ABLIM3 contains a LIM domain, a double zinc finger motif that facilitates protein-protein interactions . Its primary functions include:
Cytoskeleton regulation: Interacting with actin filaments to maintain cellular structure .
Cell adhesion: Contributing to adherens junction stability, which regulates epithelial integrity .
Cancer progression: Implicated in metastasis mechanisms, particularly in neuroblastoma, where low ABLIM3 expression correlates with poor prognosis .
ABLIM3 antibodies are employed in diverse experimental workflows:
Western Blotting (WB):
Used to quantify ABLIM3 protein levels in lysates from neuroblastoma cell lines (e.g., SK-N-AS, SK-N-BE2) . Example: ABLIM3 knockdown via shRNA in NB cells reduced ITGA3, ITGA8, and KRT19 expression, enhancing metastatic potential .
Immunohistochemistry (IHC):
Localizes ABLIM3 in tumor tissues, revealing its downregulation in metastatic neuroblastoma samples .
Immune Microenvironment Analysis:
Correlates ABLIM3 expression with tumor-infiltrating immune cells, such as CD4+ T cells and macrophages, using tools like CIBERSORT .
ABLIM3 downregulation promotes NB cell migration and invasion by disrupting cell adhesion molecules (CAMs) .
TIDE analysis indicates low ABLIM3 expression predicts poor responses to immunotherapy in NB patients .
ABLIM3 interacts with ABRA to regulate actin dynamics and transcriptional activity .
Loss of ABLIM3 impairs adherens junctions, increasing epithelial permeability .
ABLIM3 antibody-based studies highlight its potential as:
Prognostic biomarker: Low expression correlates with aggressive neuroblastoma phenotypes .
Therapeutic target: Modulating ABLIM3 levels may inhibit metastasis or enhance immunotherapy efficacy .
While ABLIM3 antibodies enable robust protein detection, further studies are needed to: