The CD4 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 786-O cell line, featuring targeted disruption of the CD4 gene. This product provides a stable loss-of-function model for studying CD4 biology without reliance on transient knockdown approaches. The polyclonal format retains genetic diversity while ensuring consistent gene disruption across the population.
The host 786-O line is a clear cell renal cell carcinoma (ccRCC) epithelial model characterized by a VHL tumor suppressor mutation, leading to constitutive stabilization of hypoxia-inducible factors. This VHL-deficient background drives pseudohypoxic signaling and tumorigenic potential, making it a widely employed system for ccRCC research and CRISPR-based genetic modification.
CD4 encodes a transmembrane glycoprotein that functions as a co-receptor for the T cell receptor by binding MHC class II molecules and recruiting the tyrosine kinase Lck to the TCR?CCD3 complex. This initiates a downstream phosphorylation cascade involving ZAP70, LAT, and PLC??1, ultimately activating NFAT and NF-??B transcription factors to drive T cell activation and cytokine production. Additionally, CD4 is the primary receptor for HIV-1 through interaction with the viral envelope glycoprotein gp120. Its expression is tightly regulated by Th-POK, RUNX3, IL-7, and TCR signaling strength.
Although 786-O cells do not endogenously express CD4, this knockout population serves as an ideal negative control for HIV-1 infectivity studies that rely on ectopic CD4 expression, or for investigating non-canonical functions of CD4 in a renal carcinoma context. The VHL-deficient pseudohypoxic state offers a unique platform to examine potential cross-talk between HIF pathways and CD4-mediated signals when CD4 is reintroduced.
Key applications include HIV entry mechanism studies, T cell activation signaling reconstitution experiments, and evaluation of CD4-targeted immunotherapies. This model is compatible with viral infectivity assays, T cell activation assays, co-immunoprecipitation, Western blot, flow cytometry, and ELISA. For more information, please contact Ascent Research.
