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)
- : 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 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 - Bone metastasis develops within a specialized marrow ecosystem where hematopoiesis, immune regulation, vascular trafficking, and skeletal remodeling intersect. Neutrophil-lineage cells occupy a unique position in this setting because they are generated, retained, mobilized, aged, and reprogrammed within the same bone marrow niches that disseminated tumor cells exploit for homing and survival. This review examines how neutrophils, tumor-associated neutrophils, immature neutrophils, low-density neutrophils, and PMN-MDSCs shape skeletal colonization. We discuss tumor-to-marrow signaling, CXCR2-dependent recruitment, CXCR4/CXCL12-mediated marrow retention, neutrophil-circulating tumor cell interactions, vascular arrest, dormancy escape, NET-mediated matrix remodeling, immune suppression, and effects on osteoclast-osteoblast coupling. Evidence is strongest in breast and prostate cancer models, where pathways such as CXCL5/CXCR2, CTNND1-CXCR4/CXCL12, PR3-RAGE, and DKK1-CKAP4-STAT6-CHI3L3 link neutrophil-lineage cells to skeletal progression and immunotherapy resistance. However, several mechanisms, including CTC-neutrophil clustering and NET-driven dormancy awakening, remain partly extrapolated from non-skeletal models. We therefore emphasize evidence hierarchy, methodological limitations, and therapeutic opportunities, arguing that selective reprogramming or functional inhibition of pro-metastatic neutrophil states may be more promising than indiscriminate neutrophil depletion in metastatic bone disease. A clearer understanding of these context-dependent neutrophil programs may help refine biomarker development and guide combination therapies for patients with skeletal metastases. - Source: PubMed
Publication date: 2026/07/03
Hamza Fatheia NZhra MahmoudHolail JasmineAlotab SamaaAlshater SidraAl-Masud Alaa AMohammad Khalid Said - Gastric cancer is the fifth most commonly diagnosed cancer. Although 10% of cases show familial clustering, a monogenic hereditary cause is rarely observed. Little is known about the molecular profile of familial gastric cancer cases in Brazil. Thus, we aimed to characterize the germline genomic profile of patients with potentially hereditary gastric cancer in the Brazilian population. - Source: PubMed
Publication date: 2026/07/14
de Souza Deivid CalebeBuranello ThalianeNeto Dario Tenorio TavaresPisani Janina PontesRibeiro Giovanna Napolitano PereiraOlandoski MarciaSchlesinger DavidKitajima João PauloViana Danilo VilelaAchatz Maria Isabel