The ICAM1 Knockout 769-P Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human renal epithelial cell line 769-P. This product features targeted disruption of the ICAM1 gene, producing a heterogeneous loss-of-function model for studying intercellular adhesion molecule 1 functions in a renal carcinoma background. The polyclonal format represents a versatile tool for investigating ICAM1-dependent processes without clonal selection bias.
The 769-P host cell line is a human clear cell renal cell carcinoma model that retains epithelial features and is widely used in cancer and immunology research. Its origin from a primary renal carcinoma makes it particularly relevant for studying tumor progression, metastasis, and immune cell interactions. As an adherent epithelial line, 769-P provides a physiologically appropriate context for examining cell adhesion, polarization, and inflammatory signaling pathways.
ICAM1 is a transmembrane adhesion receptor that binds ??2 integrins LFA-1 (ITGAL/ITGB2) and Mac-1 (ITGAM/ITGB2) to mediate firm leukocyte adhesion and transendothelial migration. This interaction triggers intracellular signaling via MAPK1/ERK2 and NFKB1, regulated by upstream stimuli such as TNF, IL1B, IFNG, and lipopolysaccharide through transcription factors NFKB1 and RELA. ICAM1 also serves as a receptor for rhinovirus and Plasmodium falciparum PfEMP1, and associates with fibrinogen and hyaluronan. Together with VCAM1, SELE, PECAM1, ITGAL, ITGAM, and CCL2, it forms a core network in leukocyte trafficking and inflammation.
In 769-P renal carcinoma cells, ICAM1 knockout disrupts the primary adhesion mechanism for leukocyte recruitment and alters tumor-stroma crosstalk. This loss-of-function model enables dissection of ICAM1??s role in renal cell carcinoma metastasis, immune evasion, and regulation of downstream effectors including NFKB1 and MAPK1. The polyclonal population reflects tumor heterogeneity, allowing researchers to assess varied cellular responses within the cancer context and to interrogate ICAM1-dependent signaling in a disease-relevant background.
These knockout cells are suitable for leukocyte adhesion and Transwell migration assays, co-culture tumor-immune interaction studies, and flow cytometry or immunofluorescence to confirm ICAM1 loss. Western blotting, NF-kB luciferase reporter assays, rhinovirus infection experiments, and malaria cytoadherence studies can be performed. The model also supports anti-inflammatory drug screening targeting ICAM1-mediated pathways. For more information or to discuss custom projects, contact Ascent Research.
