Wnt8A antibody
- Known as:
- Wnt8A (anti-)
- Catalog number:
- orb101870
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- Wnt8A antibody
Related genes to: Wnt8A antibody
- Gene:
- WNT8A NIH gene
- Name:
- Wnt family member 8A
- Previous symbol:
- -
- Synonyms:
- WNT8D
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-01
- Date modifiied:
- 2016-10-05
Related products to: Wnt8A antibody
Related articles to: Wnt8A antibody
- BACKGROUND: 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. METHODS: Whole exome sequencing was performed on a patient’s peripheral blood to identify DIAPH1 mutations. A zebrafish model was established by microinjecting mutant human DIAPH1 cDNA into one-cell embryos (no zebrafish DIAPH1 homolog exists). Phenotypic analyses (morphology, neuronal axon growth, behavior) and quantitative real-time PCR for Wnt/β-catenin pathway genes were conducted. Data were mean ± SEM; statistical tests (Student’s t-test, ANOVA, χ²) used GraphPad Prism 5.0 (P < 0.05, P < 0.0001 for significance). RESULTS: Compound heterozygous DIAPH1 mutations (c.1051 C > T, p.R351X; c.609delA, p.E203E fs*19) were found and associated with clinical symptoms. Mutant DIAPH1 zebrafish showed abnormal eye shape, shortened body length, axis defects, impaired motor axon growth, reduced locomotor activity, upregulated WNT8A, WNT9A, LRP5, LRP6, and downregulated AXIN1, AXIN2, β-CATENIN, indicating excessive Wnt/β-catenin pathway activation. CONCLUSIONS: DIAPH1 compound heterozygous mutations may trigger microcephaly and visual impairment by abnormally activating the Wnt/β-catenin pathway. The zebrafish model provides a reliable in vivo system for studying DIAPH1-related microcephaly, advancing understanding of hereditary primary microcephaly pathogenesis and potential therapeutic target exploration. - Source: PubMed
Publication date: 2026/04/10
Wang DayanLai PanjianWang KanWu ZhuanbinLi Xiaobing - In vertebrates, anterior (forelimbs and pectoral fins) and posterior (hindlimbs and pelvic fins) paired appendages arise from specific regions of the lateral plate mesoderm. In zebrafish, pectoral fin development illustrates a tightly coupled process in which fin field regionalization and subsequent bud initiation occur in close succession. Regionalization is governed by TBX5, which also promotes bud outgrowth. Canonical Wnt/β-catenin signaling is involved in these processes. In contrast, pelvic fin development is temporally dissociated: the presumptive pelvic fin field is regionalized during early embryogenesis, whereas fin bud initiation does not occur until metamorphosis, approximately 3 weeks later. This separation provides a unique opportunity to examine the distinct roles of Wnt/β-catenin signaling in early field regionalization and later bud initiation. Here, we show that canonical Wnt/β-catenin signaling is inactive during early pelvic fin field regionalization but is essential for fin bud initiation. Wnt/β-catenin activity, represented as GFP signals in , was undetectable in the pelvic region during early embryogenesis but became evident in both the epithelium and mesenchyme of the pelvic fin bud during metamorphosis. Notably, expression of , which activates this pathway in the early intermediate mesoderm, was not detected in the pelvic fin region at the time of bud formation. Pharmacological inhibition of Wnt/β-catenin signaling at metamorphic stages impaired pelvic fin bud outgrowth. These findings suggest that canonical Wnt/β-catenin signaling may not be involved in the early regionalization of the pelvic fin field but is essential for the later initiation of pelvic fin bud formation in zebrafish. - Source: PubMed
Nakamura YusakuIrifune AsatoKawanishi ToruTanaka Mikiko - The solute carriers (SLCs) are important membrane-bound transporters that regulate cellular nutrition, metabolism, homeostasis and survival. Emerging evidence highlights the critical involvement of SLCs in auditory physiology. To date, over ten SLC family members have been linked to hearing function. MFSD3 (also known as SLC33A2), is a putative plasma membrane-localized acetyl-CoA transporter regulating lipid metabolism and energy homeostasis. It has been found to be associated with the pathogenesis of neurodegenerative dementia and tumor progression. Nevertheless, its potential role in hearing remains unexplored. In this study, through qRT-PCR, we demonstrated that was predominantly expressed during early embryonic development in zebrafish. Morpholino-mediated knockdown in zebrafish induced inner ear malformations (hypoplastic otic vesicles, reduced otolith size) and hair cells loss in lateral line neuromasts. Additionally, Mfsd3 deficiency led to developmental defects (pericardial edema, body axis curvature) and impaired locomotor activity in zebrafish. The qRT-PCR analysis further revealed significant upregulation of key Wnt/β-catenin pathway components (, , , and ) in knockdown zebrafish. Our findings suggest as a potential participant in auditory function and embryogenesis, with implications for understanding hearing loss pathogenesis. - Source: PubMed
Publication date: 2025/09/15
Ma YingQiu Shi-WeiWang Wei-QianFeng Hai-FengZheng LuWei Ge-GeNie Hui-YiYang Jin-YuanChen Yi-JinDai PuGao XueYuan Yong-Yi - Brain injuries can result from accidents, warfare, sports injuries, or brain diseases. Identifying regeneration-associated genes (RAGs) during epigenome remodeling upon brain injury could have a significant impact on reducing neuronal death and subsequent neurodegeneration for patients with brain injury. We previously identified several WNT genes as RAGs involved in the neurite regrowth of injured cortical neurons. Among them, the expression of the gene increased most significantly during neurite regrowth, indicating its potential to promote neuronal regeneration. In this study, we investigated the regulatory mechanism of transcription. An algorithm was developed to predict the novel enhancer regions of candidate genes. By combining active enhancer marks, histone H3 lysine 27 acetylation (H3K27ac), and histone H3 lysine 4 mono-methylation (H3K4me1), we identified a candidate enhancer region for located 1.7 Mb upstream and 0.1 Mb downstream of the gene. This region was organized into enhancers (Ens) 1-15. Enhancer RNA expression from the predicted En1-15 regions, DNA topological dynamics, and the activity of predicted enhancers were analyzed to validate the candidate active enhancers. Our findings showed that the En8, 9, 10, 14, and 15 regions expressed higher eRNAs during neurite regrowth. Notably, the En8-2 and En14-2 subregions showed significantly up-regulated H3K4me1 modification during neurite regrowth. Using chromatin conformation capture assays and enhancer-reporter assays, we delineated that the molecular regulation of transcription during neurite regrowth occurs through looped En8-promoter interplay. - Source: PubMed
Publication date: 2025/02/20
Weng Shr-HanLiao Wen-LingChen Linyi - Wnt signaling has long been implicated in cancer development, but recent studies have revealed new insights into how Wnt ligands themselves drive metastasis. Currently, research identifies Wnt1, Wnt2, Wnt2b, Wnt3, Wnt3a, Wnt4, Wnt5a, Wnt5b, Wnt6, Wnt8a, Wnt9b, Wnt10a, Wnt10b, and Wnt16 as pro-metastatic Wnt ligands, while Wnt7a, Wnt7b, Wnt8b, Wnt9a, and Wnt11 exhibit conflicting pro- and anti-metastatic roles. These ligands arise from diverse sources in the tumor microenvironment and perform a wide range of roles in the metastatic cascade, including epithelial-to-mesenchymal transition, matrix metalloproteinase production, cell motility, angiogenesis, cell death resistance, and mesenchymal-to-epithelial transition. Their diverse and critical roles in metastasis make Wnt ligands attractive therapeutic targets. - Source: PubMed
Caroland Kailey PTrapani Jonathan BLee EthanWeiss Vivian L