CTNND1 antibody
- Known as:
- CTNND1 (anti-)
- Catalog number:
- orb48338
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CTNND1 antibody
Related genes to: CTNND1 antibody
- Gene:
- CTNND1 NIH gene
- Name:
- catenin delta 1
- Previous symbol:
- CTNND
- Synonyms:
- KIAA0384, p120, p120cas, p120ctn
- Chromosome:
- 11q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-18
- Date modifiied:
- 2015-11-19
Related products to: CTNND1 antibody
Related articles to: CTNND1 antibody
- Acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors remains the principal barrier to durable responses in non-small cell lung cancer (NSCLC), yet how the molecular interaction networks underlying this resistance reorganize over time is poorly understood. We reasoned that a systems-level signature of resistance should be visible in the way protein interaction networks remodel under sustained drug exposure, and therefore applied time-resolved network analysis to isogenic gefitinib-sensitive PC9 and gefitinib-resistant PC9R cells across 24 h of gefitinib treatment, computing network entropy and centrality measures for temporal protein interaction networks and interrogating co-expression-augmented networks for candidate resistance-associated bottleneck proteins. Network entropy rose in both phenotypes, indicating that entropic remodeling is a general response to EGFR pathway perturbation rather than a signature of resistance. In contrast, eigenvector entropy was higher in resistant cells at the earliest post-treatment time point, and resistant cells preserved giant-component connectivity and small-world topology early before fragmenting later. Temporal centrality analysis nominated BIRC3 as a resistant-cell-associated high-centrality node at 24 h, and co-expression analysis identified delta-catenin (CTNND1) as a high-betweenness bottleneck in the PC9R network, topologically bridging EGFR, VAV3, HIF3A, and NOTCH2. These findings nominate early post-treatment eigenvector entropy and a CTNND1-centered, EGFR-enriched subnetwork as candidate resistance-associated features that require validation in independent datasets and functional models. - Source: PubMed
Publication date: 2026/09/21
Tsakona Dimitra CPapanikolaou Nikolaos A - Salivary duct carcinoma is a rare, aggressive salivary gland malignancy that morphologically and immunophenotypically resembles breast ductal carcinoma. The rhabdoid variant is characterized by discohesive tumor cells with rhabdoid cytomorphology, frequent loss of E-cadherin expression, and morphologic overlap with pleomorphic invasive lobular carcinoma of the breast. We report a 74-year-old man who presented with an enlarging right buccal mass and trismus. Positron emission tomography-computed tomography demonstrated right cervical lymphadenopathy with no evidence of breast or lung primary. Resection revealed a discohesive, infiltrative tumor composed of pleomorphic rhabdoid cells, with scattered cells containing intracytoplasmic mucin imparting a signet-ring morphology, and prominent targetoid perineural invasion. Immunohistochemically, the tumor showed diffuse positivity for keratin 7, gross cystic disease fluid protein 15 (GCDFP15/PIP), androgen receptor, weak GATA3 expression, loss of E-cadherin, and cytoplasmic p120-catenin (CTNND1) staining, a profile closely resembling that of invasive lobular carcinoma. Extensive nodal metastases were identified. Despite multimodal therapy, the disease recurred. This report highlights the importance of recognizing salivary duct carcinoma with rhabdoid features to avoid misdiagnosis and guide appropriate management. - Source: PubMed
Publication date: 2026/09/19
Khalid Muhammad HassaanChristie-Nguyen Phuoc TAshfaq MaryamKakarala BhanupriyaIbrahim Nourhan GSaluja Karan - Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, with metastasis accounting for over 90% of CRC deaths. While the role of extracellular vesicles (EVs) in cancer progression is recognised, their impact on invasive behaviour and extracellular matrix (ECM) remodelling within physiologically relevant three-dimensional (3D) microenvironments remains poorly understood. This study utilised quantitative organotypic 3D models to investigate how EVs derived from primary (SW480) and metastatic (SW620) CRC cell lines influence invasion, stromal activation, and ECM remodelling. We developed models incorporating CRC cells, fibroblasts, endothelial cells, and macrophages to mimic the tumour microenvironment (TME) and lung stroma. EVs isolated from SW480 and SW620 cells were isolated and characterized according to MISEV guidelines and introduced into the models. Treatment with metastatic SW620 EVs significantly enhanced depth and extent of CRC cell invasion compared to primary SW480 EVs or controls, and increased invasion of multicellular clusters. Immunofluorescence analysis revealed elevated expression of cadherin 2 (CADH2) and catenin delta 1 (CTNND1) in SW620 EV-treated models, indicating involvement of epithelial-mesenchymal transition (EMT). In lung stroma models, SW620 EVs reduced matrix stiffness, implying ECM remodelling. Mass spectrometry and multivariate analysis identified distinct proteomic signatures in SW620 EV-treated models, with significant alterations in collagen type XI expression and unique mass-to-charge (m/z) peaks, indicating selective ECM remodelling. SW620 EVs also induced activation of stromal fibroblasts and endothelial cells, as evidenced by increased α-smooth muscle actin (α-SMA) and von Willebrand Factor (vWF) expression. These findings demonstrated that metastatic CRC-derived EVs enhance invasive behaviour and remodel the ECM, creating a permissive microenvironment for metastasis. The differential effects of primary versus metastatic EVs underscore the importance of tumour stage-specific vesicle signatures in CRC progression. This study provides a robust 3D model framework to quantify EV-mediated mechanisms and identify therapeutic targets to disrupt pro-metastatic communication in CRC. - Source: PubMed
Publication date: 2026/09/17
Guarnerio SoniaCole LauraMaani RawanTempest RobMirnezami AlexHughes PaulHunt StuartMaitre Christine LeChapple KeithPeake Nick - In breast cancer immunotherapy, Mucin 1 (MUC1) is a well-established target with promising preclinical results; however, single targeting of MUC1 has demonstrated limited efficacy in clinical trials, largely due to tumor heterogeneity, diverse glycosylation patterns, and an immunosuppressive TME. Identification of complementary co-targets enables bi-specific or dual-target immunotherapy, limiting antigen escape, improving specificity, and reducing relapse. Here, we employed a comprehensive multi-layered analytical approach to evaluate MUC1 expression, clinical relevance, and methylation status, followed by systematic screening of MUC1-correlated genes. Antigenicity prediction and protein-protein interaction analyses identified Forkhead Box A1 (FOXA1) as a potential functional partner. Expression analysis revealed concordant patterns of MUC1 and FOXA1 across breast cancer samples, while network mapping demonstrated shared interactions with adhesion-associated proteins, including CTNNB1, CTNND1, and CDH1, suggesting roles in epithelial organization and tumor progression. Further validation using gene expression datasets from Indian breast cancer cohorts confirmed consistent expression and correlation patterns, supporting reproducibility across populations. Immune profiling revealed an inverse association between MUC1-FOXA1 co-expression and immune-related gene signatures, with high co-expression linked to reduced infiltration of dendritic cells, CD4⁺ and CD8⁺ T cells, macrophages, and natural killer cells, indicative of an immunosuppressive microenvironment. Negative correlations with MHC Class I genes further suggested impaired antigen presentation. Epitope prediction identified high-affinity peptides from both targets with strong MHC Class I binding potential. Collectively, these findings support the associated role of MUC1 and FOXA1 as dual immunotherapeutic targets in breast cancer. - Source: PubMed
Publication date: 2026/09/11
Chakraborty DebolinaKundu SubhadipGupta VinitPatel MansiRawal Sudhir KumarMani Samson - Pulmonary fibrosis is a chronic progressive disease, caused by numerous factors, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Damage to the alveolar epithelial barrier (formed by junctions between alveolar epithelial cells I) has been described as a key mechanism of early fibrosis and therefore could be crucial for COVID-19-associated sequelae. The integrity of adherens junctions is regulated by p120 catenin and is crucial for barrier regulation in epithelial-mesenchymal-transition-driven diseases such as fibrogenesis and cancer. Abundance and expression of p120 catenin and intercellular contact regulating proteins (caveolin-1, P2X7R) were investigated retrospectively in COVID-19 lungs (acute, chronic) compared with healthy controls and interstitial lung disease of different etiologies (n = 6). p120 Catenin was further investigated in early injury models using profibrotic agents in murine lung and human alveolar epithelial cell culture. p120 Catenin abundance was higher in chronic COVID-19 compared with acute COVID-19, suggesting a role in fibrotic development. The interacting proteins caveolin-1 and P2X7R were simultaneously decreased in COVID-19, indicating a role in early pathophysiology. Early epithelial damage showed no changes in p120 catenin and its phospho-Y228 site in cell culture whereas p120 catenin was reduced in murine lung culture. Thus, alterations in and interactions between p120 catenin and caveolae associated proteins may represent a potential mechanism underlying COVID-19-induced pulmonary fibrosis. - Source: PubMed
Publication date: 2026/09/11
Wiegner JuliánKasper MichaelSchmidt Mirko H HBarth Kathrin