Ask about this productRelated genes to: NAP1L1 antibody
- Gene:
- NAP1L1 NIH gene
- Name:
- nucleosome assembly protein 1 like 1
- Previous symbol:
- -
- Synonyms:
- NRP, NAP1, NAP1L, MGC8688, MGC23410
- Chromosome:
- 12q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-03
- Date modifiied:
- 2016-03-10
Related products to: NAP1L1 antibody
Related articles to: NAP1L1 antibody
- Nucleosome assembly protein 1-like 1 (NAP1L1), a canonical member of the NAP1 family, orchestrates chromatin architecture and nucleosome dynamics to regulate cell cycle progression, development and proliferation. NAP1L1 is mainly expressed in actively growing cells, and its dysregulation is closely associated with the occurrence of a variety of diseases, including neurodevelopmental disorder, cardiovascular diseases and cancer. Recent studies revealed that NAP1L1 can influence disease progression through modulating multiple and classic signaling pathways such as cGAS-STING, PI3K/AKT and WNT pathways, highlighting its complex involvement in cellular signaling networks. In this review, we systematically summarized the discovery, structural features, and multifaceted biological functions of NAP1L1, with a particular focus on its pathogenic roles in cancer and cardiovascular diseases. We evaluated its potential as a druggable target by integrating computational biology approaches with structural and pharmacological evidence, identifying conserved ligandable pockets and predicting plausible interactions with known bioactive compounds. These findings position NAP1L1 as a potential druggable target with promising prospects at the intersection of chromatin plasticity and signal transduction, and provide comprehensive insights into the therapeutic potential of targeted NAP1L1, providing information and advancement for future clinical strategies. - Source: PubMed
Publication date: 2026/05/17
Wang HaoshuLiu HanyuDing JiahaoWang MengjiaYu TongShan Hongli - Osteosarcoma is a highly aggressive primary malignant bone tumor characterized by pronounced intratumoral heterogeneity and an immunosuppressive tumor microenvironment. Immunogenic cell death (ICD), a regulated form of cell death capable of activating antitumor immunity, has been implicated in cancer progression and treatment response. However, the cell type-specific distribution of ICD features and their clinical relevance in osteosarcoma remain poorly defined. - Source: PubMed
Publication date: 2026/03/23
Xu ZhaochenHan JiangboZhang MengChen FeiDeng HongliBian Weiguo - Evidence linking quaternary ammonium compounds (QACs) to cardiac function changes remains limited, particularly at the population level, and mechanistic insights are largely unexplored. To address this critical knowledge gap, we conducted a five-month longitudinal panel study that integrated epidemiological assessments with mechanistic multiomics analyses, involving 76 healthy elderly participants in Jinan, Shandong Province, China. Across five repeated measurement visits, participants underwent structured, face-to-face questionnaires, standardized physical examinations, and systematic biosample collection. Data on demographic characteristics, urinary QAC concentrations, and electrocardiogram (ECG) parameters were comprehensively gathered. Correlations between 9 QACs and 5 ECG parameters were assessed using a linear mixed-effects model (LMM), while interaction and stratified analyses examined body fat-related modulation of QAC-induced ECG disturbances. To elucidate the underlying biomolecular perturbations, multiomics analyses were further performed. Our results revealed that benzyltrimethylammonium bromide (BTMAC), dimethyldioctylammonium bromide (C8-DDAC), and diallyldimethylammonium chloride (DAD) were significantly associated with ECG alterations, suggesting potential cardiotoxicity in human populations. Specifically, both BTMAC and DAD were associated with prolonged QRS time, whereas C8-DDAC was related to increased QT interval, QTc interval, and RV5/SV1 amplitude, as well as a reduced QRS time. Interestingly, higher body fat content attenuated the adverse cardiac effects induced by QAC exposures, indicating a possible protective buffering mechanism. Moreover, the causal inference test (CIT) and ingenuity pathway analysis (IPA) collectively indicated that QAC-induced cardiac electrophysiological dysfunction may be associated with certain critical signaling pathways, particularly those involving tumor protein p53 (TP53), nucleosome assembly protein 1 like 1 (NAP1L1), dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A), and peroxisome proliferator activated receptor alpha (PPARα) signaling. Taken together, this study provides the first population-based evidence of QAC-associated cardiotoxicity and proposes the underlying biomolecular alternations. These insights offer a scientific foundation for developing targeted strategies to prevent and mitigate environmentally induced cardiovascular risks in susceptible populations. - Source: PubMed
Publication date: 2026/04/07
Guo XiaojieSitu YongjunDing EnminShi WanyingWang YuRen HuiminZhang JiranMa XiaoQian JiankunQi ChengleiWang XiaonaWang MengyaoHe YingyangLi ChenlongShao KaiyueXu YiboCha Yu'eCheng ZhipengMao ChenTong ShiluTang SongShi Xiaoming - Wnt and its crosstalk signaling pathways are involved in the modulating ischemia‒reperfusion (I/R) injury. However, whether Wnt2 is a novel therapeutic agent for I/R injury is largely unknown. Here, we show that the downregulation of serum Wnt2 levels in acute myocardial infarction (AMI) patients following reperfusion therapy, and Wnt2 levels are inversely correlated with the levels of myocardial injury markers (cTnT and CK-MB). Therapeutic administration of recombinant Wnt2 protein (rbWnt2) alleviates cardiac I/R injury and improves cardiac function by suppressing ROS levels and cardiomyocyte death in mice. Further analysis revealed that rbWnt2 downregulated Nap1L1 to reactivate the transcription of antioxidant genes (SOD, GPX, and UCP3) to reduce ROS levels and subsequently inhibit cardiomyocyte apoptosis and ferroptosis during the I/R process. Cardiac-specific Nap1L1 knockdown attenuated I/R injury, whereas overexpression of Nap1L1 partly abolished the cardiac protection mediated by rbWnt2 administration in the I/R model. Mechanistically, Wnt2 promoted Nap1L1 ubiquitination and degradation to restore ROS scavenging systems via Lrp6-mediated recruitment of the E3 ligase Trim11 in I/R hearts. Nap1L1 suppression plays a critical role in mediating the cardioprotective effects of rbWnt2. These findings establish Wnt2 as a therapeutic agent that targets compartmentalized oxidative damage, suggesting a novel strategy to mitigate I/R injury through the Lrp6/Trim11/Nap1L1 axis. - Source: PubMed
Publication date: 2025/12/16
Wang YingChen LimingLin JinyiLiu XiJin KejiaHuang ChenxingWang HaoJia JianguoWu JianDing ZhiwenGao PanGe JunboGong HuiZou Yunzeng - Cribriform adenocarcinoma of the salivary glands (CASG) is a rare tumor of minor salivary glands, predominantly of the oral cavity, characterized by distinct morphologic and immunophenotypic features. In this article, we describe a unique case of CASG arising in the sinonasal cavity of a 49-year-old female, with a novel fusion, expanding the molecular complexities of salivary gland neoplasms. This neoplasm showed typical morphology with nests of tumor cells with cribriform and papillary architecture and a classic immunohistochemical profile with tumor cells positive for S100 and p63 while negative for p40. Molecular studies showed a fusion, which has not been previously detected in cribriform adenocarcinoma. - Source: PubMed
Publication date: 2025/11/27
Duarte Ernesto MartinezGermani RossNicholson CharlesBaruch AmyShattuck Trisha