Dll1
- Known as:
- Dll1
- Catalog number:
- 043951A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Dll1
Related genes to: Dll1
- 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
Related articles to: Dll1
- Central venous catheters are a major risk factor for vascular infections, which remain challenging to manage. Although antifungal therapy is standard, the host pathways shaping vascular responses-particularly the Notch signaling pathway (NSP)-are not well characterized in this context. In addition, the potential influence of the prostaglandin pathway on vascular NSP-related responses during infection remains unclear. In this study, a rat model of central venous catheter-associated infection was used to evaluate microbiological outcomes and vascular NSP-related protein expression. Immunohistochemical analyses were performed to assess immunostaining alongside the expression of Notch receptors (Notch1-3) and ligands (DLL1/4, Jagged1/2) in vascular tissues. Experimental groups included sham, infected control, antifungal-treated (fluconazole, caspofungin, liposomal amphotericin B), and prostaglandin pathway-intervention groups (sulprostone and sulprostone followed by indomethacin). infection was associated with higher vascular NSP-related protein expression compared with sham animals. Antifungal-treated groups showed lower NSP-related protein expression, while fungicidal agents were associated with absence of fungal growth in catheter and kidney cultures. In the sulprostone-indomethacin-treated group, NSP-related protein expression levels were lower than those in the sulprostone-treated group despite persistent fungal burden. In conclusion, central venous catheter-associated infection was associated with altered vascular NSP-related protein expression. Differences in NSP-related protein expression patterns were observed across antifungal- and prostaglandin pathway-intervention groups. These findings are descriptive and do not allow causal inference but may provide a basis for future studies exploring the role of NSP in vascular responses to infection. - Source: PubMed
Publication date: 2026/07/17
Berk Cam HandeKilinc LeylaAvci Hasan HuseyinSoylu HakanCakir TugrulSeyman DeryaKizilates FilizOztoprak NefiseUstunel Ismail - Protein tyrosine phosphatase non-receptor type 14 (PTPN14) exhibits dual roles in cancer, acting as either a tumor suppressor or oncogene depending on context, while its role in colon adenocarcinoma (COAD) and liver hepatocellular carcinoma (LIHC) remains unclear. Since COAD and LIHC showed high incidence and mortality rates, we investigated PTPN14's prognostic and mechanistic significance in COAD and LIHC. Pan-cancer analysis were performed based on TCGA and GEO database. Clinical validation used IHC staining of 50 COAD and 40 LIHC specimens. In vitro functional assays and in vivo xenograft models assessed PTPN14's impact on proliferation, migration, invasion and tumorigenicity. Mechanistic studies included Co-IP, immunofluorescence, ubiquitination assay and Western blot to evaluate PTPN14-Notch1 interaction and pathway regulation. As a result, pan-cancer analysis identified PTPN14 as prognostic biomarker in COAD and LIHC. Clinical validation confirmed PTPN14 as a prognostic biomarker in COAD and LIHC and associated with survival and TNM stage progression. In vitro experiments revealed knockdown of PTPN14 suppressed the proliferation, migration and invasion of COAD and LIHC cell lines. PTPN14 stabilized Notch1 by competitively binding to prevent FBXW7-mediated ubiquitination, and increasing the expression of Notch1 intracellular domain (Notch1 ICD) and downstream targets (DLL1 and HES1). At last, in vivo experiments revealed knockdown of PTPN14 inhibited xenograft tumor formation in COAD and LIHC cell lines. In conclusion, PTPN14 drives COAD and LIHC progression via Notch signaling stabilization, serving as a prognostic biomarker and potential therapeutic target for COAD and LIHC. - Source: PubMed
Publication date: 2026/07/25
Wang YuliumingLi JingtaoWang ChunlinZhang HaoSun ZiquanChang ZewenWang YangZhang ZhongxuDong JiaojiaoShan ShuoranWang GuiyuLiu Ming - Patrolling monocytes (pMos) scavenge debris from vessel walls and mediate antibody-dependent cellular phagocytosis, making them attractive cell therapy candidates for cancer, atherosclerosis, and Alzheimer's disease. However, methods to generate enhanced numbers of pMos are not available. To address this, we developed a two-step procedure to produce pMos in vitro from murine bone-marrow (BM). First, myeloid progenitors were expanded and enriched from BM using cytokines for four days. Second, expanded progenitors were differentiated into pMos on DLL1-expressing monolayers for eight days. We confirmed that in vitro grown pMos expressed the transcription factor Nr4a1 (Nur77) and other canonical pMos surface proteins, and depended on Notch signalling for their development. RNA sequencing revealed that in vitro pMos expressed hallmark pMos genes, including Cx3cr1, Itgax (CD11c), CD43, Fcγr4, and Cd274 (PD-L1), and their gene signatures clustered closely with in vivo blood and BM pMos. Transcriptomic and phenotypic analyses further demonstrated that in vitro pMos were distinct from classical BM macrophages. Phagocytosis assays demonstrated the function of in vitro pMos in cancer cell uptake. Adoptive transfer studies demonstrated that in vitro pMos persisted within the circulation and lung vasculature during the early post-transfer period compared with BM-derived macrophages, consistent with the vascular-patrolling properties of pMos. Adoptive transfer of pMos reduced lung tumour burden in a metastatic model, supporting an anti-tumoural role for pMos and their ability to mediate immune surveillance in vivo. These findings demonstrate that the DLL1 culture system allows for propagation of functional pMos, enabling studies of pMos biology and their therapeutic potential. - Source: PubMed
Publication date: 2026/07/22
Silva Jessica A F DNagra AshinaWadhwa AbishekMar SamanthaTjoa AmeliaFlibotte StephaneBarvalia MaunishMatos IsraelPriatel JohnKrebs DanielleHarder Kenneth W - During transit in the genital tract until ejaculation, spermatozoa (SPZ) protein content and spatial distribution are remodeled through the cargo channeled by extracellular vesicles, namely epididymosomes (EpS), and the soluble luminal content. This remodeling confers the maturational competence for fertilization. This study evaluated the expression patterns of Notch components (NOTCH1-4, DLL1, 3 and 4, JAGGED1-2) in the bull genital tract tissues and their respective lumen, and their presence in EVs and SPZ, by immunocytochemistry and western blot. Results evidenced that NOTCH proteins are differentially expressed from the testis to the epididymis, the vas deferens and the accessory glands. In the testis, expression is mainly linked to acrosome biogenesis, while in post-testicular tissues is mainly localized in the adluminal cytoplasm of epithelial cells and the lumen. NOTCH1-3, DLL3 and JAGGED2 are released into the lumen via EVs, namely EpS, and are detected in SPZ of the corresponding genital tract segments. The spatial relationships support a model of region-specific acquisition of NOTCH proteins by SPZ through both testicular and EpS origins, with additional contributions from accessory glands at ejaculation. This prompts the involvement of NOTCH proteins in intercellular communication within the male reproductive tract, leading to SPZ maturation and competence for signaling in the female reproductive tract and during gamete interaction. - Source: PubMed
Publication date: 2026/07/10
Diniz PatríciaLeites InêsAlexandre-Pires GraçaTorres Ana CatarinaMateus LuísaLopes-da-Costa LuísSilva Elisabete - Mesenteric ischemia frequently causes bowel necrosis even after recirculation, known as reperfusion injury, and no effective therapy has been validated for preserving the intestine. Adipose-derived mesenchymal stem cell-conditioned medium (MSC-CM), a tissue engineering and regenerative therapy, has been suggested as a feasible acute-phase treatment for organ damages. This study aimed to elucidate the therapeutic effects of MSC-CM on intestinal tissue injuries by ischemia and reperfusion. Mice were categorized into three groups that underwent either 60-min mesenteric artery occlusion (ischemia group), 60-min reperfusion following 60-min occlusion (reperfusion group), or ischemia-reperfusion with the same duration following intravenous administration of 200-µL MSC-CM by retroorbital injection (MSC-CM group). The distal ileum was harvested, and immunofluorescence staining with caspase-3 and LGR5, an intestinal stem cell-specific marker, was performed for evaluating the injury location and type of cells protected by MSC-CM. Moreover, LGR5, Notch1, Jagged 1, Hes1, DLL1, DLL3, and DLL4 mRNA expressions were measured using quantitative polymerase chain reaction. Ischemia extensively damaged the epithelial layer, and reperfusion-induced cellular apoptosis at the epithelial layer. MSC-CM administration was associated with preservation of cells at the crypt base, which were identified as intestinal stem cells using double-immunofluorescence staining. The MSC-CM group demonstrated significantly higher LGR5 expression than the reperfusion and ischemia groups. Similarly, the MSC-CM group exhibited higher Notch1 and Jag1 expressions, whereas the reperfusion group showed a higher Notch1 expression. In conclusion, MSC-CM use was associated with preservation of the intestinal stem cells at the crypt of villi and higher Notch1 and Jag1 expressions. - Source: PubMed
Publication date: 2026/07/04
Yamamoto RyoSuzuki SayuriHomma KoichiroMaeshima KatsuyaKomura YasuoSasaki Junichi