Ctnnb1
- Known as:
- Ctnnb1
- Catalog number:
- 060587A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Ctnnb1
Related genes to: Ctnnb1
- Gene:
- CTNNB1 NIH gene
- Name:
- catenin beta 1
- Previous symbol:
- CTNNB
- Synonyms:
- beta-catenin, armadillo
- Chromosome:
- 3p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-13
- Date modifiied:
- 2019-04-23
Related products to: Ctnnb1
ACTN4 & CTNNB1 Protein Protein Interaction Antibody PairACTN4 & CTNNB1 Protein Protein Interaction Antibody Pair pairsAnserine Catenin, Beta Elisa Kit (CTNNb1)Anserine anti - Catenin, Beta Elisa Kit (CTNNb1)anti-CTNNB1 Beta Catenin (4D5)anti-CTNNB1 Beta Catenin (4D5) type: Primary antibodies host: Mouseanti-CTNNB1 Beta Catenin (EM-22)anti-CTNNB1 Beta Catenin (EM-22) type: Primary antibodies host: Mouseanti-CTNNB1 (4D5)Anti-CTNNB1 (4D5), Mouse Monoclonal to CTNNB1, Isotype IgG1, Host MouseAnti-CTNNB1 (EM-22), Mouse Monoclonal to CTNNB1, Isotype IgG1, Host Mouseanti-CTNNB1 / Beta Catenin (4D5)anti-CTNNB1 / Beta Catenin (EM-22)Anti-CTNNB1, Rabbit Polyclonal to CTNNB1, Isotype , Host RabbitAnti-CTNNB1, Rabbit Polyclonal to CTNNB1, Isotype IgG, Host Rabbit Related articles to: Ctnnb1
- Mutations in CTNNB1 are recognized oncogenic drivers of hepatocellular carcinoma (HCC); however, the downstream effector molecules and their prognostic significance remain incompletely defined. In this study, we developed a mutant CTNNB1 gene signature (MCGS) to predict CTNNB1 mutation status and to evaluate the prognostic relevance of the constituent genes. - Source: PubMed
Publication date: 2026/06/26
Zhu NingqiZhang GuoShen XiaotianChen ZuleLi YingChen DiyuJia Huliang - Molecular characterisation of odontogenic cysts and tumours has advanced recently and molecular pathogenesis for several tumour types is included in the 5th edition World Health Organisation (WHO) classification of head and neck tumours. This narrative review examines critically the genetic and signalling alterations reported in odontogenic cysts and tumours and groups them by the signalling pathways affected: MAPK/ERK (mostly BRAF and KRAS mutations), Wnt/beta-catenin (mostly CTNNB1 mutations) and HH (PTCH1 mutations). Odontogenic tumours characterized by gene rearrangements are also discussed. Apparent negative results and areas requiring further analysis are included. These genetic signatures illustrate the successes and limitations in interpreting molecular data for classification, diagnosis, pathogenesis, and targeted therapies for odontogenic tumours. - Source: PubMed
Publication date: 2026/06/18
Guimarães Letícia MartinsOdell Edward WGomes Carolina Cavalieri - Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, characterized by marked molecular heterogeneity, late-stage diagnosis, and limited therapeutic options. Emerging evidence highlights the interplay between cytoskeletal dynamics, epigenetic regulation, and oncogenic signaling pathways in hepatocarcinogenesis. Histone deacetylase 6 (HDAC6), a key regulator of cytoplasmic protein acetylation, modulates α-tubulin stability, while CTNNB1 (β-catenin) serves as a central effector of the Wnt signaling pathway. However, the existence and functional relevance of a coordinated HDAC6-TUBA1A-CTNNB1 regulatory axis in HCC remain insufficiently explored. We conducted a comprehensive integrative bioinformatic analysis using multiple publicly available datasets and platforms, including TCGA, GEO, GEPIA3, TNMplot, UALCAN, TIMER2.0, STRING, ENCORI, HPA, TargetScan, miRDB, CRISPRdb, GSCALite, and exoRBase. Gene expression, promoter methylation, survival associations, immune infiltration, regulatory RNA interactions, and therapeutic targetability were systematically evaluated. HDAC6 expression was significantly downregulated in HCC tissues, whereas TUBA1A and CTNNB1 were upregulated. Reduced HDAC6 expression was associated with poorer survival outcomes, while TUBA1A and CTNNB1 showed no significant prognostic value. Methylation analysis revealed gene-specific epigenetic alterations, including hypomethylation of CTNNB1 and differential methylation patterns in HDAC6 and TUBA1A. Immune infiltration analysis demonstrated that HDAC6 expression positively correlated with cytotoxic immune cell populations and negatively with immunosuppressive subsets. Regulatory network analyses identified lncRNA-miRNA-mRNA interactions, particularly involving SNHG1. Furthermore, in silico CRISPR targetability and extracellular vesicle (EV) transcript profiling suggested potential translational applicability of this axis. Our findings support a hypothesis of the existence of a dysregulated HDAC6-α-tubulin-β-catenin axis in HCC, linking cytoskeletal remodeling with oncogenic signaling and immune modulation. This axis may indicate a promising candidate for biomarker development and targeted therapeutic strategies, warranting further experimental validation. - Source: PubMed
Publication date: 2026/06/09
Bayram ErgulBroggi GiuseppeAyan Durmus - Gestational diabetes mellitus (GDM) is a common metabolic disorder characterized by insulin resistance and systemic inflammation. Emerging evidence suggests that the Wnt/β-catenin signaling pathway may play a role in metabolic dysregulation; however, its clinical relevance in GDM remains unclear. This study aimed to evaluate the diagnostic value of Wnt signaling-related biomarkers, including Wnt-inhibitory factor 1 (WIF-1), secreted frizzled-related protein-4 (SFRP-4), and beta-catenin-1 (CTNNB1) in GDM. This case-control study included 60 patients with GDM and 60 healthy pregnant controls. Serum levels of WIF-1, SFRP-4, and CTNNB1 were measured and compared between groups. Receiver operating characteristic (ROC) and multivariable logistic regression assessed diagnostic performance and predictors, while correlation analysis and principal component analysis (PCA) evaluated biomarker relationships. Serum levels of WIF-1, SFRP4, and CTNNB1 were significantly higher in the GDM group (all < 0.001). ROC analysis showed moderate diagnostic performance for individual biomarkers, with CTNNB1 demonstrating the highest discriminative ability. The combined biomarker model significantly improved diagnostic accuracy, yielding the highest area under the curve (AUC), sensitivity, and specificity. In multivariable analysis, all three biomarkers remained independently associated with GDM. Correlation analysis revealed moderate interrelationships, with SFRP4 acting as a central component. PCA demonstrated partial separation between GDM and control groups, supporting the ability of Wnt signaling-related biomarkers to capture disease-associated biological variation. Wnt signaling-related biomarkers, including WIF-1, SFRP4, and CTNNB1, are significantly elevated in GDM and show promising diagnostic value. The combined biomarker approach provides superior discriminative performance compared to individual markers, highlighting its potential role in improving risk stratification and personalized management. - Source: PubMed
Publication date: 2026/06/09
Dönmez Yeliz ÇeçenKeles EsraBağlar İsmailŞanlıkan FatihKara Sahra SultanAkin Öznur DündarMisirlioglu Naile FevziyeDumur SeymaUzun Hafize - Clear cell renal cell carcinoma (ccRCC) is the most prevalent subtype of renal cancer, characterized by frequent metastasis and poor prognosis. Epithelial-mesenchymal transition (EMT) plays a pivotal role in tumor progression. Protocadherin 9 (PCDH9) has emerged as a potential tumor suppressor, but its relationship with EMT markers in ccRCC remains unclear. This study aimed to investigate the expression patterns and prognostic significance of PCDH9, β-catenin (CTNNB1), Snail (SNAI1), and Vimentin (VIM) in ccRCC. Immunofluorescence analysis was performed on formalin-fixed paraffin-embedded tissue sections from 48 ccRCC patients (31 low-grade, 17 high-grade) and adjacent normal renal cortex. Findings were validated using The Cancer Genome Atlas (TCGA-KIRC) dataset via GEPIA2/GEPIA3 platforms, including differential expression, correlation, and survival analyses. mRNA was significantly downregulated in ccRCC tumors (TCGA-KIRC), while was upregulated at the transcriptomic level. Tissue-level immunofluorescence quantification revealed discordant patterns, highlighting the influence of cellular heterogeneity on bulk protein assessment. The strong positive correlation between and observed in normal kidney was completely lost in tumor tissue. Unexpectedly, showed positive correlations with EMT transcription factors (, ) in tumors. In univariate survival analysis, high and expression were associated with improved overall survival. Multivariate Cox regression revealed endpoint-specific prognostic signatures: independently predicted disease progression, while predicted overall mortality. was consistently protective across both endpoints. Our findings support a tumor-suppressive role for in ccRCC and reveal disruption of epithelial adhesion molecule co-regulation during tumorigenesis. The identification of endpoint-specific prognostic signatures has implications for patient stratification and suggests that ccRCC exhibits a partial EMT phenotype rather than classical EMT. - Source: PubMed
Publication date: 2026/05/24
Smoljo LaraMateljak TonkaRacetin AnitaTodorović PetarKomić JelenaKomić LukaĐolonga PetarGrubišić Danijel AntonioKostić SandraVukojević KatarinaKelam Nela