The ICAM1 Knockout A-549 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line. This polyclonal pool carries targeted disruptions of the ICAM1 gene, resulting in a loss-of-function model for studying ICAM-1-dependent cellular processes. As a polyclonal knockout cell population, it provides a heterogeneous genetic background that avoids clonal selection biases, making it suitable for robust functional assays.
The host cell line, A-549, is an adherent epithelial cell line established from human lung adenocarcinoma. It serves as a well-characterized model of alveolar type II epithelium and is extensively employed in respiratory research, oncology, and studies of pulmonary inflammation. A-549 cells endogenously express relevant adhesion molecules and signaling components, offering a physiologically relevant platform for investigating ICAM-1 functions in lung-derived contexts.
ICAM-1 (Intercellular Adhesion Molecule 1) is a transmembrane glycoprotein central to leukocyte adhesion and transendothelial migration. It binds integrins LFA-1 (ITGAL/ITGB2) and Mac-1 (ITGAM/ITGB2), as well as fibrinogen, activating downstream Src family kinases, MAPK/ERK (MAPK1), and Rho GTPases (RAC1). ICAM-1 expression is transcriptionally upregulated by NF-kappaB and AP-1 in response to TNF-alpha, IL-1 beta, IFN-gamma, and LPS. This signaling culminates in the production of pro-inflammatory cytokines such as IL-6 and IL-8, linking ICAM-1 to NF-kappa B-mediated inflammatory responses and cell adhesion pathways.
Knockout of ICAM1 in A-549 cells disrupts ICAM-1-dependent adhesion and leukocyte interactions, impairing inflammatory signaling and metastatic behavior. Given the A-549 background, this model is particularly valuable for dissecting ICAM-1’s role in lung cancer cell migration, invasion, and immune evasion. It enables the study of tumor-stromal crosstalk within the pulmonary microenvironment and the functional consequences of blocking ICAM-1?Cmediated leukocyte engagement.
This polyclonal knockout cell population supports a broad range of applications, including cell adhesion mechanism studies, tumor metastasis modeling, and leukocyte-cancer cell interaction assays. Researchers can assess inflammatory signaling downstream of cytokines and evaluate anti-adhesion therapeutic candidates. Compatible assays include Western blotting, RT-qPCR, flow cytometry, cell adhesion and leukocyte adhesion assays, migration/invasion assays, immunofluorescence, and ELISA-based cytokine profiling. The polyclonal nature minimizes clonal artifacts while maintaining robust knockout effects. For further information, please contact Ascent Research.
