ArticleeLife2020
Delta-like 1 and Delta-like 4 differently require their extracellular domains for triggering Notch signaling in mice.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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
10 citing papers in PubMed, 17 citations in OpenAlex.
- The Blockade of Delta-Like Ligand 1 Inhibits Atherosclerotic Lesion Formation and Attenuates Plaque Vulnerability.Journal of atherosclerosis and thrombosis · 2026Article
- Advancing adoptive cellular immunotherapy via Notch-based ex vivo T cell development platforms.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Review
- Review
- Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies.Cancer discovery · 2023Article
- Progress on methods of T lymphocyte developmentZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Review
- Dll1 Can Function as a Ligand of Notch1 and Notch2 in the Thymic Epithelium.Frontiers in immunology · 2022Article
- Thymus Functionality Needs More Than a Few TECs.Frontiers in immunology · 2022Review
- LMO2 is essential to maintain the ability of progenitors to differentiate into T-cell lineage in mice.eLife · 2021Article
- Current Views on the Roles ofBiomolecules · 2021Review
- Targeting Liver Cancer Stem Cells: An Alternative Therapeutic Approach for Liver Cancer.Cancers · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Delta-like (Dll) 1 and Dll4 differently function as Notch ligands in a context-dependent manner. As these ligands share structural properties, the molecular basis for their functional difference is poorly understood. Here, we investigated the superiority of Dll4 over Dll1 with respect to induction of T cell development using a domain-swapping approach in mice. The DOS motif, shared by Notch ligands-except Dll4-contributes to enhancing the activity of Dll for signal transduction. The module at the N-terminus of Notch ligand (MNNL) of Dll4 is inherently advantageous over Dll1. Molecular dynamic simulation revealed that the loop structure in MNNL domain of Dll1 contains unique proline residues with limited range of motion. The Dll4 mutant with Dll1-derived proline residues showed reduced activity. These results suggest that the loop structure-present within the MNNL domain-with a wide range of motion ensures the superiority of Dll4 and uniquely contributes to the triggering of Notch signaling.
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.