptide when fused to the DNA-binding domain of GAL4, with the exception of polypeptides deleted of the ankyrin repeats, which lacked transforming activity while retaining strong transactivation activity. Transforming polypeptides also demonstrated moderate to strong activation of the Su(H)/CBF1-sensitive HES-1 promoter, while polypeptides with weak or absent activity on this promoter failed to cause leukemia. These experiments define a minimal transforming region for Notch1 in T-cell progenitors and suggest that leukemogenic signaling involves recruitment of transcriptional coactivators to ICN1 nuclear complexes.
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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 Socratic graph.