AXIN2
- Known as:
- AXIN2
- Catalog number:
- 002329A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AXIN2
Related genes to: AXIN2
- 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
Related products to: AXIN2
Related articles to: AXIN2
- To explore the molecular mechanisms by which ethionine induces neural tube defects (NTD) through regulating the lysine demethylase 5A (KDM5A)/trimethylated lysine 4 of histone H3 (H3K4me3) axis and modulating the Wnt/β-catenin signaling pathway. Specific pathogen-free adult male and female C57BL/6 mice (80 females and 35 males) were housed overnight in a 2∶1 female-to-male ratio. Vaginal plugs were examined the following morning to confirm pregnancy. Pregnant mice were randomly divided into two groups: the ethionine experimental group (ethionine group) and the control group. At embryonic day 7.5 (E7.5), the ethionine group received a single intraperitoneal injection of ethionine (500 mg/kg) to establish the NTD model, while the control group was injected with an equal volume of normal saline, with 21 mice in each group. At E10.5, pregnant mice were sacrificed and embryos were collected for observation and photography under a stereomicroscope. Brain tissues from embryos of both groups were harvested for transcriptome sequencing. The expression levels of KDM5A, H3K4me3, Wnt/β-catenin pathway components [β-catenin, transcription factor 4 (TCF4), axis inhibition protein 2 (Axin2), phosphorylated glycogen synthase kinase 3β (p-GSK3β)], and cell proliferation-related proteins [G1/S-specific cyclin-D1 (Cyclin D1), proliferating cell nuclear antigen (PCNA), Myc oncogene (c-Myc)] were assessed by Western blotting, real-time quantitative polymerase chain reaction (RT-qPCR), and immunofluorescence. An additional KDM5A-specific inhibitor GSK-4J treatment group (GSK-4J group) and ethionine combined with GSK-4J treatment group (ethionine+GSK-4J group) were included to verify the regulatory role of the KDM5A/H3K4me3 axis. The pregnant mice in the GSK-4J group received intraperitoneal injection of GSK-4J (7 mg/kg) and the ethionine+GSK-4J group were injected with both 7 mg/kg GSK-4J and 500 mg/kg ethionine, with 12 mice in each group. Comparisons between the two groups were performed using independent samples t-test, one-way ANOVA was applied to evaluate the overall differences among multiple groups, and Tukey's honestly significant difference test was adopted for pairwise post-hoc comparisons. The ethionine treated group exhibited 48.79% (121/248) incidence of incomplete brain structure and morphological malformations, while the malformation rate in the control group was 3.73% (10/268), with a statistically significant difference (P<0.001). Compared with the control group, the ethionine group showed elevated KDM5A mRNA and protein levels, accompanied by reduced H3K4me3 modification levels (all P<0.001); protein expression of β-catenin, TCF4, and Axin2 were decreased (P<0.01, P<0.05), whereas p-GSK3β was increased (P<0.01). Following GSK-4J intervention, the expression of β-catenin, TCF4, and Axin2 was partially restored (all P<0.01), and the percentage of Cyclin D1-positive cells, as well as the expression of PCNA and c-Myc were increased (all P<0.05). Ethionine participates in NTD development by upregulating KDM5A to decreased H3K4me3 levels, inhibiting Wnt/β-catenin signaling pathway, and reducing neuroepithelial cell proliferation. Thus, targeting the KDM5A/H3K4me3 axis may provide a new strategy for the prevention and treatment of NTD. - Source: PubMed
Gao J JMu QZhang HZhang X BCao RZhang LGuo Y Y - This study aimed to investigate the modulatory function of microRNA-1246 (miR-1246) in the odontogenic differentiation of human dental pulp stem cells (hDPSCs) under inflammatory conditions in vitro and to elucidate its underlying molecular mechanism. - Source: PubMed
Publication date: 2026/09/17
Wu ShunyingWang YueyanYang Jiayi - We previously investigated whether maternal high-fat diet (HFD) exposure alters lupus nephritis (LN) progression in MRL/lpr offspring. Contrary to expectation, maternally HFD-exposed offspring showed delayed and attenuated nephritic progression compared with control diet offspring. The maternal HFD developmental impact on LN remains unclear. Here, integrated amniotic fluid metabolomics and fetal liver transcriptomics revealed that maternal HFD reshaped the intrauterine molecular environment, particularly involving steroid hormone biosynthesis and Wnt/β-catenin-associated regulatory networks. Methylome profiling further demonstrated broad CpG hypomethylation, immune-related differentially methylated region enrichment, and an inverse association between global CpG methylation and oxidative genomic DNA damage. Among candidate regulatory nodes, Axin2, a canonical Wnt/β-catenin target and feedback regulator, emerged as a potential link between fetal nutritional exposure, epigenetic remodeling, and persistent pathway modulation. Although whole-locus and gene body methylation of Axin2 were not markedly altered, promoter-region methylation showed an increasing tendency under maternal HFD exposure. In adult offspring, maternal HFD was associated with reduced Axin2 protein expression, decreased Wnt-responsive transcripts, increased peripheral corticosterone levels, and attenuation of LN progression. The inverse association between Axin2 expression and corticosterone further suggested coupling between suppressed Wnt pathway output and steroid hormone remodeling. Together, these findings support a developmental model in which maternal HFD reshapes the fetal intrauterine environment and establishes a persistent Wnt-steroid hormone-epigenetic regulatory axis that unexpectedly attenuates LN progression in genetically susceptible offspring. - Source: PubMed
Publication date: 2026/09/10
Liu ShuangSuzuki YasuyukiTakemasa ErikaSugiyama TakashiMogi Masaki - Wnt signaling coordinates lung specification, alveolar maturation, adult epithelial maintenance, and injury repair, but its biological output varies with developmental or disease stage, anatomical compartment, responding cell type, receptor context, and signal duration. This review organizes current evidence using a temporal-spatial framework that links Wnt ligands and receptors to source and responding cells, downstream canonical or noncanonical pathways, interacting signaling networks, and cellular outcomes. During development, mesenchymal Wnt2/2 b-β-catenin signaling specifies pulmonary endoderm, whereas canonical and noncanonical Wnt programs subsequently regulate distal progenitor expansion, branching geometry, epithelial differentiation, secondary septation, pulmonary microvascular maturation, and postnatal lung growth; maintenance of an alveolar type 2 (AT2) progenitor niche becomes a distinct function in the adult lung. After adult alveolar injury, Wnt activity is dynamically remodeled as AT2 cells proliferate and traverse damage-associated transient progenitor and keratin 8-positive (KRT8) transitional states before restoring the alveolar type 1 cell layer. This framework helps reconcile apparently discordant observations in chronic lung diseases. Bronchopulmonary dysplasia disrupts Wnt timing during alveologenesis; chronic obstructive pulmonary disease can combine deficient canonical Wnt responsiveness in the alveolar compartment with Wnt5a-associated inhibition of repair and distinct airway Wnt activation; and idiopathic pulmonary fibrosis features persistent Wnt-transforming growth factor-β signaling in abnormal epithelial and fibroblast niches. Therapeutic translation should therefore avoid indiscriminate pathway activation or inhibition and instead pursue reversible, local, biomarker-guided modulation matched to disease stage, cellular compartment, receptor profile, dose, and duration. - Source: PubMed
Publication date: 2026/08/26
Ren MingyueSong GuihuaXu YanYu SupingZhang YanSun MengmengZhang Bingxue - Aberrant repair/regeneration of alveolar epithelial stem cells is a key driver of pulmonary fibrosis (PF). While βPAK-interacting exchange factor (βPIX) is connected to stem cell signaling, its role in pulmonary fibrosis (PF) remains unknown. Here, we generated conditional βPIX knockout mice to investigate its contribution to PF pathogenesis. Selectively depleting βPIX in alveolar type 2 (AT2) cells led to progressive PF in mice, recapitulating the key features observed in human idiopathic pulmonary fibrosis (IPF), where AT2 cells exhibit significantly reduced βPIX levels. Single-nucleus RNA sequencing of the lungs of βPIX-deficient mice revealed the emergence of progenitor cells in a transitional stem cell state with senescent attributes, along with active, collagen-producing myofibroblasts. Mechanistically, the loss of βPIX impaired AT2 cell stemness by downregulating Wnt/β-catenin signaling. AT2 cells from IPF patients also presented reduced levels of β-catenin and Axin2, confirming the downregulation of Wnt/β-catenin signaling. Treatment with a glycogen synthase kinase-3β inhibitor reactivated Wnt/β-catenin signaling and attenuated fibrosis in βPIX-deficient mice. Our results establish a direct causal link between βPIX deficiency and PF, highlighting βPIX and its downstream pathway as promising therapeutic targets for this devastating disease. - Source: PubMed
Publication date: 2026/09/10
Kim Han-ByeolSong WoogilKim Sun-OkPark Jin-HeeHan JunyeolLee Ok-JunSoung Nak-KyunYang BumheeChoi JinwookSchwartz Martin AlexanderLee Jeong SeokShin Eun-YoungKim Eung-Gook