The LRRC8C Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Burkitt’s lymphoma Raji B lymphocyte line. This product features CRISPR/Cas9-mediated disruption of the LRRC8C gene, creating a heterogeneous loss-of-function model that preserves the natural diversity of polyclonal edited cells. The knockout population enables studies of LRRC8C function without clonal selection bias, suitable for experiments where population-averaged effects are informative. Cells are provided ready for functional assays and can be expanded in culture.
The Raji cell line is an Epstein-Barr virus (EBV)-positive lymphoblastoid cell line from a Burkitt’s lymphoma patient. These suspension B lymphocytes are widely used to model B-cell malignancies, immune function, and signal transduction. Raji cells retain relevant signaling pathways, exhibit rapid proliferation, and respond to extracellular stimuli. Their transformed phenotype and genetic stability provide a robust host for studying gene function in lymphoma and immune cell biology.
LRRC8C encodes a subunit of the volume-regulated anion channel (VRAC), which assembles as a heteromer with other LRRC8 family members, most notably the essential subunit LRRC8A (SWELL1). VRAC is activated by hypotonic stress, receptor tyrosine kinase signaling, and intracellular ATP depletion, promoting chloride ion and organic osmolyte efflux. In immune cells, LRRC8C-containing channels facilitate export of the cyclic dinucleotide cGAMP, produced by cGAS upon cytosolic DNA sensing. Extracellular cGAMP enters neighboring cells, activates STING, and triggers IRF3 phosphorylation and type I interferon responses. VRAC-mediated ATP release also contributes to purinergic signaling, while regulatory volume decrease (RVD) influences cell volume homeostasis, migration, and survival under osmotic insult. LRRC8C interacts with LRRC8D and LRRC8E, and may associate with integrins and cytoskeletal proteins, linking volume sensing to cellular architecture.
In Raji B lymphocytes, LRRC8C knockout disrupts regulatory volume decrease, potentially impairing adaptation to the osmotic environment of the tumor microenvironment. Loss of LRRC8C may reduce cGAMP export, attenuating paracrine STING activation and altering innate immune signaling. Given VRAC??s role in ATP release and osmosensing, this knockout population is a valuable tool for dissecting mechanical and chemical signal integration in lymphoma biology. The polyclonal nature ensures that observations reflect general loss-of-function effects rather than clonal artifacts, enhancing translational relevance.
Researchers can use these knockout cells to study VRAC-dependent volume regulation via RVD measurements under hypotonic challenge, and to assay cGAMP transport and STING activation by phospho-IRF3 flow cytometry. Migration and invasion assays can delineate LRRC8C’s role in lymphoma cell dissemination, while drug sensitivity screening under osmotic stress may identify vulnerabilities linked to volume adaptation. RNA-seq and Western blotting can profile molecular changes. This product is suited for investigating cGAS-STING signaling, ATP release, and osmosensing-immune interplay. For further information, contact Ascent Research.
