The ICAM1 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product enables loss-of-function studies of intercellular adhesion molecule 1 (ICAM1), a key adhesion receptor involved in leukocyte trafficking and viral entry. The polyclonal format provides a heterogeneous mixture of gene-disrupted cells, avoiding the clonal artifacts associated with single-cell-derived lines while maintaining robust knockout across the population.
HT29 cells are a well-established epithelial model isolated from a 44-year-old female with colorectal adenocarcinoma. These adherent cells exhibit a polarized morphology with microvilli and are widely used to investigate intestinal epithelial biology, including barrier function, inflammation, and oncogenic transformation. Their ability to form tight junctions and produce mucin makes them particularly suitable for studying cell?Ccell interactions and mucosal immune responses.
ICAM1 functions as a transmembrane glycoprotein that mediates adhesion through interactions with leukocyte integrins LFA-1 (ITGAL/CD11a) and Mac-1 (ITGAM/CD11b). Its expression is transcriptionally upregulated by pro-inflammatory cytokines such as TNF-alpha, IL-1 beta, and IFN-gamma via NF-kB and AP-1 transcription factors. Downstream, ICAM1 engagement activates signaling cascades involving RhoA, JNK, p38, and NF-kB, and modulates tight junction proteins including Occludin and ZO-1. Additionally, ICAM1 serves as a receptor for rhinovirus and associates with ERM proteins (ezrin, radixin, moesin) to link the plasma membrane to the actin cytoskeleton.
In the HT29 background, disruption of ICAM1 expression abrogates the primary adhesion receptor for leukocyte integrins, thereby impairing leukocyte adhesion and transendothelial migration. This knockout model attenuates NF-kB and MAPK signaling pathways downstream of ICAM1, reducing inflammatory cytokine production and potentially altering epithelial barrier integrity. Consequently, these polyclonal knockout cells are valuable for dissecting the molecular mechanisms governing immune?Cepithelial crosstalk and for studying how loss of ICAM1 affects intestinal homeostasis under inflammatory conditions.
Researchers can employ this knockout model in a variety of experimental setups, including leukocyte adhesion and transmigration assays using Transwell systems, measurement of transepithelial electrical resistance (TEER) to assess barrier function, and flow cytometry or immunofluorescence microscopy to confirm ICAM1 depletion. Additional applications encompass rhinovirus infection studies to examine viral entry mechanisms, cancer immuno-oncology research focusing on immune evasion and metastasis, and screening of anti-inflammatory compounds targeting the ICAM1?Cintegrin axis. For further technical details and ordering information, please contact Ascent Research.
