The ITGAM Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the ITGAM gene has been disrupted to impair expression of integrin subunit alpha M (CD11b). This product offers a genetically heterogeneous loss-of-function model of ITGAM without requiring clonal isolation, enabling functional studies of CD11b-dependent biology in a malignant bone-forming context. The polyclonal format simplifies experimental setup while providing a robust platform for assays that benefit from population-level gene disruption.
The host cell line 143B is a human osteosarcoma line derived from a 13-year-old female patient. These malignant bone-forming cells are widely used in bone cancer and metastasis research, providing a relevant model for studying tumor cell adhesion, invasion, and interaction with the bone microenvironment. The 143B background makes this knockout model particularly relevant for investigating how loss of ITGAM influences osteosarcoma cell behavior.
ITGAM encodes integrin ??M, which pairs with the ??2 subunit (ITGB2/CD18) to form the Mac-1 (CR3) receptor. Mac-1 is activated by ligands including ICAM-1, iC3b, and fibrinogen, and mediates critical processes such as leukocyte adhesion, transendothelial migration, and complement-mediated phagocytosis. ITGAM transcription is upregulated by pro-inflammatory stimuli TNF-??, IL-1, and LPS through transcription factors PU.1, C/EBP, and AP-1. Ligand-bound Mac-1 signals via the associated kinases Syk and FAK, culminating in activation of the PI3K/AKT and NF-??B pathways, which promote expression of inflammatory mediators like IL-6 and TNF-??. In this knockout model, disruption of ITGAM impairs these signaling cascades, providing a clear background to investigate CD11b-dependent cellular responses.
In the 143B osteosarcoma context, ITGAM knockout allows investigation of integrin ??M in tumor cell adhesion, migration, and matrix interactions. The model facilitates study of Mac-1-independent mechanisms, serves as a control for antibody specificity assays, and helps elucidate CR3 roles in tumor microenvironment communication.
These polyclonal knockout cells are suitable for a wide range of assays, including flow cytometry and Western blotting for verification of CD11b depletion, adhesion assays to dissect integrin binding properties, phagocytosis assays to evaluate pathogen clearance mechanisms, RT-qPCR for analyzing downstream gene expression changes, and migration/invasion assays to model metastatic behavior. They also serve as an ideal negative control for antibody specificity testing and can be used to study how loss of CR3 affects tumor-microenvironment crosstalk. For additional information or to discuss custom requirements, please contact Ascent Research.
