NCSTN Antibody
- Known as:
- NCSTN Antibody
- Catalog number:
- 32159
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- NCSTN Antibody
Related genes to: NCSTN Antibody
- Gene:
- NCSTN NIH gene
- Name:
- nicastrin
- Previous symbol:
- -
- Synonyms:
- KIAA0253, APH2
- Chromosome:
- 1q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-08
- Date modifiied:
- 2019-04-23
Related products to: NCSTN Antibody
Related articles to: NCSTN Antibody
- This study aimed to explore the anti-neuroinflammatory mechanism of Ganoderma lucidum against Alzheimer's disease (AD) using network pharmacology and molecular docking, and verify its neuroprotective and anti-neuroinflammatory effects in Aβ1-42-induced AD mice. - Source: PubMed
Sheng FeiyaYu Jia-MeiYang QiaoJipei RiguXie Wen-QiZhan GuZhang YanZhang Le-Le - Hidradenitis suppurativa (HS) is a chronic, recurrent inflammatory disease originating from the folliculosebaceous unit (FPSU), characterized by abundant neutrophil infiltration in the skin. We aimed to address the lack of systemic evidence regarding lipid metabolic dysregulation within the FPSU in disease pathogenesis. By integrating the lipidomic features of lesional hair, skin tissue, and pus, we found prominent dysregulation of arachidonic acid (ARA) and leukotriene B4 (LTB4) across all specimens. Notably, the lipidomic features in lesional hair directly correlated with disease severity. Mechanistically, HS lesions exhibited activation of a bacterial-keratinocyte-neutrophil cascade, in which sustained exposure to lipopolysaccharide (LPS) derived from Gram-negative bacteria induced phosphorylation of cytosolic phospholipase Aα (cPLA2α) in keratinocytes. This response was further amplified by recruited neutrophils through 5-lipoxygenase (5-LO) activation, resulting in increased production of LTB4 and extensive neutrophil extracellular traps (NETs) formation. These findings were further validated in Ncstn mice, where lipid profiles in lesional hair mirrored those of HS patients. Our study provided evidence that lipid mediators in HS lesional hair served as sensitive markers for disease activity, suggesting that targeting Gram-negative colonization or the ARA-LTB4 pathway represented a promising therapeutic intervention for HS. - Source: PubMed
Publication date: 2026/09/12
Ye QianLi YiZhang ChongTang XinLai XiaodongZhu LiuluanHe YanyanYan YanWang Baoxi - Cutaneous squamous cell carcinoma (cSCC) is among the most common epithelial malignancies. Although cSCC arising in long-standing acne inversa (AI) lesions is rare, it is a severe and clinically important complication of AI. Approximately one-third of patients with AI harbour loss-of-function mutations in NCSTN. Whether NCSTN loss contributes to cSCC development remains unclear. To address this, we first examined its expression pattern in cSCC tissues. Interestingly, NCSTN expression was significantly decreased in cSCC tissues by immunohistochemistry (IHC) and Western blotting. Furthermore, loss of NCSTN promoted cSCC cell proliferation and migration in vitro and tumour growth in vivo. Proteomic analysis revealed that NCSTN deficiency promoted cell proliferation through activation of the MAPK/ERK signalling pathway, accompanied by reduced CLDN3 expression and alterations in cell-adhesion-related pathways. To validate the functional relevance of this signalling axis in vivo, we treated NCSTN-knockdown tumour-bearing mice with the ERK inhibitor SCH772984, which effectively suppressed tumour growth. Collectively, these findings demonstrate that loss of NCSTN drives cSCC progression through activation of MAPK/ERK signalling, and identify ERK signalling as a potential therapeutic vulnerability in NCSTN-deficient cSCC. - Source: PubMed
Xue ShumengShen YuanxingZhang ChongYe QianZhang YiXu HaoxiangHe Yanyan - Cigarette smoke is a major risk factor for chronic obstructive pulmonary disease (COPD), but its toxicity results from multiple harmful constituents. Nicotine is a chemically defined and biologically active tobacco-related compound, yet its COPD-related molecular features remain unclear. This study aimed to identify nicotine-related transcriptomic signatures in COPD and explore their immune and single-cell relevance. - Source: PubMed
Publication date: 2026/07/27
Zhang WeiSheng HongmeiShi YueyueJiang YuhangPeng Haiying - Chronic obstructive pulmonary disease (COPD) ranks as the third leading cause of death worldwide and is primarily caused by cigarette smoke (CS) exposure. A reduction in the number of ciliated cells significantly contributes to the development and progression of COPD. Nicastrin (NCSTN), a core subunit of γ-secretase, plays an important role in the pathogenesis of various tumors. However, to date, no studies have demonstrated its role in COPD. The aim of this study was to investigate the effect and underlying mechanism of NCSTN on the differentiation of airway epithelial basal cells into ciliated cells under cigarette smoke extract (CSE) exposure. Mouse tracheal epithelial basal cells were differentiated at the air-liquid interface (ALI) and exposed to CSE for 7 days. Lentiviral overexpression and knockdown of NCSTN in basal cells were performed. The effects on cell differentiation, NCSTN expression and the Notch signaling pathway in response to CSE were assessed using reverse transcription‑quantitative PCR (RT-qPCR) and western blotting (WB). We found that CSE exposure inhibited ciliated cell differentiation, while simultaneously increasing the expression of NCSTN, Notch3, and Hes1. Overexpression of NCSTN suppressed ciliated cell differentiation and induced Notch3 activation. Conversely, knockdown of NCSTN attenuated the CSE-mediated reduction in ciliated cell differentiation and inhibited Notch3 activation. Our findings indicate that CSE exposure inhibits basal cell differentiation into ciliated cells by upregulating the NCSTN-Notch3-Hes1 pathway. Inhibition of the NCSTN-Notch3-Hes1 pathway promoted ciliated cell differentiation and ameliorated the CSE-induced reduction in ciliated cells. - Source: PubMed
Publication date: 2026/05/09
Lan MaohuaWang CaimeiGu YanhuiHe ZhiquanLi ZhengluLan YiLiu NanHu JinyangYuan Guocheng