Affinage

DLL1

Delta-like protein 1 · UniProt O00548

Length
723 aa
Mass
78.1 kDa
Annotated
2026-04-28
100 papers in source corpus 34 papers cited in narrative 34 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DLL1 is a transmembrane Notch ligand that functions as a trans-activating signal in diverse developmental and adult tissue contexts, including somitogenesis, neural progenitor maintenance, intestinal stem cell fate, arterial identity, mammary gland morphogenesis, myogenesis, and pancreatic β-cell insulin secretion (PMID:7671806, PMID:12900443, PMID:21238454, PMID:19144989, PMID:29773667, PMID:34370738, PMID:32029480). Its signaling competence requires ubiquitination-dependent endocytic recycling to acquire high Notch-binding affinity, followed by transendocytosis of the Notch extracellular domain; surface presentation is further regulated by MAGI1 scaffolding at adherens junctions, SYNJ2BP-mediated stabilization, Arp2/3-dependent vesicular trafficking, phosphorylation of its intracellular domain, USP11 deubiquitination, estrogen-mediated protection from proteasomal degradation, and proteolytic shedding by MT1-MMP (PMID:18676613, PMID:15908431, PMID:24025447, PMID:28380416, PMID:24449764, PMID:39904982, PMID:30442981, PMID:21572390). DLL1 transcription is directly activated by WNT–LEF/TCF in synergy with TBX6 in presomitic mesoderm, by MyoD through E-box elements in myoblasts, and by NF-κB in inflammatory contexts, while the MNNL–DSL–EGF3 ectodomain region determines receptor selectivity, enabling DLL1 to activate NOTCH1 and NOTCH2 with comparable efficiency—unlike DLL4, which preferentially activates NOTCH1 and also acts as a potent cis-inhibitor (PMID:15545628, PMID:34370738, PMID:35750470, PMID:30289388, PMID:26114479). In the intestine, DLL1-expressing secretory progenitors mark the immediate progeny of Lgr5+ stem cells and can revert to stemness upon tissue damage, while in breast cancer, DLL1+ tumor-initiating cells activate Notch in stromal fibroblasts and macrophages to create Wnt-dependent feedback loops that drive chemoresistance and immune evasion (PMID:23000963, PMID:33462238, PMID:36007109, PMID:41191774).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1995 High

    Identification of DLL1 as the first mammalian Delta homologue established that the Notch ligand-receptor paradigm is conserved in vertebrates and provided the molecular entry point for studying Notch signaling in mammalian development.

    Evidence Molecular cloning, sequence analysis, and in situ hybridization in mouse embryos

    PMID:7671806

    Open questions at the time
    • No functional assay confirming signaling activity
    • Receptor binding affinity not measured
  2. 2003 High

    Genetic epistasis in somite patterning placed DLL1 upstream of MESP2 and dependent on PRESENILIN1, establishing the first in vivo pathway hierarchy for DLL1-Notch signaling in a specific developmental context and distinguishing its pathway from the DLL3-dependent branch.

    Evidence Systematic double-mutant analysis of Dll1, Dll3, Mesp2, and Psen1 knockout mice

    PMID:12900443

    Open questions at the time
    • Biochemical basis of DLL3 antagonism to DLL1 unknown
    • Whether DLL1 feeds back on its own transcription not resolved molecularly
  3. 2004 High

    Demonstration that WNT–LEF/TCF and TBX6 synergistically activate Dll1 transcription answered how DLL1 expression is initiated in the presomitic mesoderm, linking Wnt and Notch pathways in the segmentation clock.

    Evidence Transgenic reporter assays with mutated promoter elements in vivo, plus in vitro transactivation assays

    PMID:15545628 PMID:15986483

    Open questions at the time
    • Chromatin-level regulation (enhancer accessibility) not examined
    • Whether other T-box factors compensate in non-PSM tissues unclear
  4. 2005 High

    Discovery that MAGI1 recruits and stabilizes DLL1 at adherens junctions revealed a scaffolding mechanism governing ligand surface presentation, explaining how cell-cell contact geometry can regulate Notch signaling strength.

    Evidence Yeast two-hybrid, reciprocal co-immunoprecipitation, and co-localization at adherens junctions in neural tube and fibroblasts

    PMID:15908431

    Open questions at the time
    • Whether MAGI1 loss phenocopies DLL1 loss in vivo not tested
    • Stoichiometry and competitive binding with other PDZ ligands unknown
  5. 2008 High

    Ubiquitination-dependent recycling was shown to be essential for DLL1 to acquire Notch-binding competence, and a separate transendocytosis step was demonstrated as necessary for signal activation, resolving the longstanding question of why endocytosis is required in the signal-sending cell.

    Evidence Ubiquitination-defective DLL1 mutants, recycling and Notch1 binding assays, DLL1-DLL3 chimera transendocytosis assays, lipid microdomain fractionation

    PMID:18676613

    Open questions at the time
    • Identity of the E3 ligase responsible for this recycling-promoting ubiquitination not pinpointed in this study
    • Structural basis for how recycling confers binding competence unknown
  6. 2009 High

    Endothelial-specific DLL1 deletion revealed a non-redundant role in maintaining fetal arterial identity through VEGFR2/NRP1 regulation, distinguishing DLL1 from DLL4 in vascular Notch signaling.

    Evidence Conditional endothelial-specific Dll1 knockout mice with immunofluorescence and Nrp1 promoter-RBPJκ reporter assays

    PMID:19144989

    Open questions at the time
    • Whether DLL1 loss affects adult arterial maintenance not addressed
    • Direct vs. indirect mechanism of VEGFR2 regulation unclear
  7. 2011 High

    MT1-MMP was identified as a metalloprotease that cleaves DLL1 on stromal cells, providing a mechanism to negatively regulate Notch ligand availability; this explained how the bone marrow niche tunes Notch signaling for B-lymphopoiesis.

    Evidence Recombinant enzyme cleavage of synthetic DLL1 peptide, MT1-MMP knockout mouse phenotype rescued by Notch inhibitor DAPT

    PMID:21572390

    Open questions at the time
    • Cleavage site specificity and whether other MMPs contribute not fully resolved
    • Whether MT1-MMP regulates DLL1 outside the bone marrow niche untested
  8. 2011 High

    Combinatorial conditional knockout of Dll1 and Dll4 in the intestinal epithelium established these as the essential Notch ligands maintaining intestinal stem cells, while Elavl1/HuR was shown to post-transcriptionally stabilize Dll1 mRNA during neural progenitor mitosis — together revealing both tissue-level redundancy and cell-cycle-coupled mRNA regulation.

    Evidence Inducible gut-specific Dll1/Dll4/Jag1 single and compound knockouts; RNA immunoprecipitation and mRNA stability assays for Elavl1 plus Elavl1 heterozygous retinal analysis

    PMID:21238454 PMID:21346194

    Open questions at the time
    • Which cell type supplies DLL1 vs DLL4 signal to stem cells not resolved
    • Whether Elavl1 stabilization operates in non-neural tissues unknown
  9. 2012 High

    Lineage tracing showed that Dll1-high intestinal cells are secretory progenitors that can revert to stemness upon tissue damage, establishing DLL1 expression as a marker of facultative stem cell potential and demonstrating plasticity in the intestinal hierarchy.

    Evidence Dll1(GFP-ires-CreERT2) knock-in mice with lineage tracing and organoid formation after tissue damage

    PMID:23000963

    Open questions at the time
    • Molecular mechanism of de-differentiation not defined
    • Whether DLL1 is functionally required for reversion or is merely a marker unclear
  10. 2013 High

    Multiple studies converged to show that DLL1 serves as a niche signal from progeny to parent stem cells: in the adult SVZ, activated NSC progeny asymmetrically inherit DLL1 and maintain neighboring quiescent NSCs; in the neocortex, intermediate progenitors supply DLL1 to radial glia via dynamic processes; and SYNJ2BP was identified as a stabilizer of DLL1 protein that modulates endothelial Notch signaling.

    Evidence Conditional Dll1 KO in SVZ with live-cell imaging of asymmetric segregation; multiphoton live imaging with Notch reporters in cortical slices; Co-IP and protein stability assays for SYNJ2BP

    PMID:23695674 PMID:23699523 PMID:24025447

    Open questions at the time
    • Mechanism of asymmetric DLL1 segregation at the molecular level unknown
    • Whether SYNJ2BP competes with MAGI1 for DLL1 PDZ-binding motif untested
  11. 2013 High

    Ubiquitous overexpression of the DLL1 intracellular domain in mice produced no developmental phenotype, arguing against a physiologically relevant 'reverse signaling' function for the DLL1 cytoplasmic fragment.

    Evidence Multiple transgenic mouse lines expressing DLL1 intracellular domain ubiquitously, with nuclear fractionation and Notch target gene analysis

    PMID:24167636

    Open questions at the time
    • Cannot exclude context-specific reverse signaling below detection threshold
    • Does not rule out functions requiring ligand-receptor interaction to release ICD
  12. 2014 High

    Mass spectrometry identified sequential phosphorylation sites in the DLL1 intracellular domain that increase protein stability and Notch1 activation in vitro, though knock-in mice with phospho-deficient DLL1 developed normally, indicating phosphorylation is dispensable under standard conditions.

    Evidence Mass spectrometry, phospho-deficient mutagenesis, coculture Notch activation assays, knock-in mice

    PMID:24449764

    Open questions at the time
    • Whether phosphorylation becomes essential under stress or in specific tissues unknown
    • Kinase identity for the threonine site not identified
  13. 2015 High

    Direct comparison showed DLL1 functions as a pure trans-activator whereas DLL4 also acts as a potent cis-inhibitor; DLL4 knocked into the Dll1 locus cannot rescue somitogenesis, establishing that functional non-equivalence derives from cis-inhibition capacity rather than trans-activation potency.

    Evidence DLL4 knock-in at Dll1 locus mice, conditional overexpression from HPRT locus, quantitative Notch trans/cis assays in vitro

    PMID:26114479

    Open questions at the time
    • Structural basis for why DLL1 lacks cis-inhibition not determined
    • Whether intermediate cis-inhibition occurs at supraphysiological DLL1 levels unknown
  14. 2016 High

    Systematic EGF-repeat mutagenesis revealed that all eight EGF repeats contribute to DLL1 activity, and MIB1 E3 ligase was shown to couple Notch ligand-receptor engagement to DLL1 endocytosis through SNX18-dynamin2, linking the ubiquitination and endocytic machineries.

    Evidence Allelic series of disulfide-bridge mutations at Dll1 locus in mice with in vitro Notch activation assays; Co-IP and endocytosis assays for MIB1-SNX18-dynamin2

    PMID:26801181 PMID:26923255

    Open questions at the time
    • Which EGF repeats contact Notch directly vs. play structural roles unresolved
    • MIB1-SNX18-dynamin2 axis not validated in vivo
  15. 2018 High

    The MNNL–DSL–EGF3 ectodomain region was mapped as the determinant of DLL1 vs. DLL4 receptor selectivity, with DLL1 activating NOTCH1 and NOTCH2 equivalently while DLL4 preferentially activates NOTCH1; separately, mammary stem cell–expressed DLL1 was shown to activate Notch in stromal macrophages, triggering Wnt ligand production in a feedback loop essential for ductal morphogenesis.

    Evidence Chimeric ligand knock-in mice plus cell-based binding and activation assays for ectodomain mapping; conditional Dll1 KO in mammary gland with co-culture Wnt ligand measurements

    PMID:29773667 PMID:30289388

    Open questions at the time
    • Atomic-resolution structure of DLL1-NOTCH2 complex unavailable
    • How macrophage Wnt secretion feeds back specifically to DLL1+ stem cells mechanistically undefined
  16. 2018 High

    Estrogen signaling was found to stabilize DLL1 protein by blocking its ubiquitination and proteasomal/lysosomal degradation in ERα+ breast cancer, revealing a hormone-dependent post-translational regulatory axis for DLL1 and linking it to cancer stem cell maintenance.

    Evidence DLL1 conditional KO in breast cancer mouse models, ubiquitination assays, proteasome and lysosome inhibitor treatments

    PMID:30442981

    Open questions at the time
    • The E3 ligase targeted by estrogen signaling not identified
    • Whether this mechanism operates in normal mammary epithelium unclear
  17. 2020 High

    Oscillatory Dll1/Hes1 expression was shown to drive multipotent pancreatic progenitor expansion, and loss of DLL1/DLL4 in adult β-cells improved insulin secretion, establishing DLL1-Notch as a functional regulator of pancreatic endocrine physiology beyond development.

    Evidence Conditional Dll1/Jag1 knockouts with Hes1 oscillation live imaging in pancreatic progenitors; β-cell-specific Dll1/Dll4 double KO with glucose tolerance and insulin secretion assays

    PMID:32029480 PMID:32059775

    Open questions at the time
    • Whether DLL1 and DLL4 have distinct roles in β-cells not resolved
    • Downstream effectors of DLL1-Notch in β-cell insulin granule dynamics unknown
  18. 2021 High

    MyoD was shown to directly activate Dll1 through E-box elements, and DLL1 simultaneously trans-activates Notch in neighbors and cis-inhibits Notch in the DLL1-expressing myoblast itself, creating a feedback loop that coordinates the balance between differentiation and progenitor maintenance during myogenesis.

    Evidence CRISPR E-box disruption in human myoblasts, E-box-deficient mouse model, functional rescue experiments

    PMID:34370738

    Open questions at the time
    • Whether DLL1 cis-inhibition in myoblasts contradicts the general finding that DLL1 lacks cis-inhibition needs resolution
    • Quantitative contribution of DLL1 vs. DLL4 in adult muscle regeneration unclear
  19. 2022 Medium

    Several cancer-context studies established DLL1 as a node in tumor-stroma crosstalk: DLL1+ tumor cells activate Notch in CAFs to induce Wnt-driven radioresistance, NF-κB directly transactivates DLL1 in esophageal adenocarcinoma downstream of APE1, and HUWE1 suppresses the N-Myc–DLL1–NOTCH1 axis in glioblastoma.

    Evidence Conditional DLL1 KO with co-culture and radiation assays; ChIP of NF-κB on DLL1 promoter; HUWE1 ubiquitination assays and orthotopic xenografts

    PMID:35750470 PMID:35848447 PMID:36007109

    Open questions at the time
    • DLL1 transcriptional regulation in esophageal context from single study
    • Whether HUWE1 regulates DLL1 directly or only indirectly via N-Myc not clear
    • CAF Wnt-Notch loop not validated in human patient samples
  20. 2025 Medium

    USP11 was identified as a deubiquitinase that stabilizes DLL1 in marginal zone B cells, and DLL1+ tumor cells were shown to recruit immunosuppressive PD-L1+ macrophages via CCR3/CCL7, revealing new layers of DLL1 post-translational control and immune-modulatory function in the tumor microenvironment.

    Evidence Usp11 KO mice with ubiquitination assays and flow cytometry; conditional DLL1 KO mouse breast cancer models with combination anti-DLL1/anti-PD-L1 therapy

    PMID:39904982 PMID:41191774

    Open questions at the time
    • USP11-DLL1 interaction not validated by reciprocal IP or structural data
    • CCR3/CCL7 axis specificity to DLL1-expressing tumors vs. general Notch activation unclear
    • O-glycosylation of NOTCH1 affecting DLL1 binding (PMID:41129232) studied mainly from receptor side

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: (1) the atomic-resolution structural basis for DLL1-NOTCH2 vs. DLL1-NOTCH1 binding equivalence and DLL1's lack of cis-inhibitory capacity; (2) how ubiquitination-dependent recycling conformationally activates DLL1; (3) whether DLL1 reverse signaling has any context-dependent physiological role despite negative in vivo evidence; and (4) the therapeutic window for anti-DLL1 strategies in cancer given its essential roles in adult tissue homeostasis.
  • No high-resolution DLL1-Notch co-crystal structure available
  • Conformational change upon recycling not demonstrated
  • Reverse signaling tested only in standard developmental conditions

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 6 GO:0060089 molecular transducer activity 3
Localization
GO:0005886 plasma membrane 4 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-1266738 Developmental Biology 8 R-HSA-162582 Signal Transduction 8 R-HSA-1643685 Disease 6
Partners
ELAVL1MAGI1MIB1MT1-MMPNOTCH1NOTCH2SYNJ2BPUSP11

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 DLL1 (Delta-like 1) was identified as the first mammalian homologue of Drosophila Delta, encoding a transmembrane protein with EGF-like repeats in the extracellular domain that directly interacts with Notch receptors in a ligand-receptor manner, expressed in paraxial mesoderm and nervous system overlapping with Notch1 expression. Molecular cloning, sequence analysis, whole-mount in situ hybridization Development High 7671806
2004 WNT signaling, acting through LEF/TCF factors in synergy with the T-box transcription factor TBX6, directly activates transcription of Dll1 in the tailbud and presomitic mesoderm (PSM), controlling Notch activity and somite formation; mutation of either T or LEF/TCF binding sites in the Dll1 promoter abolishes reporter expression in transgenic embryos. Transgenic reporter assays in vivo, in vitro promoter transactivation assays with LEF/TCF and TBX6, mutational analysis of Dll1 promoter elements Genes & Development High 15545628
2005 TBX6 directly binds to two of four putative Tbx6 binding sites in the Dll1 paraxial mesoderm enhancer in vitro, and Dll1 expression is lost in Tbx6 mutants, establishing Dll1 as a direct transcriptional target of TBX6 in the presomitic mesoderm. Electrophoretic mobility shift assay (EMSA/in vitro DNA binding), in vivo genetic analysis of Tbx6 mutant embryos Genesis High 15986483
2005 MAGI1, a PDZ scaffolding molecule, directly binds DLL1 at cadherin-based adherens junctions in the developing neural tube, recruits DLL1 to these junctions, and stabilizes DLL1 on the cell surface, providing a mechanism for DLL1 presentation to activate Notch in neighboring cells. Co-immunoprecipitation, yeast two-hybrid, immunofluorescence localization in developing spinal cord and cultured AJ-forming fibroblasts Journal of Biological Chemistry High 15908431
2003 Positive and negative feedback loops comprising DLL1 and the transcription factor MESP2 are crucial for rostrocaudal patterning of somites; epistatic analysis revealed that PRESENILIN1 (Psen1) is required for DLL1-Notch signaling to activate DLL1 itself, while a Psen1-independent DLL3-Notch pathway may counteract the Psen1-dependent DLL1-Notch pathway. Genetic epistasis analysis using Dll1, Dll3, Mesp2, and Psen1 mutant and double-mutant mice Development High 12900443
2008 Ubiquitination of DLL1 is required for its recycling back to the cell surface after endocytosis and for acquiring high affinity for Notch1; an ubiquitination-defective DLL1 mutant is endocytosed but fails to recycle and cannot efficiently bind Notch1. A DLL1-DLL3 chimera can be recycled and bind Notch1 but cannot perform transendocytosis of the Notch1 extracellular domain, indicating transendocytosis is required for Notch signaling activation. DLL1 partially localizes to lipid microdomains required for its signaling activity. Ubiquitination-defective mutagenesis, endocytosis/recycling assays, Notch1 binding assays, transendocytosis assays, lipid microdomain fractionation PNAS High 18676613
2009 DLL1 is an essential Notch ligand in fetal arterial endothelial cells that activates Notch1 to maintain arterial identity; loss of DLL1 function leads to downregulation of VEGFR2 and its co-receptor NRP1, followed by upregulation of the venous fate repressor COUP-TFII, establishing DLL1 as distinct from DLL4 in the vasculature. Conditional knockout mice (endothelial-specific DLL1 deletion), immunofluorescence, in vitro Nrp1 promoter-RBPJκ reporter assays Blood High 19144989
2011 MT1-MMP (MMP14) expressed on bone marrow stromal cells directly cleaves DLL1 on the cell surface; recombinant MT1-MMP cleaves a synthetic DLL1 peptide at the same site as cell-surface cleavage. Loss of MT1-MMP in stromal cells increases Notch signaling in hematopoietic progenitor cells and specifically impairs B-lymphocyte development, which is rescued by the Notch inhibitor DAPT. Co-IP (MT1-MMP–DLL1 interaction), in vitro cleavage of synthetic DLL1 peptide by recombinant MT1-MMP, Notch inhibitor rescue experiments in vitro and in vivo with MT1-MMP knockout mice EMBO Journal High 21572390
2011 Inactivation of Dll1 alone in the intestinal epithelium causes a moderate increase in goblet cells; simultaneous inactivation of Dll1 and Dll4 causes complete conversion of proliferating progenitors to postmitotic goblet cells with loss of intestinal stem cells (Olfm4+, Lgr5+, Ascl2+), establishing DLL1 and DLL4 as the physiological Notch ligands required for intestinal stem cell maintenance. Inducible gut-specific conditional knockout (Vil-Cre-ERT2) of Dll1, Dll4, and Jag1 singly and in combination; lineage tracing with Notch1 reporter Gastroenterology High 21238454
2011 Elavl1/HuR ribonucleoprotein binds the 3' UTR of Dll1 mRNA and stabilizes it during mitosis in neuroepithelial cells; RNAi against Elavl1 reduces Dll1-3'UTR transcript stability in mitosis-arrested cells, and Elavl1 heterozygous null mice show decreased Dll1 expression and increased neurogenesis in the developing retina. RNAi knockdown, RNA immunoprecipitation (RIP), mRNA stability assay, in vivo analysis of Elavl1 heterozygous mouse retina Molecular Biology of the Cell High 21346194
2012 Dll1-expressing secretory progenitor cells (immediate daughters of Lgr5+ intestinal stem cells) generate all four secretory cell types through Notch lateral inhibition; upon tissue damage, Dll1-high cells reacquire stem cell properties (form organoids with Wnt3A exposure and undergo stem cell tracing events). Lineage tracing using Dll1(GFP-ires-CreERT2) knock-in mice, organoid culture, genetic marking before tissue damage Nature Cell Biology High 23000963
2013 DLL1 protein is induced in activated neural stem cells (NSCs) in the adult mouse subventricular zone and segregates asymmetrically to one daughter cell during mitosis; DLL1-expressing cells reside adjacent to quiescent NSCs and are required to maintain quiescent NSC identity, suggesting a feedback niche signal from progeny to parent NSC. Conditional knockout of Dll1 in the adult SVZ, live-cell imaging of DLL1 segregation during mitosis, proximity analysis of DLL1-expressing cells and quiescent NSCs Nature Communications High 23695674
2013 Intermediate neurogenic progenitors (INPs) serve as a source of DLL1 and interact with radial glia (RG) via dynamic elongate processes (some long-range, some filopodia-like) to transmit Notch signals in the embryonic neocortical niche; live multiphoton microscopy and Notch-pathway reporters confirmed these dynamic cell–cell contacts. High-resolution live-cell multiphoton microscopy with Notch reporter in organotypic brain slices, gene expression profiling of sorted RG and INP populations Journal of Neuroscience Medium 23699523
2013 SYNJ2BP (synaptojanin-2 binding protein) interacts with the PDZ-binding motif at the C-terminus of DLL1 (and DLL4 but not JAG1), enhances DLL1 protein stability, promotes Notch signaling (inducing HEY1, LFNG, ephrin-B2), and inhibits endothelial tip cell formation and sprouting angiogenesis. Co-immunoprecipitation, protein stability assays, Notch target gene qPCR, endothelial cell functional assays (migration, proliferation), in vivo vascular network formation in immunocompromised mice Circulation Research High 24025447
2014 Phosphorylation of DLL1 occurs sequentially at two serine residues (one likely by protein kinase B/AKT) and one threonine residue in the intracellular domain; phosphorylation requires membrane association, increases DLL1 stability, affects surface levels, and phosphorylation-deficient DLL1 activates Notch1 significantly less efficiently in vitro, though mice with the phosphorylation-deficient DLL1 develop normally. Mass spectrometry identification of phosphorylation sites, site-directed mutagenesis, Notch1 coculture activation assays, knock-in mice expressing phosphorylation-deficient DLL1 Molecular and Cellular Biology High 24449764
2015 DLL4, but not DLL1, efficiently acts as a cis-inhibitor of Notch signaling in cells co-expressing Notch receptor and ligand; both ligands have similar trans-activation potential but DLL4 causes reduced net Notch activation through cis-inhibition, explaining context-dependent functional divergence. In the presomitic mesoderm (PSM), DLL4 cannot replace DLL1 for somitogenesis despite equivalent expression from the Dll1 locus. Conditional overexpression from HPRT locus, DLL4 knock-in into Dll1 locus (Dll1Dll4ki mice), Notch transactivation and cis-inhibition assays in vitro, in vivo analysis of somitogenesis and retinal progenitor maintenance PLoS Genetics High 26114479
2016 The structural integrity of each individual EGF repeat in the extracellular domain of DLL1 is required for full DLL1 activity; disulfide-bridge-disrupting mutations in each EGF repeat impair both NOTCH1 and NOTCH2 activation similarly in vitro, and certain mutations (particularly in specific EGF repeats) affect somite patterning in vivo resembling spondylocostal dysostosis. Site-directed mutagenesis of each EGF repeat, Notch transactivation coculture assays in vitro, allelic series of point mutations knocked into endogenous Dll1 locus in mice Genetics High 26801181
2016 MIB1 (mind bomb 1 ubiquitin ligase) is required for efficient DLL1 endocytosis by promoting dynamin 2 recruitment via SNX18; MIB1 ubiquitin ligase activity is induced by Notch ligand–receptor interaction, and MIB1 promotes the SNX18–dynamin 2 interaction in an ubiquitin-ligase-activity-dependent manner. Co-immunoprecipitation, endocytosis assays, ubiquitin ligase activity assays Genes to Cells Medium 26923255
2017 Osteoblast-specific overexpression of DLL1 (but not JAG1) promotes proliferation of committed but immature osteoblasts while inhibiting their further maturation; this maturational arrest impairs osteoclast coupling and suppresses bone metabolic turnover, establishing DLL1-Notch signaling as critical for bone remodeling. Osteoblast-specific transgenic overexpression of DLL1 and JAG1 in mice, bone histomorphometry, osteoblast and osteoclast differentiation assays Journal of Cellular Physiology Medium 27735989
2017 Arp2/3 complex is required for vesicular transport of DLL1 from cytoplasm to the cell membrane in glioma-initiating cells; Arp2/3 inhibition prevents DLL1 from reaching the surface (and activating Notch1), impairing stem cell phenotype maintenance, which can be rescued by exogenous soluble DLL1 but not by endogenous DLL1. shRNA knockdown of DLL1 and Arp2/3 components, Arp2/3 pharmacological inhibition, rescue with soluble DLL1, intracranial xenograft model Oncotarget Medium 28380416
2018 Estrogen signaling stabilizes DLL1 protein by preventing its proteasomal and lysosomal degradation and inhibiting DLL1 ubiquitination, thereby maintaining DLL1-mediated Notch signaling specifically in ERα+ luminal breast cancer to promote tumor proliferation, angiogenesis, and cancer stem cell function. Conditional DLL1 knockout in breast cancer mouse models, ubiquitination assays, proteasome/lysosome inhibitor treatments, tumor growth and metastasis assays Oncogene High 30442981
2018 MaSC-expressed DLL1 activates Notch signaling in stromal macrophages, which increases macrophage expression of Wnt ligands (Wnt3, Wnt10A, Wnt16), creating a feedback loop that promotes the function of Dll1-expressing mammary stem cells; conditional deletion of Dll1 reduces MaSC number and impairs ductal morphogenesis. Conditional knockout of Dll1 in mammary gland stem cells, co-culture assays, measurement of Wnt ligand expression in macrophages Science High 29773667
2018 The ectodomains of DLL1 and DLL4 determine their differential receptor selectivity: DLL4 preferentially activates NOTCH1 over NOTCH2, whereas DLL1 is equally effective in activating NOTCH1 and NOTCH2; the region between the N-terminus and EGF repeat 3 (MNNL and DSL domains) confers this selectivity in cell-based assays, and chimeric ligand knock-in mice confirm ectodomain-driven function in vivo. Cellular co-culture Notch activation assays, biochemical binding studies, chimeric ligand knock-in mice, mutagenesis of NOTCH1-interface residues in DLL1 eLife High 30289388
2020 Oscillatory expression of DLL1 and HES1 in multipotent pancreatic progenitor cells (MPCs) drives MPC expansion, with changes in Hes1 oscillation parameters associated with bipotent progenitor versus pro-acinar cell fate; JAG1 restrains MPC growth but later drives bipotent progenitor specification in combination with DLL1. Conditional knockout of Dll1 and Jag1 (single and double mutants), live imaging of oscillatory reporters (Hes1), lineage analysis of pancreatic progenitor fates Developmental Cell High 32059775
2020 DLL1 and DLL4 are specifically expressed in adult pancreatic β-cells; mice lacking both DLL1 and DLL4 in adult β-cells show improved glucose tolerance and increased glucose-stimulated insulin secretion, while overexpression of the DLL1 intracellular domain in β-cells impairs glucose tolerance and insulin secretion, establishing a role for DLL1-Notch signaling in β-cell function. Conditional knockout of Dll1 and Dll4 in adult β-cells (Ins-Cre), overexpression of DLL1 intracellular domain in β-cells, glucose tolerance tests, insulin secretion assays in vitro and in vivo Diabetes High 32029480
2021 MyoD directly activates Dll1 transcription through E-box motifs in the Dll1 cis-regulatory region in myoblasts; Dll1-expressing cells activate Notch in neighboring myoblasts (trans-activation) to prevent premature differentiation, while autonomously inhibiting Notch in Dll1-expressing cells (cis-inhibition) to facilitate myogenic differentiation, creating a feedback loop. Gain/loss-of-function experiments in mouse and human myoblasts, CRISPR-mediated E-box disruption, novel E-box deficient mouse model, ChIP (implied by promoter analysis), in vivo myogenesis assays PLoS Genetics High 34370738
2021 Dll1+ breast tumor cells bearing NF-κB activation represent quiescent tumor-initiating cancer cells (TICs) that drive chemoresistance; RNA-seq and ATAC-seq show NF-κB activation is downstream of Dll1, and pharmacological blocking of Dll1 or NF-κB completely sensitizes Dll1+ tumors to chemotherapy. Conditional knockout mouse models, Dll1 reporter models, RNA-seq, ATAC-seq, pharmacological NF-κB and Dll1 blockade, in vivo tumor growth and metastasis assays Nature Communications High 33462238
2022 Dll1+ breast cancer cells activate Notch signaling in cancer-associated fibroblasts (CAFs), which increases CAF Wnt ligand secretion and leads to β-catenin-driven radioresistance and metastasis. Conditional Dll1 knockout, co-culture assays between tumor cells and CAFs, Notch signaling reporter assays, β-catenin pathway analysis, radiation resistance assays Cancer Research Medium 36007109
2022 HUWE1 E3 ubiquitin ligase ubiquitinates and degrades N-Myc, which in turn inactivates downstream DLL1-NOTCH1 signaling, thereby suppressing GBM proliferation, invasion and migration; HUWE1 acts as a tumor suppressor through the N-Myc–DLL1–NOTCH1 axis. Ubiquitination assays, KO/overexpression in GBM cell lines and orthotopic xenografts, dCas9 synergistic activation mediator (SAM) system for HUWE1 overexpression in vivo Cancer Communications Medium 35848447
2022 APE1 redox function activates NF-κB, which directly binds to and induces DLL1 expression in esophageal adenocarcinoma cells in response to acidic bile salts (reflux conditions); DLL1 is the predominant Notch ligand activating NOTCH1 in this context, and the APE1–NF-κB–DLL1–NOTCH1 axis promotes cancer stem-like properties. NF-κB chromatin immunoprecipitation on DLL1 promoter, APE1 redox inhibitor experiments, Notch intracellular domain nuclear accumulation assays, transgenic mouse model (L2-IL1β), cell line knockdown/overexpression Gut Medium 35750470
2013 Normal development in mice ubiquitously overexpressing the intracellular domain of DLL1 (DICD), with no alteration in Notch target gene expression or early Notch-dependent processes, argues against a physiologically relevant reverse signaling function of the DLL1 intracellular domain in vivo; mouse DICD also enters the nucleus inefficiently. Ubiquitous transgenic overexpression of DLL1 intracellular domain (multiple versions) in mice, nuclear fractionation, Notch target gene expression analysis PLoS ONE High 24167636
2025 USP11 deubiquitinase sustains survival of marginal zone B cells by regulating ubiquitination of the Notch ligands DLL1 and JAG2; loss of Usp11 leads to increased DLL1 ubiquitination and reduced MZ B cell survival after irradiation. Co-IP, ubiquitination assays in Usp11-/- mice, single-cell sequencing, flow cytometry, pharmacological Usp11 inhibition with mitoxantrone Cell Death & Disease Medium 39904982
2025 DLL1-expressing tumor cells recruit PD-L1+ immunosuppressive M2-like tumor-associated macrophages through the CCR3/CCL7 axis, which maintain cancer stem cell activity and drive tamoxifen/fulvestrant resistance in ER+ luminal breast cancer; combination of anti-DLL1 and anti-PD-L1 antibodies with tamoxifen reduced tumor growth and reprogrammed the immunosuppressive tumor microenvironment. Conditional DLL1 knockout mouse models, patient-derived explants, cytokine/chemokine axis analysis (CCR3/CCL7), combination antibody therapy, CSC functional assays Science Translational Medicine Medium 41191774
2025 Site-specific elongation of O-glucose glycan on NOTCH1 EGF10 (synthesized by B4GALT1 and ST3GAL4 to form a 3'-sialyllactose-like structure) significantly impacts DLL1- and DLL4-dependent NOTCH1 ligand binding and signal transduction; C4-2 amino acid position in the EGF domain is crucial for galactose elongation, affecting T cell differentiation through DLL1-NOTCH1 signaling. Mass spectrometry, site-directed mutagenesis, NOTCH1 activation assays with DLL1/DLL4 ligands, T cell differentiation assays in vivo PNAS Medium 41129232

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Dll1+ secretory progenitor cells revert to stem cells upon crypt damage. Nature cell biology 627 23000963
1995 Transient and restricted expression during mouse embryogenesis of Dll1, a murine gene closely related to Drosophila Delta. Development (Cambridge, England) 406 7671806
2009 DLL1-mediated Notch activation regulates endothelial identity in mouse fetal arteries. Blood 377 19144989
2011 Dll1- and dll4-mediated notch signaling are required for homeostasis of intestinal stem cells. Gastroenterology 350 21238454
2005 The Notch ligands DLL1 and JAG2 act synergistically to regulate hair cell development in the mammalian inner ear. Development (Cambridge, England) 228 16141228
2018 Notch ligand Dll1 mediates cross-talk between mammary stem cells and the macrophageal niche. Science (New York, N.Y.) 164 29773667
2004 WNT signaling, in synergy with T/TBX6, controls Notch signaling by regulating Dll1 expression in the presomitic mesoderm of mouse embryos. Genes & development 147 15545628
2010 Direct comparison of Dll1- and Dll4-mediated Notch activation levels shows differential lymphomyeloid lineage commitment outcomes. Journal of immunology (Baltimore, Md. : 1950) 129 20548034
2013 Dll1 maintains quiescence of adult neural stem cells and segregates asymmetrically during mitosis. Nature communications 114 23695674
2013 Dynamic interactions between intermediate neurogenic progenitors and radial glia in embryonic mouse neocortex: potential role in Dll1-Notch signaling. The Journal of neuroscience : the official journal of the Society for Neuroscience 82 23699523
2018 Estrogen-dependent DLL1-mediated Notch signaling promotes luminal breast cancer. Oncogene 78 30442981
2003 Feedback loops comprising Dll1, Dll3 and Mesp2, and differential involvement of Psen1 are essential for rostrocaudal patterning of somites. Development (Cambridge, England) 77 12900443
2008 The intracellular region of Notch ligands Dll1 and Dll3 regulates their trafficking and signaling activity. Proceedings of the National Academy of Sciences of the United States of America 71 18676613
2021 Dll1+ quiescent tumor stem cells drive chemoresistance in breast cancer through NF-κB survival pathway. Nature communications 60 33462238
2011 Resuscitating cancer immunosurveillance: selective stimulation of DLL1-Notch signaling in T cells rescues T-cell function and inhibits tumor growth. Cancer research 60 21825014
2005 MAGI1 recruits Dll1 to cadherin-based adherens junctions and stabilizes it on the cell surface. The Journal of biological chemistry 58 15908431
2019 Haploinsufficiency of the Notch Ligand DLL1 Causes Variable Neurodevelopmental Disorders. American journal of human genetics 56 31353024
2011 Ptf1a-mediated control of Dll1 reveals an alternative to the lateral inhibition mechanism. Development (Cambridge, England) 55 22096075
2020 Jag1 Modulates an Oscillatory Dll1-Notch-Hes1 Signaling Module to Coordinate Growth and Fate of Pancreatic Progenitors. Developmental cell 54 32059775
2009 Dll1 and Dll4 function sequentially in the retina and pV2 domain of the spinal cord to regulate neurogenesis and create cell diversity. Developmental biology 53 19389377
2014 Spatiotemporal oscillations of Notch1, Dll1 and NICD are coordinated across the mouse PSM. Development (Cambridge, England) 51 25468943
2005 Dll1 is a downstream target of Tbx6 in the paraxial mesoderm. Genesis (New York, N.Y. : 2000) 50 15986483
2021 DLL1 orchestrates CD8+ T cells to induce long-term vascular normalization and tumor regression. Proceedings of the National Academy of Sciences of the United States of America 47 34035167
2018 MiR-34a Enhances Chondrocyte Apoptosis, Senescence and Facilitates Development of Osteoarthritis by Targeting DLL1 and Regulating PI3K/AKT Pathway. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 47 30048987
2017 MiR-34a-5p promotes multi-chemoresistance of osteosarcoma through down-regulation of the DLL1 gene. Scientific reports 46 28281638
2012 Dll1/Notch activation contributes to bortezomib resistance by upregulating CYP1A1 in multiple myeloma. Biochemical and biophysical research communications 45 23111325
2011 MT1-MMP cleaves Dll1 to negatively regulate Notch signalling to maintain normal B-cell development. The EMBO journal 45 21572390
2015 Multivalent Forms of the Notch Ligand DLL-1 Enhance Antitumor T-cell Immunity in Lung Cancer and Improve Efficacy of EGFR-Targeted Therapy. Cancer research 44 26404003
2013 Synaptojanin-2 binding protein stabilizes the Notch ligands DLL1 and DLL4 and inhibits sprouting angiogenesis. Circulation research 39 24025447
2002 The Arabidopsis gain-of-function mutant dll1 spontaneously develops lesions mimicking cell death associated with disease. The Plant journal : for cell and molecular biology 35 11967093
2015 Context-Dependent Functional Divergence of the Notch Ligands DLL1 and DLL4 In Vivo. PLoS genetics 34 26114479
2022 Dll1-Mediated Notch Signaling Drives Tumor Cell Cross-talk with Cancer-Associated Fibroblasts to Promote Radioresistance in Breast Cancer. Cancer research 31 36007109
2017 Actin cytoskeleton regulator Arp2/3 complex is required for DLL1 activating Notch1 signaling to maintain the stem cell phenotype of glioma initiating cells. Oncotarget 31 28380416
2018 The ectodomains determine ligand function in vivo and selectivity of DLL1 and DLL4 toward NOTCH1 and NOTCH2 in vitro. eLife 30 30289388
2014 Distinct expression patterns of Notch ligands, Dll1 and Dll4, in normal and inflamed mice intestine. PeerJ 29 24860699
2012 Delta-like ligand (DLL)1 expression in early mouse decidua and its localization to uterine natural killer cells. PloS one 29 23284862
2022 Activation of NOTCH signaling via DLL1 is mediated by APE1-redox-dependent NF-κB activation in oesophageal adenocarcinoma. Gut 28 35750470
2018 CCN3 and DLL1 co-regulate osteogenic differentiation of mouse embryonic fibroblasts in a Hey1-dependent manner. Cell death & disease 27 30538222
2020 DLL1- and DLL4-Mediated Notch Signaling Is Essential for Adult Pancreatic Islet Homeostasis. Diabetes 26 32029480
2022 The E3 ubiquitin ligase HUWE1 acts through the N-Myc-DLL1-NOTCH1 signaling axis to suppress glioblastoma progression. Cancer communications (London, England) 25 35848447
2016 Effect of Jagged-1 and Dll-1 on osteogenic differentiation by stem cells from human exfoliated deciduous teeth. Archives of oral biology 25 26826998
2015 Increased Serum Levels of the Notch Ligand DLL1 are Associated with Diastolic Dysfunction, Reduced Exercise Capacity, and Adverse Outcome in Chronic Heart Failure. Journal of cardiac failure 25 26211721
2010 Two Notch ligands, Dll1 and Jag1, are differently restricted in their range of action to control neurogenesis in the mammalian spinal cord. PloS one 25 21124801
2015 Dengue virus up-regulates expression of notch ligands Dll1 and Dll4 through interferon-β signalling pathway. Immunology 24 25041739
2014 Divergent and conserved roles of Dll1 signaling in development of craniofacial and trunk muscle. Developmental biology 23 25220152
2021 Feedback regulation of Notch signaling and myogenesis connected by MyoD-Dll1 axis. PLoS genetics 21 34370738
2020 Overexpressing microRNA-34a overcomes ABCG2-mediated drug resistance to 5-FU in side population cells from colon cancer via suppressing DLL1. Journal of biochemistry 21 32044957
2017 DISC1 Regulates the Proliferation and Migration of Mouse Neural Stem/Progenitor Cells through Pax5, Sox2, Dll1 and Neurog2. Frontiers in cellular neuroscience 21 28900388
2013 Sustained vs. oscillating expressions of Ngn2, Dll1 and Hes1: a model of neural differentiation of embryonic telencephalon. Journal of theoretical biology 21 23499991
2011 Stabilization of Dll1 mRNA by Elavl1/HuR in neuroepithelial cells undergoing mitosis. Molecular biology of the cell 21 21346194
2011 Overexpression of Notch ligand Dll1 in B16 melanoma cells leads to reduced tumor growth due to attenuated vascularization. Cancer letters 21 21752535
2017 The Notch Ligands DLL1 and Periostin Are Associated with Symptom Severity and Diastolic Function in Dilated Cardiomyopathy. Journal of cardiovascular translational research 20 28474304
2005 Identification of Dll1 (Delta1) target genes during mouse embryogenesis using differential expression profiling. Gene expression patterns : GEP 20 15979417
2017 Maintenance of Bone Homeostasis by DLL1-Mediated Notch Signaling. Journal of cellular physiology 17 27735989
2009 Dll1 haploinsufficiency in adult mice leads to a complex phenotype affecting metabolic and immunological processes. PloS one 16 19562077
2019 MIR148A family regulates cardiomyocyte differentiation of human embryonic stem cells by inhibiting the DLL1-mediated NOTCH signaling pathway. Journal of molecular and cellular cardiology 15 31233755
2012 Genetic and functional evaluation of the role of DLL1 in susceptibility to visceral leishmaniasis in India. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases 14 22561395
2011 Cdx regulates Dll1 in multiple lineages. Developmental biology 14 22015720
2023 The phenotypic spectrum of terminal 6q deletions based on a large cohort derived from social media and literature: a prominent role for DLL1. Orphanet journal of rare diseases 13 36935482
2011 Genetic and functional evidence implicating DLL1 as the gene that influences susceptibility to visceral leishmaniasis at chromosome 6q27. The Journal of infectious diseases 13 21742847
2010 Combination of in silico and in situ hybridisation approaches to identify potential Dll1 associated miRNAs during mouse embryogenesis. Gene expression patterns : GEP 13 20558326
2016 Mib1 modulates dynamin 2 recruitment via Snx18 to promote Dll1 endocytosis for efficient Notch signaling. Genes to cells : devoted to molecular & cellular mechanisms 12 26923255
2016 Context-Dependent Sensitivity to Mutations Disrupting the Structural Integrity of Individual EGF Repeats in the Mouse Notch Ligand DLL1. Genetics 11 26801181
2016 Disruption of Notch signaling aggravates irradiation-induced bone marrow injury, which is ameliorated by a soluble Dll1 ligand through Csf2rb2 upregulation. Scientific reports 11 27188577
2013 Normal development in mice over-expressing the intracellular domain of DLL1 argues against reverse signaling by DLL1 in vivo. PloS one 10 24167636
2021 Terminal 6q deletions cause brain malformations, a phenotype mimicking heterozygous DLL1 pathogenic variants: A multicenter retrospective case series. Prenatal diagnosis 9 34894355
2009 Generation of transgenic mice expressing Cre recombinase under the control of the Dll1 mesoderm enhancer element. Genesis (New York, N.Y. : 2000) 9 19298012
2024 Cooperation of Wnt/β-catenin and Dll1-mediated Notch pathway in Lgr5-positive intestinal stem cells regulates the mucosal injury and repair in DSS-induced colitis mice model. Gastroenterology report 8 39444950
2021 Development of Dl1.72, a Novel Anti-DLL1 Antibody with Anti-Tumor Efficacy against Estrogen Receptor-Positive Breast Cancer. Cancers 8 34439228
2020 The potential mechanism of miR-130b on promotion of the invasion and metastasis of hepatocellular carcinoma by inhibiting Notch-Dll1. Journal of receptor and signal transduction research 8 32019397
2023 MicroRNA-143 acts as a tumor suppressor through Musashi-2/DLL1/Notch1 and Musashi-2/Snail1/MMPs axes in acute myeloid leukemia. Journal of translational medicine 7 37149661
2023 LINC00460 promotes neuroblastoma tumorigenesis and cisplatin resistance by targeting miR-149-5p/DLL1 axis and activating Notch pathway in vitro and in vivo. Drug delivery and translational research 7 38161194
2021 miR-130b suppresses the invasion and migration of prostate cancer via inhibiting DLL1 and regulating the PI3K/Akt pathways. Experimental and therapeutic medicine 7 34976140
2020 Association of DLL1 with type 1 diabetes in patients characterized by low polygenic risk score. Metabolism: clinical and experimental 7 33157082
2022 Dll1 Can Function as a Ligand of Notch1 and Notch2 in the Thymic Epithelium. Frontiers in immunology 6 35371023
2021 MALAT1: A Pivotal lncRNA in the Phenotypic Switch of Gastric Smooth Muscle Cells via the Targeting of the miR-449a/DLL1 Axis in Diabetic Gastroparesis. Frontiers in pharmacology 6 34385927
2014 S/T phosphorylation of DLL1 is required for full ligand activity in vitro but dispensable for DLL1 function in vivo during embryonic patterning and marginal zone B cell development. Molecular and cellular biology 6 24449764
2021 Tamoxifen Downregulates the Expression of Notch1 and DLL1 Genes in MKN-45 Gastric Cancer Cells. Journal of gastrointestinal cancer 5 32901446
2007 [Effect of mutation of chemotaxis signal transduction gene cheA in Pseudomonas putida DLL-1 on its chemotaxis and methyl parathion biodegradation]. Wei sheng wu xue bao = Acta microbiologica Sinica 5 17672308
2018 Dll1 Marks Cells of Origin of Ras-Induced Cancer in Mouse Squamous Epithelia. Translational oncology 4 30081298
2017 Glioma cell fate decisions mediated by Dll1-Jag1-Fringe in Notch1 signaling pathway. BMC systems biology 4 28950865
2013 [Up-regulation of DLL1 may promote the chemotherapeutic sensitivity in small cell lung cancer]. Zhongguo fei ai za zhi = Chinese journal of lung cancer 4 23769341
2024 Low-intensity pulsed ultrasound combined with ST36 modulate gastric smooth muscle contractile marker expression via RhoA/Rock and MALAT1/miR-449a/DLL1 signaling in diabetic rats. Neurogastroenterology and motility 3 38873849
2022 Dll1 haploinsufficiency causes brain abnormalities with functional relevance. Frontiers in neuroscience 3 36590296
2021 Computationally-obtained structural insights into the molecular interactions between Pidilizumab and binding partners DLL1 and PD-1. Journal of biomolecular structure & dynamics 3 33559526
2020 Localization of DLL1- and NICD-positive osteoblasts in cortical bone during postnatal growth in rats. Biochemical and biophysical research communications 3 32703409
2024 Novel small molecule DMAMCL induces differentiation in rhabdomyosarcoma by downregulating of DLL1. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2 38626518
2012 [Expression of JAG1 and DLL1 genes in colorectal cancer and its clinical significance]. Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery 2 22539391
2025 Usp11 maintained the survival of marginal zone B cells under ionizing radiation by deubiquitinating DLL1 and JAG2. Cell death & disease 1 39904982
2019 Loss of Pax6 Causes Regional Changes in Dll1 Expression in Developing Cerebral Cortex. Frontiers in cellular neuroscience 1 30894800
2018 A fusion protein composed of the DSL domain of Dll1 and RGD motif protects cryptic stem cells in irradiation injury. Bioscience reports 1 29444821
2026 Discovery of guaianolide-eudesmanolide dimers as antihepatoma agents by targeting NEURL1B to disrupt the DLL1/Notch signaling pathway. Bioorganic chemistry 0 41861701
2025 A Serum DLL1 and CRP dual-marker model for bacterial infection detection in patients with decompensated cirrhosis: A dual-cohort diagnostic study. Science progress 0 40629898
2025 Soluble DLL1 as an Indicator of acute kidney injury and postoperative delirium following cardiac surgery: a secondary analysis of a prospective study. Perioperative medicine (London, England) 0 40775336
2025 Differential O-glucose elongation on a specific EGF repeat within the canonical ligand-binding domain regulates DLL1/4-NOTCH1 signaling. Proceedings of the National Academy of Sciences of the United States of America 0 41129232
2025 DLL1-responsive PD-L1+ tumor-associated macrophages promote endocrine resistance in breast cancer. Science translational medicine 0 41191774
2024 DLL1/NOTCH1 signaling pathway maintain angiogenesis in meniscus development and degeneration. The international journal of biochemistry & cell biology 0 38772475
2024 GMNN and DLL1 mutation-related spondylocarpotarsal synostosis: a case report. Journal of Yeungnam medical science 0 39659197
2021 Activity of the mouse Notch ligand DLL1 is sensitive to C-terminal tagging in vivo. BMC research notes 0 34583743
2017 Differential expression of the Notch1 receptor, and its ligands Dll1, Dll3 and Dll4 in distinct human pituitary adenoma subtypes. Oncology letters 0 28599454