NEK7 antibody
- Known as:
- NEK7 (anti-)
- Catalog number:
- orb101596
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- NEK7 antibody
Related genes to: NEK7 antibody
- 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: NEK7 antibody
Related articles to: NEK7 antibody
- The NLRP3 inflammasome is a multiprotein complex that primes cytokine production in the innate immune system. The inflammasome activation involves the cage-to-disk transition of NLRP3 oligomers, facilitated by the co-factor NEK7 protein. While NEK7's role in promoting cage disassembly has been reported, its involvement in the large conformational changes of the NLRP3 monomer during activation remains elusive. Here, by using multi-scale simulations, we uncovered a stage-dependent role of NEK7 in the inactive-to-active transition. In the early stage, NEK7 reshapes the dynamics of the highly unstable inactive NLRP3 monomer to resemble active state, priming the conformational transition. In the middle stage, NEK7 impedes progression by populating an intermediate state farther from the active conformation than the NEK7-free counterpart, and structures in this state exhibit reduced allosteric potential toward activation. In the late stage, NEK7 has negligible impact, as the active conformation remains inherently isolated by a high energy barrier regardless of NEK7 presence. This highlights the critical role of oligomeric assembly in enabling monomeric NLRP3 to complete its conformational transition, in agreement with experiment observations. Our work suggests a multilayered activation mechanism where oligomer-level assembly and monomeric conformational changes are coupled, providing new mechanistic insights into this physiologically essential macromolecular process. - Source: PubMed
Publication date: 2026/06/12
Peng JinLi WenjianWang HaoChen XiaohuiZhang ManjieSun Bin - The NLRP3 inflammasome responds to chemically and biologically diverse stimuli, yet growing evidence indicates that this apparent diversity converges on a limited set of structural and spatial licensing steps. Here, we argue that NLRP3 regulation is best understood through an assembly-centered framework rather than as another stimulus-centered catalog of activators. Cryo-electron microscopy (Cryo-EM), biochemical, and cell-biological studies support a model in which NLRP3 is maintained in inactive cage-like assemblies, undergoes nucleotide-dependent conformational rearrangements, engages NEK7, and nucleates ordered supramolecular complexes containing apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC). We synthesize current evidence for structural licensing, interface-level restraint, subcellular trafficking, phase-separation-linked organization, and post-translational and proteostatic control of NLRP3 assembly. We then examine a less explored question with translational implications: whether peptide-scale regulators, particularly endogenous microproteins, may control defined assembly transitions. Available evidence supports the existence of synthetic peptides that inhibit inflammasome interfaces and of endogenous microproteins that intersect with inflammatory signaling. However, direct evidence that endogenous microproteins act as dedicated interface-mimic inhibitors of NLRP3 assembly remains lacking. This review integrates mature structural models of NLRP3 regulation with the emerging microprotein field while clearly distinguishing established mechanisms from plausible but unproven hypotheses. This perspective defines a mechanistically explicit agenda for future work, including rigorous validation of translated small open reading frames (smORFs), direct interaction mapping to defined NLRP3 surfaces, and quantitative testing of effects on assembly, signaling output, and cellular context. - Source: PubMed
Hamad Rabab SSuliman Safwan Abid Al-HameedKadhim Mustafa EglaHasan Waseem AliElmorsy Elsayed AHamza EmanIbrahim Etedal Ahmed AMohamed Renad M SEissa HananFarrag Alshaimaa ASaber Sameh - Gestational diabetes mellitus (GDM) affects 15.6% of pregnancies globally, with Vietnam exhibiting one of the highest prevalences at 21%. Current diagnostic approaches at 24-28 weeks limit early intervention opportunities. We developed a multi-modal machine learning framework integrating cell-free DNA (cfDNA) structural features and genetic information for early GDM prediction at 10-12 weeks of gestation in Vietnamese women. - Source: PubMed
Publication date: 2026/05/26
Dao Vinh NguyenTran Nhat-ThangVo Ta-SonLe Hong-ThinhThi Nguyen Thu-HaNguyen Quoc-Huy VuThi Ha Minh-ThiLe Tam MinhHoang Diem-Tuyet ThiNguyen Huynh Khanh-TrangNguyen Nhan VietNguyen Chuong CanhBui Thuong ChiNguyen Xuan ThanhLe Sa VietTran Vinh DinhNguyen My-Nhi BaNguyen Thong VanNguyen Tuyet-Anh ThiHoang Ba PhuocNguyen Trong VanNguyen Thuy-Ai ThuyNguyen Toa TriDuong Thang DucPham Cuong HuyLuong Kim-Oanh ThiDao Cuong NgocHoang Khanh VanHuynh Thu-Thanh ThiNguyen Khuong ManhTran Son-Tra ThiTran Hoanh TrungNguyen Son CanhTran Thuy DinhNguyen Phương Thi LanPham Thanh VietPham Kong ChiThai Minh DoanTruong My-Hang ThiPham Hieu HaDo Thanh-Thuy ThiTang Sang HungNguyen Hoai-NghiaPhan Minh-DuyDao Hoa ThiGiang Hoa - Chronic low-grade inflammation driven by persistent NLRP3 inflammasome activation is a unifying pathophysiological feature of most non-communicable diseases (NCDs). Whereas single-target pharmacological inhibitors exhibit limited breadth and durability, regular moderate-intensity exercise confers robust multi-system protection through a diverse network of exerkines. This narrative review synthesizes evidence that exercise-released myokines (irisin, Metrnl, context-reprogrammed IL-6), hepatokines/adipokines (FGF21, adropin, adiponectin), metabolites (lactate, β-hydroxybutyrate), microbiota-derived factors (SCFAs, betulinic acid), and extracellular vesicle (EV)-delivered non-coding RNAs converge on every regulatory node of the canonical NLRP3 inflammasome to achieve multi-nodal suppression that is currently unmatched by any single pharmacological approach based on available evidence. Acute high-intensity exercise transiently activates NLRP3 via canonical danger signals, whereas chronic moderate-intensity training (150-300 min·wk, 60%-75% HRmax) induces profound basal suppression through NF-κB attenuation, mitochondrial protection, direct interference with NEK7-NLRP3 interaction and ASC oligomerization, post-transcriptional silencing, and enhanced autophagic clearance. These mechanisms are supported by preclinical structural data and human biomarker studies across cardiovascular, metabolic, neurodegenerative, and musculoskeletal disorders. We propose a precision exercise medicine framework integrating exerkine/genetic/microbiome profiling to minimize non-responders, together with emerging mimetics, RNA therapeutics, and synergistic pharmacology, to deliver scalable systems-level modification of NLRP3-driven metaflammation. - Source: PubMed
Publication date: 2026/05/25
Wang HuaimingJin ZongqiangDi ShijingAlizadeh Hamid - Microglia's role in epilepsy through neuroimmune communication is poorly understood. Mechanisms by which neurons activate microglia and how microglia affect neuronal activity to drive seizure-related inflammation remain unclear. Here, we elucidated a crucial axis connecting pathological adenosine triphosphate (ATP) release induced by epileptiform neuronal activity to microglial MEF2A-dependent hyperactivation, which exacerbates epilepsy pathology. In epilepsy models, seizures cause excessive ATP release, activating microglial P2X7 receptors, causing CAMKII phosphorylation. This triggers HDAC5 translocation, freeing MEF2A for acetylation, and enhancing transcription. Acetylated MEF2A increases CD74 and NEK7 expressions, enhancing NLRP3 inflammasome activation and microglial hyperactivation, worsening neuronal hyperexcitability by increasing inhibitory synapses clearance. Targeting microglial MEF2A with parecoxib or AAV knockdown reduced seizure severity and cognitive deficits and maintained synaptic inhibition by reducing excessive microglial phagocytosis. This reveals an ATP-P2X7-Ca⁺- MEF2A signaling axis connecting neuronal injury with pathogenic microglial activation, suggesting MEF2A as a therapeutic target for microglial-neuronal homeostasis restoration in epilepsy pathology. - Source: PubMed
Publication date: 2026/05/22
Wu JinghengFu JiayuanyuanWang ShuaiWu YuzhangWang XuFeng ShangangShi QiWang YuhaoShi YetongFang YehongLan YuWu QiaoliDu ChuanYin ShaoyaXu LixiaYan Hua