AXIN2 ELISA kit
- Known as:
- AXIN2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-AXIN2-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- AXIN2 ELISA kit
Related genes to: AXIN2 ELISA kit
- Gene:
- AXIN2 NIH gene
- Name:
- axin 2
- Previous symbol:
- -
- Synonyms:
- MGC126582, DKFZp781B0869
- Chromosome:
- 17q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2019-04-23
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- Tooth agenesis, including hypodontia and oligodontia, is one of the most common developmental dental anomalies. Emerging evidence suggests a potential association between tooth agenesis and colorectal cancer (CRC), particularly in the context of shared genetic pathways such as WNT signalling and AXIN2 mutations. However, findings across epidemiological and genetic studies remain inconsistent. - Source: PubMed
Publication date: 2026/08/03
Hashmi Ahmad ShoebRanganathan RajiVats KunalBaburaj DianaSampaio PedroChauhan DhvaniKulsum OnaizaTiwari Rahul - Dynamic monitoring of cell-matrix interfacial remodeling remains challenging with conventional endpoint assays, particularly in degeneration-relevant microenvironments. The cartilage endplate (CEP), a key structure for load transmission and solute exchange in the intervertebral disc, provides a model in which early pathological changes involve abnormal cell-matrix adhesion and extracellular matrix remodeling. Here, we established a label-free, long-term monitoring platform based on metasurface-enhanced surface plasmon resonance microscopy (Meta-SPRM) to quantify CEP chondrocyte interfacial dynamics under mechanical, genetic, and inflammatory perturbations. Under perfusion-induced shear, CEP chondrocytes exhibited magnitude-dependent interfacial adaptation, with high shear causing a more sustained reduction in interfacial coupling and contact area. FGFBP1 knockdown further exacerbated this shear-associated loss, supporting a protective role for FGFBP1 in interfacial stability under mechanical stress. Under inflammatory stimulation with M1 macrophage-conditioned medium, interfacial signals increased despite a late decrease in cell spreading, consistent with enhanced interfacial adhesion and matrix remodeling. Axin2 expression increased under shear, was further increased by FGFBP1 knockdown in the shear model, and was also elevated under inflammatory stimulation, supporting its use as an endpoint readout of Wnt/β-catenin-associated transcription across the tested perturbations. Collectively, Meta-SPRM enables continuous live-cell monitoring of CEP chondrocyte interfacial dynamics and relates these changes to endpoint molecular readouts, providing a reproducible platform for comparative biointerface studies and in vitro screening of candidate interventions. - Source: PubMed
Publication date: 2026/08/13
Li WenWang QiongGu XiaofengChen MingqianXu QiangLi DingChen YouqianYang YihuiLi ZhenyuHu WenjunWang Junfang - β-catenin plays a pivotal role in oncogenesis through its involvement in cell-cell adhesion, Wnt signaling, and transcriptional regulation. Dysregulation of β-catenin contributes to tumorigenesis by promoting proliferation, bypassing senescence, and enhancing migration and invasion. In melanoma, however, its role has been controversial, with studies reporting conflicting effects on proliferation, metastasis, and patient survival. Here, we demonstrate that activation of β-catenin is associated with a poor prognosis in melanoma. This conclusion is based on immunohistochemical analysis of a cohort of 157 patients and the identification of a genetic signature for melanoma upon β-catenin activation. This signature includes known targets such as APCDD1 and AXIN2, as well as previously unknown targets like MICAL2 and SLC1A5. Notably, MICAL2 (Molecule Interacting with CasL 2) emerged as a key regulator of the invasive phenotype, with high expression levels correlating with adverse outcomes. Functional studies confirmed that MICAL2 is transcriptionally regulated by β-catenin. Nras and Braf mouse melanoma models further validated the conserved regulation of MICAL2 by β-catenin, linking it to melanoma initiation and metastasis. Moreover, MICAL2 expression is enriched in melanoma cells resistant to BRAF inhibitors, and MICAL2 downregulation restores therapeutic sensitivity. These findings highlight MICAL2 as a central effector of β-catenin signaling and a mediator of melanoma progression and resistance. Given the therapeutic challenges of directly targeting β-catenin, inhibiting the enzymatic activity of MICAL2 offers a promising and innovative strategy to improve outcomes in β-catenin-driven melanoma. - Source: PubMed
Publication date: 2026/08/14
Sohier PierreRaymond Jérémy HAktary ZackieZidi NourAraktingi LaraCharoenchon NisamaneePisibon CélineCaberia SylviePasmant EricMacagno NicolasDelmas VéroniqueGaudy-Marqueste CarolineSteingrimsson EirikurBallotti RobertPetit ValérieLarue Lionel - Parabens are antimicrobial preservatives with endocrine-disrupting potential. Because methylparaben (MeP), ethylparaben (EtP), and butylparaben (BuP) differ in alkyl-chain length and biological potency, their comparison may reveal structure-dependent cellular responses. Using K562 chronic myeloid leukemia cells, we compared the effects of MeP, EtP, and BuP on cytotoxicity, metabolic activity assessed by resazurin reduction, proliferation- and stress-related markers, and WNT/β-catenin- and PPARγ-associated signaling. Cells were exposed to MeP, EtP, or BuP for 24 or 48 h; pathway-focused experiments used 1 μM parabens alone or with methyl 3-{[(4-methylphenyl)sulfonyl]amino}benzoate (MSAB), a β-catenin-directed WNT/β-catenin inhibitor, or GW9662, a PPARγ antagonist. MeP did not significantly affect LDH release or resazurin reduction. In contrast, EtP and BuP increased resazurin reduction at nanomolar and low-micromolar concentrations. At 1 μM, this response was not accompanied by marked LDH release, ROS generation, or cell-cycle alterations and therefore did not indicate overt acute cytotoxicity or robust proliferation. This response was accompanied by increased expression of WNT-related and glycolysis-associated genes, including AXIN2, LEF1, SLC2A1, HK2, PDK1, and PFKFB3. Parabens also induced divergent c-MYC regulation, with decreased c-MYC mRNA but increased protein abundance, and modulated PPARγ-associated signaling, antioxidant enzymes, caspase-related responses, and p-p62-related signaling. MSAB and GW9662 modified the resazurin-reduction response; however, these pharmacological effects did not establish direct β-catenin or PPARγ dependence. Overall, EtP and BuP, particularly BuP, produced stronger effects than MeP on resazurin reduction and several WNT/β-catenin-, PPARγ-, and p-p62-associated readouts. - Source: PubMed
Publication date: 2026/08/12
Szychowski Konrad ASkóra Bartosz - In this investigation, we examined the functional mechanism of the transcription factor zinc finger protein 695 (ZNF695) and its target gene chromobox protein homolog 8 (CBX8) in colorectal cancer (CRC) migration and invasion. HCT-116 and LOVO cell lines were used to establish cell models with knocked-down ZNF695 and knocked-down or over-expressed CBX8. To comprehensively evaluate the functional contributions of ZNF695 and CBX8 to cellular phenotypes, we employed CCK-8, wound-healing, and Transwell assays to evaluate cell proliferation, migration, and invasion, respectively. To assess the impact of ZNF695 on tumor progression, we generated a xenograft model utilizing nude mice. A FLAG-ZNF695 expression plasmid was constructed, and ChIP-seq experiments were performed. By integrating mRNA sequencing data following ZNF695 knockdown with highly expressed genes in CRC from the TCGA database, CBX8 was identified as a putative downstream target of ZNF695. We employed a dual-luciferase reporter assay to validate the specific binding affinity of ZNF695 toward the CBX8 promoter region. To elucidate the specific biological cascades modulated by ZNF695 and CBX8, we conducted a comprehensive pathway enrichment analysis. Rescue experiments were conducted to determine whether the ZNF695/CBX8 regulatory axis upregulates the expression of the Wnt signaling pathway downstream targets, AXIN2 and CCND1. Both in vitro assays and in vivo models confirmed that silencing ZNF695 dramatically suppresses CRC cell proliferation, migration, and invasion, while concurrently impeding tumor progression. ChIP-seq coupled with dual-luciferase reporter assays substantiated the direct binding of ZNF695 to the CBX8 promoter. Furthermore, CBX8 depletion significantly attenuated the migratory and invasive phenotypes of CRC cells. Restoring CBX8 expression effectively rescued the migratory and invasive deficits in CRC cells induced by ZNF695 silencing. Re-expression of CBX8 in ZNF695-silenced cells restored Wnt/β-catenin signaling activity, accompanied by increased expression of AXIN2 and CCND1. ZNF695 promotes CRC progression by transcriptionally activating CBX8 and subsequently enhancing Wnt/β-catenin signaling, thereby promoting tumor cell proliferation, migration, and invasion. - Source: PubMed
Publication date: 2026/07/19
Tang XiaozhunKe HailinHuang Ying