Ask about this productRelated genes to: DLL1 antibody
- Gene:
- DLL1 NIH gene
- Name:
- delta like canonical Notch ligand 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-11
- Date modifiied:
- 2019-01-03
Related products to: DLL1 antibody
Related articles to: DLL1 antibody
- The early identification of patients with sepsis among those presenting with suspected infection in the emergency department (ED) remains challenging. Delta-like canonical Notch ligand-1 (DLL-1), a Notch pathway ligand involved in immune and endothelial signaling, has been shown to reflect disease severity and outcomes in ICU-based sepsis cohorts. Its value for early risk stratification at ED presentation is less well defined. - Source: PubMed
Publication date: 2026/04/13
Hübner AureliaFriedrich KatharinaGaltung NoaTheobald VivienneSchenz JudithHecke BrittaKraß MelanieWeigand Markus AKappert KaiBauer Wolfgang - Temperature plays a crucial role in embryonic development, particularly in oviparous species that experience natural fluctuations during incubation. Unlike viviparous embryos developing under stable maternal conditions, chick embryos are exposed to external temperature variability that can influence cellular regulatory processes. Notch signaling, a conserved pathway essential for maintaining the neural progenitor cell (NPC) pool, is regulated by endosomal recycling; however, the mechanism by which temperature modulates this process across species remains poorly understood. To model environmental challenges experienced by chick embryos, we examined the effects of a physiologically relevant low temperature (30°C) on Dll1-mediated Notch signaling in chick and mouse NPCs. Under hypothermic conditions, Dll1 reporter signals increased in chick NPCs but decreased in mouse NPCs, correlating with corresponding changes in Notch activity. Chick NPCs maintained progenitor gene expression at low temperature, whereas mouse NPCs showed reduced expression. Mechanistic analyses revealed that distinct recycling pathways are differentially required for Notch signaling across temperatures and species. Chick NPCs maintained Notch signaling through both fast and slow recycling under normothermia and additional degradation under hypothermia, whereas mouse NPCs relied on slow recycling and degradation under normothermia and showed impaired recycling under hypothermia. Together, these findings reveal species-specific adaptations in the temperature-dependent endocytic regulation of Notch signaling, highlighting how environmental temperature influences the maintenance of neural progenitors across species. - Source: PubMed
Publication date: 2026/04/07
Lin Kai-WeiWu Pei-RongChen Cheng-ChangHalim AlexanderLiao Bo-KaiHou Pei-Shan - Critical limb ischemia (CLI) is a severe vascular disease with limited pharmacologic treatments and a high risk of amputation. Conventional therapeutic angiogenesis, mainly based on single growth factors, has failed to achieve stable and functional vessel formation. Recent insights indicate that interactions between endothelial cells and immune cells, particularly perivascular macrophages, are critical for durable vascular remodeling. Here, we engineered a pH-responsive intein-based platform to load extracellular vesicles (EVs) with a stabilized, constitutively active form of hypoxia-inducible factor-1α (HIF-1α). In this study, we demonstrate that EV-mediated HIF-1α delivery markedly improves perfusion and reduces necrosis in a murine hindlimb ischemia model. HIF-1α-EVs activated a regenerative vascular program that coupled new vessel growth with structural maturation, resulting in enlarged collateral arteries and an expansion of type H and CD34 endothelial populations. Notably, HIF-1α-EV treatment also increased CD163 perivascular macrophages, which are known to support arteriogenesis by vessel stabilization. Mechanistically, EV-mediated delivery of HIF-1α upregulated endothelial Delta-like ligand 1 (Dll1), which directed macrophage differentiation toward a CD163 reparative phenotype, thereby reinforcing vascular maturation and restoring blood flow. Collectively, this transcription factor delivery strategy offers a promising therapeutic avenue for durable revascularization in CLI and potentially other ischemic diseases. - Source: PubMed
Publication date: 2026/03/24
Cho SeongeonLee YejiHwang Yeong HaGoo JiyoungHan JihoonWoo JiwanNam Gi-HoonJeong CherlhyunKim IljinKim In-San - Control of cell identity and number is central to tissue function, yet principles governing the organization of malignant cells remain poorly understood. Using genetically engineered mouse models and orthotopic allografts with dual WNT reporter systems, we discover that pancreatic ductal adenocarcinoma (PDAC) organizes in a stereotypical pattern, whereby PDAC cells responding to WNT signals (WNT-R) neighbor WNT-secreting cancer cells (WNT-S). Lineage tracing reveals that the WNT-R state is transient and gives rise to a stable WNT-S state. A subset of WNT-S cells expressing DLL1 forms a functional niche for WNT-R cells. The genetic inactivation of WNT secretion or Notch pathway components, or the cytoablation of WNT-S cells, disrupts PDAC tissue organization, suppressing tumor growth and metastasis. Analysis of human PDAC tissues confirms conservation of these populations. PDAC growth depends on an intricately controlled equilibrium of functionally distinct cancer cell states, revealing the fundamental principles governing solid tumor organization and therapeutic opportunities. - Source: PubMed
Publication date: 2026/03/23
Torborg Stefan RKim Jung YunSinghal AnupriyaGrbovic-Huezo OliveraHolm MatildaWu KatherineHan XuexiangHo Yu-JuiHaglund CajMitchell Michael JLowe Scott WDow Lukas EPitter Kenneth LSanchez-Rivera Francisco JLevchenko AndreTammela Tuomas - Given the high incidence of hepatocellular carcinoma (HCC) and its limited therapeutic options, and building on our previous work on anti-HCC sesquiterpenoid dimers, a series of natural product-like guaianolide-eudesmanolide dimers were designed and synthesized as potential anti-HCC agents in this study. Among them, compound 1 showed significantly antihepatoma effects on HepG2, Huh-7, and SK-Hep-1 cells with IC values of 5.6, 4.8, and 4.6 μM, respectively; induced cell cycle arrest and apoptosis; and inhibited the migration of HCC cells. Bioinformatic analysis and experimental validation indicated that compound 1 directly targeted NEURL1B, which was further established as a critical regulator of HCC proliferation and migration. Mechanistically, compound 1 bound to Arg422 within the NHR2 domain of NEURL1B, triggering its autoubiquitination and degradation, which stabilized DLL1 by suppressing its ubiquitination and ultimately attenuated the Notch signaling pathway. In vivo experiments showed that compound 1 (60 mg/kg) inhibited tumor weight up to 69% in SK-Hep-1 xenograft nude mice, which was comparable to that of sorafenib (67%) at the same dose. This study revealed that the previously unrecognized oncogenic role of NEURL1B acted as upstream of DLL1 in HCC, and suggested that compound 1 might be an antihepatoma candidate that inhibited Notch signaling by disrupting the NEURL1B-DLL1 interaction. - Source: PubMed
Publication date: 2026/03/12
Ma Wen-JingLi Qi-HaoHu JingWang Yong-CuiMa Yun-BaoChen Ji-JunLi Tian-Ze