Human Netrin-4,Ntn4 ELISA Kit
- Known as:
- Human Netrin-4,Ntn4 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-1298
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Netrin-4 Ntn4 ELISA Kit
Related genes to: Human Netrin-4,Ntn4 ELISA Kit
- Gene:
- NTN4 NIH gene
- Name:
- netrin 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q22
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-27
- Date modifiied:
- 2014-11-19
Related products to: Human Netrin-4,Ntn4 ELISA Kit
Related articles to: Human Netrin-4,Ntn4 ELISA Kit
- The pronounced heterogeneity of bladder cancer (BLCA) drives divergent patient outcomes and therapy responses. Mitophagy, a pivotal cellular quality-control and metabolic mechanism, modulates the dynamics of the tumor microenvironment (TME). Its prognostic significance and potential for guiding precision oncology, however, remain incompletely defined. This investigation aimed to evaluate the translational utility of mitophagy-associated signatures for the risk stratification of BLCA, profiling of TME, and prediction of therapeutic response. - Source: PubMed
Publication date: 2026/06/25
Han ChenyuMiao LiuyangLiu YanWang YitianWu JiaxuanDu Peng - Adult neuronal survival underlies lifelong brain function, yet its sustaining mechanisms remain unclear. We identify a neurovascular survival axis at intracranial arteries in mice, where superior cervical ganglion (SCG) sympathetic terminals form synapse-like neurosmooth muscular junctions (NsMJs) with arterial smooth muscle cells (aSMCs) that secrete netrin-4 (Ntn4). Adult aSMC-restricted Ntn4 deletion selectively reduces rostral, intracranial-projecting (cerebrospinal fluid-traced) SCG neurons; the denervation of the intracranial arterial plexus follows soma loss. Local recombinant Ntn4 delivery to the SCG rescues these phenotypes. Ntn4 withdrawal engages a receptor-interacting serine/threonine kinase 1 (RIPK1)/mixed lineage kinase domain-like pseudokinase (MLKL)-linked, caspase-independent, non-inflammatory death program via deleted in colorectal cancer (DCC): unliganded DCC triggers neuronal loss, whereas Dcc knockout preserves vulnerable neurons. Arterial Ntn4 declines from young adulthood and precedes selective neuronal attrition before midlife; aSMC-targeted Ntn4 overexpression prevents this loss. Together, intracranial arteries provide a local, non-cell-autonomous trophic niche that maintains this adult sympathetic subset and becomes compromised as vascular Ntn4 output wanes with age. - Source: PubMed
Publication date: 2026/05/07
Zhu ZhuLin WanlingXiao LiangQian ZhihaoHe TingWang WentaoWang YuanjiaoZhang XiaoxuanZhao BingruiXie HuiqiQuan XinghuaZhang YanxiaoJiang MinLi XuzhaoZhou LiliZhang DongdongYu HualinLiu ZiyuBao LingyunJia Jie-Min - SMARCB1-deficient sinonasal carcinoma (SDSC) is a rare, highly aggressive malignancy with limited therapeutic options and no established preclinical models. Here, single-nucleus RNA sequencing (snRNAseq), spatial transcriptomics, and ex vivo patient-derived tissue slice culture (TSC) were combined to resolve intratumoral heterogeneity, niche organization, and treatment vulnerabilities in an index SDSC. snRNAseq identified three malignant subpopulations, including two specialized states marked by ALDH1A1 and NTN4. Spatial profiling mapped these states to distinct niches. The ALDH1A1+ compartment localized to a basal-associated niche with intermingled p63-positive basal cells adjacent to stroma, showed reduced proliferative activity, and displayed stem-like transcriptional features. Ex vivo drug testing revealed a striking response: the mTOR inhibitor Sapanisertib induced extensive tumor necrosis and was associated with near-complete depletion of ALDH1A1+ and NTN4+ states, accompanied by strong stress/apoptosis signatures and reduced endothelial cells. In an additional retrospective cohort of 12 SDSC, ALDH1A1 was present in all cases with heterogeneous spatial patterns and higher levels in recurrences. Mesothelin was expressed in the index case and a subset of tumors, supporting mesothelin-directed therapeutic strategies. - Source: PubMed
Publication date: 2026/05/02
Jurmeister PhilippFlach SusanneBergmayr LindaSchleich KonstanzeChimal Calderon EdgarH Mochmann LilianaZhdanovich YauheniyaKlingler DoreenPusztai AdaKübler AnnaWalz ChristophWestphalen Christoph BenediktBeck AlexanderLeitheiser MaximilianBreimer Gerben ERijken Johannes ADevriese LotBaumeister PhilippSkálová AlenaSchallenberg SimonKlauschen FrederickMock Andreas - Remote ischemic postconditioning (RIPC) confers neuroprotection in ischemic stroke partly via promoting angiogenesis and neurogenesis, but its precise molecular mechanisms remain unclear; here, we investigated the role of the secreted guidance protein Netrin-4 (NTN4) and its upstream regulator hypoxia-inducible factor 1α (HIF-1α) in mediating RIPC's reparative effects, using endothelial-specific Ntn4 knockout (KO) mice subjected to transient middle cerebral artery occlusion (MCAO) and RIPC, alongside in vitro assays with brain microvascular endothelial cells (BMECs) and neural stem cells (NSCs) and molecular interaction analyses, including DNA pull-down and chromatin immunoprecipitation (ChIP), finding that RIPC significantly upregulated NTN4 expression in the ischemic penumbra of MCAO mice, that endothelial-specific Ntn4 knockout abolished RIPC's protective effects-impairing neurological recovery, angiogenesis and neurogenesis, which were rescued by recombinant NTN4 administration, that NTN4 promoted BMEC proliferation and tube formation via an integrin β1-PI3K/AKT pathway while conditioned medium from Ntn4-overexpressing BMECs enhanced NSC neuronal differentiation through an integrin β1-MAPK/ERK axis, and that RIPC stabilised HIF-1α, which directly bound the Ntn4 promoter to drive its transcription, collectively establishing that RIPC orchestrates brain repair by stabilising HIF-1α to transcriptionally activate endothelial NTN4, which signals through integrin β1 to drive parallel PI3K/AKT and MAPK/ERK pathways for angiogenesis and neurogenesis, highlighting this axis as a key therapeutic target in stroke. - Source: PubMed
Feng ZhaoweiLiu ZhenqianTang SiyuPan MeihuaZhu KaishenLiu YiweiWang ChunyuYao RuiqinWei XiueLiu Haiyan - Observational studies suggest that plasma proteins play a crucial role in the development and progression of obstructive sleep apnea (OSA); however, the causal relationship between plasma proteins and OSA remains controversial. This study conducted a comprehensive evaluation of the causal relationships between 4,907 plasma proteins and OSA by employing bidirectional Mendelian randomization (MR) analysis, network pharmacology strategies, and single-cell sequencing techniques. The plasma protein data used in this study were derived from Ferkingstad et al.'s research (n = 35,559), and OSA-related data were obtained from genome-wide association studies (GWAS) conducted on European populations through Finland's biobank (FinnGen). This study utilized multi-omics integration strategies, including enrichment analysis, protein-protein interaction (PPI) network construction, drug target prediction, molecular docking simulation, and single-cell transcriptome sequencing, to investigate the biological mechanisms of identified targets and evaluate their potential applications in drug development. MR analysis identified 62 plasma proteins significantly associated with OSA risk, including NTN4 (p = 0.003, OR = 1.076, CI [1.024, 1.129]) and TFF2 (p = 0.004, OR = 1.098, CI [1.029, 1.174]). Further reverse Mendelian analysis revealed causal relationships between OSA and the CELF2, NTRK3, ANTXR2, and MYOM2 genes. PPI network analysis identified 10 core genes, including IL1β, TGFβ1, EGF, SHH, and SMAD2, which participate in critical pathological processes in OSA, such as oxidative stress, inflammatory responses, and immune regulation. Through drug prediction analysis, this study identified compounds with potential therapeutic effectiveness, including 3,4-DHB, BIM IX, and 1,9-Pyrazoloanthrone, and molecular docking studies further confirmed their high binding affinity to target proteins. Single-cell sequencing revealed high expression levels of key genes in T cells and dendritic cells, thereby confirming the critical role of these cells in the pathological progression of OSA. A total of 62 candidate therapeutic targets for OSA were identified in this study, with 10 of these targets deemed important candidates for clinical trials. These findings not only enrich the understanding of the molecular pathological mechanisms underlying OSA but also offer new perspectives for developing targeted therapeutic strategies to treat the condition. By facilitating the establishment of more precise and personalized disease management approaches, these results are expected to advance the development of therapeutic drugs for OSA and substantially reduce the economic costs associated with new drug development. - Source: PubMed
Publication date: 2026/02/19
Duan LingzhiWang YanJing HaiqingWang YanqiongNing ShuyeYang ZhengfuZhang Aihua