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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- The present study aimed to investigate the expression and biological behaviour of the six-transmembrane epithelial antigen of the prostate 1 (STEAP1) in oral squamous cell carcinoma (OSCC), and to further analyse its underlying mechanisms. - Source: PubMed
Jin KuangyuLiu ShitongJin HuiZhang DongLu RunzeWang Wei - Neutralizing sclerostin antibodies (Scl-Ab) mitigate bone loss and promote bone formation to address fracture risk in postmenopausal osteoporosis. Clinically, this treatment is administered monthly for women at high risk of fragility fractures, who are often years into menopause. Preclinical studies have demonstrated that dampening of bone formation occurs with continuous dosing at supraphysiological doses. Osteoporotic bone loss occurs rapidly during early menopause, followed by longer-term changes in bone mineralization and osteocyte activity. Whether earlier administration of lower-exposure Scl-Ab can mitigate bone loss and osteocyte-mediated mineralization is unknown. The objective of this study was to evaluate the effects of early intermittent low-dose Scl-Ab on: (1) osteoclastogenesis and bone resorption, (2) perilacunar remodelling, (3) secondary mineralization, and (4) osteocyte mechanosensitivity. Female retired breeder Wistar rats underwent bilateral ovariectomy and received monthly low-dose Scl-Ab injections (2 mg/kg/month) from 3 to 14 weeks post-OVX, while a control group remained untreated. Early intermittent low-dose Scl-Ab treatment increased bone formation and reduced osteoclastogenesis and catabolic gene expression ((Sost, Ctsk, Mmp9) compared to untreated rats. Treatment also decreased the percentage of empty lacunae and the number of MMP14+ osteocytes, accompanied by lower perilacunar mineral density and smaller lacunar size, indicating improved osteocyte survival and reduced perilacunar remodelling. Conversely, expression of osteocyte-mediated mineralization genes (DMP1, PHEX, OPN, ALP) and mechanotransduction-related genes (Vcl, integrins α5, αV, β1, CX43, Axin2, IFT88, Adcy6, Pkd1, Cav1) were reduced. Together, these findings suggest that early intermittent low-dose Scl-Ab therapy promotes surface bone formation while attenuating osteocyte-mediated mineralization after initial bone loss. - Source: PubMed
Publication date: 2026/04/07
Naqvi Syeda MasoomaAli WahaajAllison HollieO'Sullivan Laura MHoldsworth GillPanadero-Perez Juan AlbertoSchiavi-Tritz JessicaMcNamara Laoise M - Worldwide, colorectal cancer continues to be a major contributor to cancer mortality. The main reasons for high-colorectal cancer death rates are tumor progression, metastasis, and resistance to existing therapies. Wnt/β-catenin and PI3K/AKT/mTOR pathways have been shown to be involved in the development of colorectal cancer as well as in resistance to available therapies. Therefore, agents that can target both pathways simultaneously would be advantageous. Baicalein, a bioactive flavonoid from the plant Scutellaria baicalensis, has been shown to have anticancer activity against multiple cancers, but its dual effects on the Wnt/β-catenin and PI3K/AKT/mTOR pathways in human colorectal cancer remain undefined. In this study, we aimed to determine whether baicalein has antitumor activity and the molecular mechanism through which it acts in human colorectal cancer cell lines SW480 and HCT116. We assessed baicalein's antitumor activity using PrestoBlue cell viability, flow cytometry for determining apoptosis, wound-healing assay for migration, and colony formation assay for determining clonogenic survival. The molecular mechanisms by which baicalein inhibits tumors were evaluated using various molecular techniques including reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blotting, and nuclear-cytoplasmic fractionation to measure the activity of the Wnt/β-catenin and PI3K/AKT/mTOR pathways. In addition, the clinical relevance of baicalein's targets was evaluated using in silico analysis of the Cancer Genome Atlas (TCGA) dataset. The compound baicalein decreased proliferation, migration and colony forming ability of colorectal cancer cells and increased apoptosis. These actions were dependent upon time and concentration of baicalein treatment. The anti-proliferative actions of baicalein occurred through inhibition of Wnt/β-catenin signaling by decreasing AXIN2 and GSK3β expression and nuclear accumulation of β-catenin. Baicalein also inhibited PI3K/AKT/mTOR signaling by decreasing mTOR expression as well as phosphorylation of AKT, mTOR, and S6. In addition, the results of the in silico analyses suggested that these targets may be clinically relevant and correlate with drug resistance. Therefore, baicalein is identified to be a potent dual inhibitor of Wnt/β-catenin and PI3K/AKT/mTOR signaling pathways and provides evidence for its use as a novel therapeutic agent for colorectal cancer. - Source: PubMed
Publication date: 2026/04/13
Anlei WangKaihao WangYazhao GongBeibei RenGuanglei YangShuqing Xu - Prostate cancer (PCa) is a biologically heterogeneous disease that frequently progresses to castration-resistant prostate cancer (CRPC), a challenging clinical stage. The underlying mechanisms driving CRPC progression and resistance to androgen receptor (AR) signaling inhibition (ARSI) remain incompletely understood. Emerging evidence implicates the canonical Wnt pathway as a key contributor to CRPC progression. This study elucidates the role of Wnt pathway activation in mediating resistance to ARSI and identifies a robust molecular signature for predicting treatment outcomes. By integrating genomic and transcriptomic data from PCa patients, patient-derived xenografts (PDXs), and experimental models harboring or not Wnt-activating mutations, we performed differential expression analysis, unsupervised clustering, survival, and viability analysis to assess Wnt/β-catenin pathway activation and its interaction with AR signaling. A specific Wnt transcriptional signature (AXIN2, RNF43, ZNRF3, NKD1) was found to reliably reflect pathway activation in advanced PCa. AR was found to suppress mutation-driven Wnt signaling, which was upregulated upon AR inhibition, contributing to treatment resistance. Targeting β-catenin interactions with co-activators p300/CBP using selective inhibitors (IQ-1 and ICG-001) effectively mitigated Wnt-driven ARSI resistance, restoring sensitivity to therapy in preclinical models. Thus, canonical Wnt pathway activation emerges as a critical mediator of resistance to ARSI in CRPC. The identified Wnt signature holds potential as a biomarker for predicting and monitoring therapeutic outcomes. Concurrent targeting of AR and Wnt signaling represents a promising strategy to overcome treatment resistance, particularly in patients with Wnt-activating mutations. - Source: PubMed
Publication date: 2026/04/14
Anselmino NicolasSanchis PabloBizzotto JuanLabanca EstefaniaDong JiabinShepherd Peter D AYang JunVazquez Elba SMateo JoaquinGueron GeraldineLogothetis Christopher J - Biallelic DIAPH1 mutations are linked to hereditary microcephaly syndrome, yet the underlying pathogenic mechanism remains unelucidated. This study aimed to clarify how DIAPH1 biallelic mutations cause microcephaly and visual impairment, focusing on the gene's regulatory role in the Wnt/β-catenin signaling pathway. - Source: PubMed
Publication date: 2026/04/10
Wang DayanLai PanjianWang KanWu ZhuanbinLi Xiaobing