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
- 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 - We searched for oncogenes activated by copy number increases using whole-genome sequencing data of 535 pancreatic ductal adenocarcinomas (PDACs). We found that gains of 1q were the second most common gain, occurring in 213 (39.8%) of PDACs. Single-cell analysis via fluorescence in situ hybridization on 33 cancers confirmed these results. A portion of 1q, rather than the entire 1q arm, was gained in 75 (14.0%) PDACs, allowing us to pinpoint two ~3-megabase regions of 1q that were nearly always gained. These two regions contained and , genes that code two subunits of the γ-secretase complex. Evaluation of 267 precancerous lesions revealed that extra copies of and were common (49%) in noninvasive neoplasms (high-grade pancreatic intraepithelial neoplasms), which are at relatively high risk for progression to PDACs, but uncommon (6%) in low-grade pancreatic intraepithelial neoplasia lesions, which have low malignant potential. We hypothesize that γ-secretase genes are genetically activated oncogenes in the early phases of pancreatic neoplasia. - Source: PubMed
Publication date: 2026/02/20
Douville ChristopherParksong JeeunDal Molin MarcoGraham SarahGreipp Patricia TKnudson RyanCurtis SamuelWang YuxuanDobbyn LisaPopoli MariaPtak JanineSilliman NatalieRomans KatharineIacobuzio-Donahue Christine AMakoohon-Moore Alvin PLennon Anne MarieGoggins MichaelHruban Ralph HKiemen AshleyBettegowda ChetanKinzler Kenneth WPapadopoulos NickolasWood Laura DVogelstein Bert - Mutations in the NCSTN gene are believed to be involved in the pathogenesis of acne inversa (AI). Further, certain cytokines are overexpressed in the inflammatory milieu of AI skin. Considering its central role in cytokine regulation, the JAK/STAT signaling pathway should be examined as a pathogenic factor and potential therapeutic target in AI. - Source: PubMed
Shi Zhe-YeJin Xiao-JieSun Shu-YuanDu Shi-YouWang Guo-FangWu-Zhou Chen Yan-HuiLi Jian-GuoZhang Si-SenShi Tian-Wei - - Source: PubMed
Meena AkshaySusan Saka SowmyaGanesh Rajesh NachiappaKumar Sheetanshu