DLL1 Blocking Peptide, Blocking Peptides
- Known as:
- DLL1 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-3580
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- DLL1 Blocking Peptide Peptides
Related genes to: DLL1 Blocking Peptide, Blocking Peptides
- 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 Blocking Peptide, Blocking Peptides
Related articles to: DLL1 Blocking Peptide, Blocking Peptides
- This Mendelian randomization study aimed to systematically investigate the causal associations of 2,821 plasma protein ratios with UC susceptibility and validate potential biomarkers through multi-omics approaches. - Source: PubMed
Publication date: 2026/08/10
Kang KuoWei LinfengLi XuanxuanWang ShalongHuang ChanghaoWu Zhiwei - Osteoporosis (OP) is a common skeletal disease mainly caused by the imbalance between bone formation and bone resorption. Dysfunction and senescence of bone marrow mesenchymal stem cells (BMSCs) are critical pathogenic factors for OP, resulting in impaired osteogenic differentiation, increased adipogenic shift, and enhanced susceptibility to inflammation and oxidative stress. Therefore, the purpose of this review is to systematically synthesize current evidence on how Icariin (ICA)-a major bioactive flavonoid from Epimedium-exhibits therapeutic potential against OP by targeting BMSC senescence and regulating multiple underlying signaling networks. - Source: PubMed
Publication date: 2026/07/28
Wang ChengjieWu ZhenyuXu YaweiLi YuyiMan ZhenweiLiu KangWang JianLin WenlinQie FengqingShi XiaolinYuan Yifeng - 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 pMos for cell therapy are not available. To address this, we developed a 2-step procedure to produce pMos in vitro from murine bone marrow (BM). First, myeloid progenitors were expanded and enriched from BM using cytokines for 4 d. Second, expanded progenitors were differentiated into pMos on delta-like ligand 1 (DLL1)-expressing monolayers for 8 d. We confirmed that in vitro grown pMos expressed the transcription factor Nr4a1 (Nur77) and other canonical pMos surface proteins, and depended on Notch signaling 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 tumor burden in a metastatic model, supporting an anti-tumoral 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
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