Human Netrin-1,Ntn1 ELISA Kit
- Known as:
- Human Netrin-1,Ntn1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-1278
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Netrin-1 Ntn1 ELISA Kit
Related genes to: Human Netrin-1,Ntn1 ELISA Kit
- Gene:
- NTN1 NIH gene
- Name:
- netrin 1
- Previous symbol:
- -
- Synonyms:
- NTN1L
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-15
- Date modifiied:
- 2015-02-16
Related products to: Human Netrin-1,Ntn1 ELISA Kit
Related articles to: Human Netrin-1,Ntn1 ELISA Kit
- Deregulation of the Sonic Hedgehog (SHH)/GLI signaling pathway has been strongly implicated in carcinogenesis, particularly in brain and skin tumors, through mutations affecting various pathway components. Given its central role in tumor development, the SHH/GLI axis has emerged as a key target for therapeutic intervention, underscoring the need to identify GLI-specific targets in cancer cells. Netrin-1, a multifunctional signaling molecule with pro-oncogenic properties, is overexpressed in diverse tumor types. While its tumor-promoting functions are well documented, the regulatory mechanisms governing its expression remain poorly understood. Here, we provide through gene expression profiling and in vitro and ex vivo analyses evidence demonstrating that Netrin-1 (NTN1) is a direct transcriptional target of canonical SHH signaling. We further show that in conditions of SHH pathway hyperactivation-such as in SHH-driven medulloblastoma (MB) NTN1 is significantly upregulated. This overexpression promotes the self-renewal of MB stem-like cells through the modulation of ERK signaling, thereby contributing to enhanced cancer stemness. Our findings identify NTN1 as a novel downstream effector of the SHH/GLI pathway and demonstrate that quantifying NTN1 levels can refine molecular classification of SHH-subtype medulloblastomas-distinguishing tumors with high SHH pathway activation and enhanced stem-like properties, with potential implications for prognosis and targeted therapy selection. - Source: PubMed
Publication date: 2026/06/15
Falcón PFernández-Caniulén EZúñiga-Hernández J MGaete-Ramírez BPrieto CPfister S MKool MSchüller UWainwright BRemke MTaylor M DAlvarez-Astudillo FArmisén RVaras-Godoy MPalma V - Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality, primarily attributed to distant metastasis. The trimethoxyflavone eupatilin (Eup), a major flavonoid derived from the leaves of Artemisia argyi, exhibits potential antitumor properties. However, its effects and underlying mechanisms in NSCLC have been inadequately elucidated. - Source: PubMed
Publication date: 2026/05/18
Xu BoHu LinlingJiang BoQi YuYan LeZhang JixianYu YihanMiao Qing - Total rib number (TRN) and total teat number (TTN) are key anatomical and economic traits in pigs, linked to carcass yield and reproductive performance, respectively, and are genetically correlated. However, the shared genetic basis underlying these traits remains incompletely understood. This study aimed to dissect the genetic architecture of TRN and TTN and to identify pleiotropic genes affecting both traits. Single-population genome-wide association studies (GWASs), multi-population meta-analysis, and multi-trait meta-analysis were conducted using phenotypic and genotypic data from three pig populations: Yorkshire (YY, n = 413), Suhuai (SH, n = 655), and Landrace × Yorkshire (LY, n = 678). Significant genetic and phenotypic correlations were observed between TRN and TTN, with genetic correlations of 0.82 in YY, 0.46 in SH, and 0.35 in LY. Ten quantitative trait loci (QTLs) associated with TRN were identified, including novel loci on SSC2 (39.38-40.49 Mb), SSC3 (123.79-125.58 Mb), SSC6 (103.40-104.53 Mb), SSC12 (53.30-54.84 Mb), and SSC18 (45.29-46.91 Mb). For TTN, eight QTLs were detected, including three newly discovered regions on SSC13 (142.82-143.99 Mb), SSC14 (7.26-8.54 Mb), and SSC16 (10.19-12.18 Mb). Candidate genes were identified through functional annotation and phenome-wide association analysis. For TRN, the prioritised genes included GREB1, SMCHD1, HES7, VRTN, ABCD4, NTN1, and members of the HOX gene family, whereas for TTN, the identified genes included FRMD4A, STC1, GREB1, and ABCD4. Colocalisation analysis integrating GWAS and multi-tissue expression QTL data suggested shared genetic signals for several genes, including EMILIN2, PTGR2, PSEN1, and ABCD4 for TRN, and PTGR2 and ENSSSCG00000033037 for TTN. Notably, GREB1, PTGR2, and ABCD4 were identified as pleiotropic genes potentially regulating both traits. These results clarify the shared genetic architecture of rib and teat number and provide candidate genes for future functional validation and genetic improvement in pig breeding. - Source: PubMed
Publication date: 2026/04/29
Liu QYu JYin YChen JXu LMa JZhou JZhao QHuang RLi P - Cadmium (Cd) is a persistent environmental pollutant that poses a significant health risk to humans and animals, with acute exposure known to induce kidney injury. Fucoidan (Fc), a natural bioactive polysaccharide derived from brown algae, exhibits diverse biological activities; however, its potential to protect against Cd-induced kidney damage and the underlying mechanisms remain unclear. In this study, we investigated the effects of Fc on Cd-induced renal injury in vitro and further explored the role of transcription factor EB (TFEB) in regulating autophagy in its protective mechanism. Our results demonstrate that in Cd-exposed porcine kidney cells (PK-15), Fc suppressed the expression of renal inflammatory factors (TNF-α, IL-1β) and kidney injury markers (NGAL, NTN-1, KIM-1), reduced reactive oxygen species (ROS) production, and downregulated apoptosis-related proteins (cleaved caspase-3 and cleaved caspase-9). Mechanistically, Fc upregulated TFEB protein expression, enhanced the levels of lysosomal function-related proteins (Cathepsin B, CTSB; Cathepsin D, CTSD), and reversed Cd-induced autophagic flux blockade. Importantly, TFEB silencing abolished the protective effects of Fc. Collectively, these findings suggest that Fc exerts renoprotective effects against Cd-induced injury by restoring autophagic flux, a process that involves TFEB. - Source: PubMed
Publication date: 2026/05/13
Qu HaoboZhao XiaoyuWang YifanMao SichaoChen XingxiangHuang KeheXu Xinyi - Doxorubicin (DOX)-induced cardiotoxicity is strongly associated with ferroptosis and oxidative stress, yet the endogenous protective mechanisms remain incompletely understood. This study aimed to determine whether Netrin-1 protects against DOX-induced cardiomyocyte and myocardial injury and to elucidate the underlying signaling pathway. H9C2 cardiomyocytes and DOX-treated mice were used to evaluate the effects of Netrin-1 on ferroptosis, oxidative stress, and cardiac function. Ferroptosis markers, antioxidant proteins, and signaling molecules were assessed by biochemical assays, immunofluorescence, and Western blotting. Loss-of-function experiments were conducted using si-UNC5B, si-LKB1, si-CaMKKβ, Compound C, and AAV-shUNC5B to dissect pathway dependence. Netrin-1 significantly restored DOX-impaired cell viability, reduced membrane damage, and suppressed ferroptosis by decreasing Fe²⁺, MDA, and ROS while replenishing GSH. It normalized GPX4, ACSL4, ferritin, and TFR1 expression, uniquely activated AMPK, suppressed BACH1, enhanced HO-1, and promoted robust NRF2 nuclear translocation. UNC5B knockdown abolished these effects, indicating its essential role. Mechanistically, Netrin-1 activated AMPK through both LKB1 and CaMKKβ pathways, with dual knockdown producing additive suppression. In DOX-treated mice, Netrin-1 markedly improved cardiac function, lowered serum injury markers, alleviated histological damage, reduced apoptosis, and inhibited ferroptosis; these benefits were negated by AMPK inhibition or UNC5B depletion. Netrin-1 mitigated DOX-induced cardiotoxicity by suppressing ferroptosis and restoring antioxidant defenses through the UNC5B-LKB1/CaMKKβ-AMPK-NRF2 axis, highlighting Netrin-1 as a promising therapeutic candidate for preventing chemotherapy-induced cardiac injury. - Source: PubMed
Publication date: 2026/05/22
Lu WeiWu HaiboWang YanqingDuan YaweiGao PengLi HongxiaoDu Rongpin