CTNND1 antibody - N-terminal region (ARP51889_P050)
- Known as:
- CTNND1 (anti-) - N-terminal region (ARP51889_P050)
- Catalog number:
- arp51889_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CTNND1 antibody - N-terminal region (ARP51889_P050)
Related genes to: CTNND1 antibody - N-terminal region (ARP51889_P050)
- 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 - N-terminal region (ARP51889_P050)
Related articles to: CTNND1 antibody - N-terminal region (ARP51889_P050)
- 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 - This study was conducted at both the clinical and cellular levels, utilizing patient-derived vaginal wall tissues and cultured vaginal wall fibroblasts (VWFs). - Source: PubMed
Publication date: 2026/08/17
Liang ChunyanJiang YunJiang YiyangLin QiuhuiCao QingliSun Haishi - KIF21A, a member of the Kinesin-4 family of motor proteins, is involved in the regulation of microtubule dynamics and intracellular transport, with emerging evidence suggesting its potential role in cancer progression. In this study, we performed an integrative analysis of over 3825 human phosphoproteomics studies to characterize site-specific phosphorylation of KIF21A. Three predominant phosphosites were identified in KIF21A (S853, S1212, and S1239) with the highest detection frequency across phosphoproteomics studies, and were analyzed for co-regulation patterns to identify potential kinase associations and functional networks. Phosphosite S853 showed a strong association with cytoskeletal organization and cortical microtubule stabilization complexes (CMSCs) components, including KANK1 (S186), PHLDB2 (S513, S42) and CLASP1 (S600, S572, S646), indicating its role in cytoskeletal organization. Upstream kinase analysis identified potential regulators, such as PAK2, RPS6KA1/A3, RPS6KB1, CHEK1/2 and CDK18/16 with site-specific variability in their associations with KIF21A predominant sites. Interestingly, phosphosite-specific correlation analysis between KIF21A and candidate kinases revealed that the KIF21A S1239 phosphosite exhibited tumor-specific correlations with CDK18 across multiple cancer types. Functional enrichment revealed that co-regulated phosphoproteins were involved in cytoskeleton regulation, cell cycle regulation, and carcinogenesis. Pan-cancer analysis demonstrated dysregulated expression of KIF21A in multiple tumor types, with stage-associated upregulation in selected cancers. Gene-level validation further supported these findings, showing consistent positive correlations between KIF21A and key regulators such as CTNND1 and PTK2, as well as other cytoskeleton and cancer-associated genes. Overall, this study highlights site-specific phosphorylation as a key regulatory mechanism of KIF21A and suggests its involvement in cytoskeleton-associated signaling networks in cancer. - Source: PubMed
Publication date: 2026/07/18
Rai Shanmitha BSujina AyadathilAhmed MukhtarKammarambath Sreeshma RavindranSubair SuhailGopalakrishnan Athira PerunellyKalasa Anil Kumar Apoorva PaiJohn LevinRaju RajeshPalollathil Akhina