Human Polyclonal Notch1 Ab
- Known as:
- Human Polyclonal Notch1 Antibody
- Catalog number:
- a0473
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal Notch1
Related genes to: Human Polyclonal Notch1 Ab
- 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: Human Polyclonal Notch1 Ab
Related articles to: Human Polyclonal Notch1 Ab
- Collision tumors, characterized by the coexistence of distinct histological tumor types in adjacent regions, are rare in neuro-oncology. While meningioma-glioma collisions are documented, sequential occurrence without a history of radiotherapy is exceptionally uncommon, posing diagnostic challenges and implying elusive pathogenic mechanisms. - Source: PubMed
Publication date: 2026/06/15
Wang FeiChang MeiYan MengQiu YoujiaWang MenghanYou WanchunZhang JuyiWang Zhong - Intervertebral disc degeneration (IVDD) is the major pathological cause of low back pain and global disability. Its chronic and persistent inflammatory microenvironment, resembling a flowing flood to erode the ecosystems relentlessly, disrupts the intervertebral disc homeostasis. In the present study, we first verified that Notch signaling is negatively correlated with inflammation in IVDD samples. Meanwhile, we identified a natural flavonoid hesperetin (Hes) as a potential agonist of Notch1 by molecular docking predicting. Herein, we developed an EV-inspired bioactive reservoir system, in which the natural extracts hes was encapsulated into liposomes (Hes@lipo) and embedded within a gelatin methacryloyl (GM) hydrogel (GM/Hes@lipo)to achieve sustained release. By mimicking the extracellular matrix (ECM)-like microenvironment of the intervertebral disc (IVD), GM/Hes@lipo provided physiological environment for nucleus pulposus cells (NPCs) adhesion and growth maintenance. Furthermore, by activating Notch signaling, GM/Hes@lipo effectively restored the dynamic balance between pro- and anti-inflammatory cytokines and maintained ECM metabolic homeostasis, attenuating NOD-like receptor signaling, thereby inhibiting NPC pyroptosis. Based on these aspects, GM/Hes@lipo relieved the IVDD process, maintained annulus fibrosus integrity, and effectively alleviated discogenic pain after the platform was administrated into the intervertebral disc of the rats. Collectively, as an anti-inflammatory "flood-control" system, the Notch signaling-targeted biomimetic hydrogel presents a biomimetic-natural compound combinatorial strategy offering promising therapy for mitigating IVDD progression. - Source: PubMed
Publication date: 2026/05/29
Zhang RuiZhang XiaoyuGuo JiangboYang YilinNiu JunjieShen HaoZheng YiWang JiaqiWang SuhaoNi LiYang HuilinShi Qin - Alzheimer's Disease (AD) is a prevalent neurodegenerative disorder which involves a complex pathobiology driven by amyloid-beta (Aβ) and tau pathologies, among other factors. Aβ peptides are generated β-secretase (BACE1) and γ-secretase cleavage of amyloid precursor protein (APP). While long isoforms like Aβ42 are neurotoxic and aggregation-prone, shorter isoforms (Aβ38, Aβ37) are non-amyloidogenic. γ-secretase modulators (GSMs) shift production from longer to shorter peptides which is expected to slow down or halt (prevent) amyloid accumulation and its downstream effects. - Source: PubMed
Publication date: 2026/05/28
Lindemann LotharLambotte JulieRothe JudithMesser JürgDiener CatherinePichereau SolenCantrill CarinaMueggler ThomasHoner MichaelBeck JenniferSteinbrecher ThomasTortelli RosannaGerlach IreneRatni HasaneRodriguez Sarmiento Rosa MariaBaumann Karlheinz - Pancreatic cancer cell metastasis is a major factor influencing prognosis. A Ras homologue member I (ARHI) was reported to regulate proliferation and apoptosis in pancreatic cancer; however, its role in invasion remains unclear. This study aimed to explore the role and related mechanisms of ARHI in pancreatic cancer metastasis. We revealed that in pancreatic cancer ARHI expression levels were consistent with aggressive cellular phenotypes, and that changes in endogenous ARHI protein expression led to corresponding alterations in epithelial-mesenchymal transition (EMT) markers. Furthermore, ARHI accelerated tumor invasion in pancreatic cancer cells and in a mouse hepatic metastasis model. Notably, this unusual promoting effect of ARHI on EMT and invasion in pancreatic cancer was primarily exerted through the Notch-1 signaling pathway. Collectively, our findings provide insight into the function and molecular mechanisms of ARHI in pancreatic cancer metastasis. - Source: PubMed
Publication date: 2026/06/14
Liu JingjingZhao YiqunWang YingShi YingZhi QiangChen LinlinKe YuhaoRen Jianlin - Lung adenocarcinoma (LUAD) is a major cause of cancer-related mortality worldwide. Understanding the mechanism of LUAD progression will aid in the development of therapeutic approaches targeting this malignancy. Hypoxia is characteristic of solid tumors and contributes significantly to LUAD progression, although the molecular mechanisms involved have not been fully elucidated. Long noncoding RNAs (lncRNAs) are key regulators of cancer progression. Here, we identify SLC9A3-AS1 as a previously unrecognized hypoxia-induced lncRNA that is aberrantly upregulated in LUAD tissues. Functional analyses demonstrated that SLC9A3-AS1 promotes LUAD cell proliferation, migration, and invasion in vitro, as well as tumor growth in vivo. Mechanistically, SLC9A3-AS1 acts as a competing endogenous RNA (ceRNA) by binding to miR-506-5p, alleviating the post-transcriptional repression of aspartate β-hydroxylase (ASPH) and activating NOTCH1 signaling. ASPH overexpression or miR-506-5p inhibition counteracts the effects of SLC9A3-AS1 knockdown, restoring LUAD cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) capacity. Furthermore, we report that SLC9A3-AS1 is a hypoxia-responsive gene that is transcriptionally activated by hypoxia-inducible factor-1α (HIF-1α) in LUAD cells. Collectively, these results identify SLC9A3-AS1 as a key hypoxia-induced regulator of LUAD progression and reveal a miR-506-5p/ASPH/NOTCH1 signaling pathway that drives oncogenic activity. These findings provide new insights for the diagnosis and treatment of LUAD. - Source: PubMed
Publication date: 2026/06/14
Yao WeipingZhang KaiyuanFei WenjingLi YilongCheng KeyuChu XiaoyuanHuang Guichun