The BCAM Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the BCAM gene. As polyclonal knockout cells, this product comprises a heterogeneous pool of edited cells, offering a versatile loss-of-function model to study BCAM in cell adhesion, migration, and signaling without clonal bias.
These cells originate from the HEK293T cell line, a human embryonic kidney epithelial model renowned for high transfection efficiency and episomal plasmid replication driven by the SV40 large T antigen. Derived from HEK293 cells transformed with adenovirus 5 DNA, HEK293T cells are widely employed for protein expression, viral production, and gene function analyses, making them an ideal host for studying cell-matrix interactions.
BCAM (basal cell adhesion molecule) functions as a specific receptor for laminin subunit alpha-5 (LAMA5) and forms complexes with integrin ??1 (ITGB1) and cytoskeletal adaptors alpha-actinin and filamin A. Ligand binding activates focal adhesion kinase (PTK2) and SRC, which in turn regulate RhoA and ROCK1 to drive actin polymerization. This LAMA5?CBCAM?CITGB1?CPTK2?CSRC?CRhoA?CROCK1 signaling cascade governs cell-matrix adhesion, migration, and epithelial barrier maintenance, and BCAM contributes to sickle red cell adhesion to endothelium.
Disruption of BCAM in HEK293T cells eliminates laminin-511-dependent adhesion and perturbs downstream Rho GTPase activities, providing a clean background to dissect these pathways. The polyclonal knockout pool recapitulates heterogeneous gene inactivation, enabling rapid phenotypic screening while HEK293T??s high transfectability facilitates rescue experiments with wild-type or mutant BCAM constructs. This model is therefore well-suited for dissecting BCAM-mediated signal transduction, analyzing its role in focal adhesion dynamics, and exploring crosstalk with integrin-mediated pathways.
Key applications include investigating laminin-511-dependent adhesion and migration, modeling sickle cell adhesion to endothelium, examining epithelial barrier dysfunction in disease contexts, and screening for small-molecule modulators of BCAM function. Researchers can validate the knockout by Western blotting and TIDE analysis, and assess functional consequences via laminin-511 adhesion assays, transwell migration/invasion, immunofluorescence for focal adhesion markers such as vinculin, and RhoA activation pull-downs. For additional information or to place an order, please contact Ascent Research.
