Notch1 Monoclonal Antibody (3E12)
- Known as:
- Notch1 Monoclonal Antibody (3E12)
- Catalog number:
- ASA905-897
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Notch1 Monoclonal Antibody (3E12)
Related genes to: Notch1 Monoclonal Antibody (3E12)
- Gene:
- NOTCH1 NIH gene
- Name:
- notch receptor 1
- Previous symbol:
- TAN1
- Synonyms:
- -
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-13
- Date modifiied:
- 2019-04-23
Related products to: Notch1 Monoclonal Antibody (3E12)
Related articles to: Notch1 Monoclonal Antibody (3E12)
- Vitamin phenol has anti-glioma potential but low bioavailability. Liposomal nanoparticles are effective drug delivery systems. Whether vitamin phenol-encapsulated liposomal nanoparticles can regulate ferroptosis in glioma cells remains unknown. - Source: PubMed
Gao ZhaoWang YuxinSu ShichaoLiu Jiayu - Sepsis remains a leading cause of death. Reverse migrated (RM) neutrophils, characterized as ICAM1hiCXCR1lo, have been recognized as a key driver of systemic inflammation and organ injury in sepsis. We have recently discovered a distinct DLL4+ subset of neutrophils that accumulate in the lungs, contributing to lung injury; however, the underlying mechanism is less understood. In sepsis, ICAM1hiCXCR1lo neutrophils, being hyperactive, were shown to be detrimental. Here, we investigated how DLL4+ neutrophils activate alveolar macrophages (AMs) to cause endothelial cell barrier disruption and promote neutrophil reverse migration. AMs were treated with DLL4+ neutrophils or recombinant mouse DLL4 (rmDLL4), and a disintegrin and metalloprotease (ADAM17) generated by AMs was assessed at both mRNA and protein levels. Conditioned medium was subsequently applied to pulmonary vascular endothelial cells (PVECs); junctional adhesion molecule-C (JAM-C) protein was detected by Western blot assays, and ICAM1hiCXCR1lo neutrophils were detected by flow cytometry. We demonstrate that during sepsis induced by cecal ligation and puncture (CLP), DLL4+ neutrophils interact with AMs via the Notch1 pathway, leading to increase of ADAM17 expression. ADAM17 decreased JAM-C on PVECs, causing endothelial barrier disruption and ICAM1hiCXCR1lo neutrophils generation. Small-molecule inhibitor of ADAM17 effectively preserved pulmonary endothelial barrier integrity, and reduced ICAM1hiCXCR1lo neutrophils accumulation. Importantly, we have developed a novel DLL4-Notch1 inhibitory peptide (NDI) that effectively suppresses ADAM17 expression, restores JAM-C, and reduces ICAM1hiCXCR1lo neutrophils accumulation in sepsis. These findings identify DLL4+ neutrophils as a critical inflammatory mediator that exacerbate systemic inflammation and worsen sepsis, highlight the DLL4-Notch1-ADAM17 axis as a promising therapeutic target. - Source: PubMed
Publication date: 2026/07/10
Jin HuiHolland SaoirseJha AlokAziz MonowarWang Ping - Fowler syndrome is an embryonic lethal disease with proliferative vasculopathy and hydranencephaly-hydrocephaly of the central nervous system caused by mutations in feline leukemia virus subgroup C receptor-related protein 2 (FLVCR2) characterized by large regions of hypovascularization along with glomeruloid formation of poorly organized vascular endothelial cell masses. The purpose of the current study is to elucidate the mechanisms by which FLVCR2 regulates retinal angiogenesis. - Source: PubMed
Goncalves AndreiaStanley AlexanderSantander NicolasMukherjee DibyantiLiu XuwenCleuren AudreyArnold ThomasAntonetti David - Aniridia is a rare congenital vision-loss disorder caused primarily by loss-of-function variants of the paired box 6 () gene. There is currently no cure. Augmentation gene therapy has emerged as a successful treatment for inherited ocular diseases. Here, we conducted the first pilot preclinical intrastromal augmentation gene therapy for aniridic cornea. It was undertaken in an aniridia mouse model, using adeno-associated virus 9 (AAV9), with a ubiquitous promoter driving PAX6, delivered by injection at 3 months, and harvest at 5 months post-injection (PI). The primary endpoint was histologically quantified epithelial thickness. The secondary endpoints were the slit lamp assessment of keratopathy and the RT-ddPCR measurement of four key signaling genes in the cornea. At 5 months PI, we demonstrated virally delivered PAX6 protein in the aniridic mouse corneal stroma. Critically, we found a statistically significant, albeit suggestive due to low values, structural improvement in the corneal epithelial thickness. When the data were pooled, we also demonstrated a significant and complete transcription correction of four key genes-, , , and . We explore a variety of hypothesizes to explain these initial results, including that the virally delivered PAX6 is acting non-cell autonomously, moving from the non-dividing stroma into the epithelium, causing structural and molecular improvement. - Source: PubMed
Publication date: 2026/06/17
Kaad Sif GLengyell Tess CMirjalili Mohanna Seyedeh ZeinabDjaksigulova DianaKorecki Andrea JSimpson Elizabeth M - This study aimed to investigate the biological effects of Picroside II on colorectal cancer (CRC) cells, including its impacts on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), and to explore whether its mechanism of action involves modulation of the Notch1 signaling pathway. Human CRC cell lines SW480 and SW620 were treated with various concentrations of Picroside II (10-100 μM). Cell proliferation was assessed using the CCK-8 assay, colony formation assay, and EdU incorporation assay. Migration and invasion capacities were evaluated by wound healing and Transwell assays. The expression levels of EMT-related markers (E-cadherin, N-cadherin, Vimentin, ZEB2) and key proteins in the Notch1 pathway (Notch1, Cleaved Notch1, RBP, HES1) were analyzed by Western blotting. Statistical analysis was performed using one-way ANOVA and Student's t-test. Picroside II inhibited the proliferation of SW480 and SW620 cells in a dose- and time-dependent manner, reduced colony formation ability, and decreased DNA synthesis activity. Treatment with Picroside II suppressed the migratory and invasive abilities of CRC cells, accompanied by upregulation of E-cadherin and downregulation of N-cadherin, Vimentin, and ZEB2. Furthermore, Picroside II exposure led to a decrease in the expression of Notch1, Cleaved Notch1, RBP, and HES1 proteins in a concentration-dependent manner. Picroside II suppresses CRC cell progression in vitro by inhibiting the Notch1 signaling pathway, providing a preliminary molecular basis for further in vivo investigation. - Source: PubMed
Wang RuiZhang WeiWang FangZhang YongLi Jiayi