CTNND1 antibody Monoclonal Antibodies Primary antibodies
- Known as:
- CTNND1 (anti-) Monoclonal Antibodies Primary antibodies
- Catalog number:
- orb45432
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- CTNND1 antibody Monoclonal Antibodies Primary antibodies
Related genes to: CTNND1 antibody Monoclonal Antibodies Primary antibodies
- 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 Monoclonal Antibodies Primary antibodies
Related articles to: CTNND1 antibody Monoclonal Antibodies Primary antibodies
- 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 - : The aims of this study were to explore the genetic variants identified by Next-Generation Sequencing (NGS) in patients presenting syndromic/non-syndromic cleft palate (CP) associated with tooth agenesis (TA) and to describe the observed phenotype-genotype correlations. : A systematic review exploring PubMed, Scopus and Web of Science was conducted. Data extraction and bias assessment were performed. : From 227 screened articles, 8 studies were included. Second premolars were the most frequently missing teeth, followed by central incisors in non-syndromic CP cases. Genetic variants were most commonly reported in , , , , and . Several mutations in these genes were associated with syndromic forms such as Pierre Robin Sequence, Kallmann syndrome, and Van der Woude syndrome. : This study suggests a potential shared genetic pathway between CP and TA and supports further exploration of TA as a possible clinical indicator of syndromic cases. NGS emerges as a valuable exploratory tool for identifying such associations, though validation in larger patient cohorts remains necessary. - Source: PubMed
Publication date: 2026/08/02
Boutahari NisrineBelayachi LamiaeGhoul Sonia