The Human CD300LD Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 786-O human renal cell carcinoma line. This product features targeted disruption of the CD300LD gene, which encodes an inhibitory immune receptor containing immunoreceptor tyrosine-based inhibitory motifs (ITIMs). The polyclonal knockout format comprises a heterogeneous mix of cells carrying various loss-of-function mutations, avoiding clonal selection biases and providing a robust model for functional investigations. These cells are optimized for studying CD300LD-mediated signaling within a renal carcinoma background.
The parental 786-O cell line is an adherent epithelial line established from a primary clear cell renal adenocarcinoma. It harbors a well-characterized mutation in the von Hippel-Lindau (VHL) tumor suppressor gene, making it a widely accepted model for clear cell renal cell carcinoma (ccRCC). The VHL deficiency drives constitutive activation of hypoxia-response pathways, recapitulating key tumorigenic features of ccRCC. This genetic context is clinically relevant for exploring immune checkpoint receptors, as ccRCC is considered an immunogenic tumor type.
CD300LD functions as an inhibitory immune receptor that negatively regulates myeloid cell activation. Upon ligand binding, the ITIM motifs become phosphorylated by Src family kinases, leading to recruitment of the tyrosine phosphatases SHP-1 and SHP-2. These phosphatases dephosphorylate downstream effectors including ERK and NF-??B, thereby suppressing pro-inflammatory cytokine secretion. Expression of CD300LD is induced by upstream stimuli such as IL-4, IL-13, LPS, and the transcription factor PU.1. Consequently, CD300LD serves as a critical node in immune inhibitory signaling, and its deletion in 786-O cells facilitates analysis of these transduction pathways.
In ccRCC, CD300LD may shape the immune microenvironment by restraining myeloid cell activity. The 786-O knockout cells enable exploration of how CD300LD loss affects signaling in tumor-associated myeloid populations. With a VHL-mutant background, this model is ideal for investigating crosstalk between oncogenic and immune inhibitory pathways, potentially informing immune checkpoint strategies.
Research applications include functional analysis of CD300LD in myeloid cell signaling, immune checkpoint research, and drug screening campaigns. Researchers can employ Western blotting and flow cytometry to verify knockout, ELISA to quantify cytokine secretion changes, phospho-ERK analysis to assess pathway activity, and RNA-sequencing to profile transcriptional alterations. Co-culture assays with immune cells can reveal functional consequences of CD300LD loss. This polyclonal knockout product supports both basic and translational studies in cancer immunology. For ordering or technical inquiries, please contact Ascent Research.
