Active NEK7
- Known as:
- Active NEK7
- Catalog number:
- ASAPPK-436Z
- Product Quantity:
- 5 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Active NEK7
Related genes to: Active NEK7
- Gene:
- NEK7 NIH gene
- Name:
- NIMA related kinase 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-19
- Date modifiied:
- 2016-01-13
Related products to: Active NEK7
Related articles to: Active NEK7
- To investigate the protective effect of M2 macrophage-derived exosomes (M2-Exo) on high glucose-induced podocyte injury and the underlying molecular mechanism. - Source: PubMed
Publication date: 2026/07/21
Zhang YanZhan QingZhao MinyangLiu HuiyunHuang Haihua - Ginkgo biloba L. has been widely utilized in traditional Chinese medicine for its potential to enhance memory-related functions. In traditional medical practices, it is also commonly prescribed for conditions associated with cognitive decline and age-related disorders. These ethnopharmacological uses are closely linked to neurodegenerative disorders, in which neuroinflammation plays a central role. Ginkgo biloba has shown anti-inflammatory and neuroprotective properties, yet its underlying mechanisms in modulating neuroinflammation are still not fully understood. - Source: PubMed
Publication date: 2026/07/18
Hu KaifanGao WaimaoPan JieXu XiaoYou PingpingLi KunYang GuangWang DandanJiang MeifangWang XingyuZhao YanXu Ying - Urinary tract infections (UTIs) are among the most common bacterial infections, yet the genetic factors influencing susceptibility remain poorly understood. We performed a genome-wide association study of recurrent UTI involving 1,860,836 individuals (213,869 cases and 1,646,967 controls). We identified 36 independent non-HLA genome-wide significant loci encoding kidney epithelial and immune response genes and demonstrated that some loci have sex-specific effects. Integrative functional annotation, expression and protein quantitative trait locus colocalization, and single-cell multi-omic analyses revealed that UTI risk alleles preferentially modulated gene expression in kidney, ureter, and bladder epithelia. Multi-omic prioritization converged on a number of pathogenic pathways: epithelial barrier and mucosal glycocalyx defense ( , , , ), innate immune regulation ( , , ), infection resolution and regulated cell death ( , , ), epithelial identity maintenance ( , , ), urinary tract development ( , , , , ), and nutritional immunity through iron sequestration ( ). Approximately one-third of loci colocalized with gene expression in kidney tubules, suggesting direct modulation of epithelial host-defense programs. Among all loci, , which encodes a GPI-anchored epithelial surface protein expressed in the kidney papilla and urinary tract epithelia, emerged as the strongest candidate causal gene. We demonstrated that PSCA was secreted into urine, bound uropathogenic , and inhibited bacterial growth , implicating it as a constitutive epithelial defense factor. We also demonstrated that while was protective against urinary infections and duodenal ulcers, it was associated with increased risk of bladder, prostate, and gastric cancers, suggesting antagonistic pleiotropy between mucosal defenses and oncogenesis. Together, our findings define the polygenic architecture of UTI susceptibility, highlighting epithelial surface defense, innate immune regulation, developmental patterning, and nutritional immunity as central components of host defense, providing a new framework for host-directed, non-antibiotic interventions. - Source: PubMed
Publication date: 2026/07/10
Xu KatherineKhan AtlasShang NingZeng WenjieWang ChenBerrouet CeciliaShen Tian HuaiNarayanan PadmaDeng JennyDiPerna ChiaraWilliams CharlotteCuacuas SarahOlsen Timothy RArace JeffreyGhotra AryanMonical WayneBorisov OlegHaug StefanLiu HongboHa EunjiBanlengchit RunLevitman AbrahamPatel DiyaChou ClaireHalibart BartlomiejGuo Tai WeiSimmons ShawnGoswami SanyaNesanir KivancFujita MasashiKullo Iftikhar JJarvik Gail PWei Wei-QiFeng QiPingJiang LanStein C MichaelWeng ChunhuaHripscak GeorgeGharavi Ali GSusztak KatalinDe Jager Philip LKöttgen AnnaBarasch JonathanSims Peter AKiryluk Krzysztof - Dysregulated activation of the NLRP3 inflammasome is a key driver in the pathogenesis of numerous inflammatory disorders. This study aimed to evaluate the protective effect of polysaccharide (PGPS) against NLRP3-inflammasome-mediated inflammation and elucidate its underlying mechanisms. An in vitro inflammatory model was established in porcine alveolar macrophages (3D4/21) using LPS/ATP co-stimulation. The effects of PGPS were assessed by measuring inflammasome activation, intracellular reactive oxygen species (ROS) generation, and pro-inflammatory cytokine secretion. Molecular docking, alongside inhibitors (NAC, MCC950) and siRNA targeting NEK7, was employed to probe the involved mechanisms. PGPS significantly suppressed NLRP3 inflammasome assembly and activation, reduced caspase-1 cleavage, and decreased the maturation and release of IL-1β and IL-18. It exerted its inhibitory effects through dual mechanisms: scavenging intracellular ROS and directly binding to NEK7 and NLRP3 to disrupt their interaction, as supported by molecular docking. The anti-inflammatory effect was diminished upon NEK7 knockdown. In conclusion, PGPS is an effective natural inhibitor of the NLRP3 inflammasome, functioning through ROS clearance and direct interference with the NLRP3-NEK7 interaction. These findings propose PGPS as a promising therapeutic candidate and further validate NEK7 as a potential target for treating NLRP3-driven inflammatory diseases. - Source: PubMed
Publication date: 2026/06/29
Lv MeiyunYu YueLi LinjueLiu YangLi ZhaolongZhang XiaoranDai XinyiZheng PimiaoLiu JianzhuZhao Xiaona - Cardiac remodeling (CR) is a critical risk factor for the development and progression of cardiovascular diseases. CR is accompanied by activation of the innate immune response, with NLRP3 inflammasome emerging as a key player in morphological and functional changes. However, the mechanisms underlying NLRP3 inflammasome assembly and activation in the heart upon beta-adrenergic overactivation remain poorly understood. This study aims to investigate the temporal profile of NLRP3 inflammasome activation and its upstream signaling P2X7-NEK7 in isoproterenol (ISO)-induced CR. - Source: PubMed
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