CTNNAL1抗体

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     The image is immunohistochemistry of paraffin-embedded Human liver cancer tissue using P00231(CTNNAL1 Antibody) at dilution 1/30. (Original magnification: ×200)    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human gastric cancer tissue using P00231(CTNNAL1 Antibody) at dilution 1/30. (Original magnification: ×200)    

  
  

**Background of CTNNAL1 Antibody**

CTNNAL1 (Catenin Alpha-Like 1), also known as α-catulin, is a cytoplasmic protein belonging to the α-catenin family. It shares structural homology with αE-catenin and αN-catenin, featuring an N-terminal vinculin-binding domain and a C-terminal actin-binding region. Unlike classical α-catenins, CTNNAL1 does not directly interact with β-catenin or participate in cadherin-mediated cell adhesion. Instead, it functions as a scaffolding protein involved in regulating cytoskeletal dynamics, cell motility, and signal transduction pathways, including Rho GTPase and NF-κB signaling.

CTNNAL1 is implicated in various physiological and pathological processes. Studies highlight its role in cancer progression, particularly in promoting tumor invasion, metastasis, and epithelial-mesenchymal transition (EMT) in cancers such as lung adenocarcinoma and hepatocellular carcinoma. It also contributes to cardiovascular development and neuronal differentiation. Dysregulation of CTNNAL1 has been linked to inflammatory diseases and fibrosis.

CTNNAL1 antibodies are essential tools for detecting and quantifying CTNNAL1 expression in research applications like Western blotting, immunohistochemistry, and immunofluorescence. These antibodies aid in elucidating CTNNAL1's molecular interactions, subcellular localization, and mechanistic roles in disease models. Commercial CTNNAL1 antibodies are typically raised against specific epitopes, with validation in multiple species and sample types, ensuring specificity for experimental reproducibility. Their use continues to advance understanding of CTNNAL1's dual roles in cellular homeostasis and disease pathogenesis.