The DENND4C Knockout Raji Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte cell line. This population introduces a loss-of-function model for the DENND4C gene, enabling investigation of its role in macropinocytosis, endosomal trafficking, and autophagy. Unlike clonal isolates, the polyclonal format retains cellular heterogeneity, reflecting a more natural distribution of edited cells for population-level studies.
The Raji cell line, established from a human Epstein-Barr virus (EBV)-positive Burkitt lymphoma, is a well-characterized lymphoblastoid model. It originates from malignant B cells and retains features of B-cell biology, including antigen presentation and signaling pathways. Raji cells are widely employed in immunological and oncological research, providing a physiologically relevant context to study processes such as macropinocytosis, autophagy, and drug resistance in B-cell lymphomas.
DENND4C encodes a guanine nucleotide exchange factor (GEF) that specifically activates Rab10 by promoting GTP loading. This activity drives macropinocytosis and endosomal trafficking, with Rab10 localizing to macropinocytic cups and early endosomes. Functionally, DENND4C is regulated by upstream signals from mTORC1, AMPK, and growth factor receptors such as EGFR, integrating nutrient status and growth factor cues. It also physically interacts with DENND4A and DENND4B and associates with endosomal sorting complexes, positioning DENND4C at a nexus controlling cellular uptake and autophagy.
In Raji B lymphoma cells, DENND4C-mediated macropinocytosis can influence nutrient scavenging and mTORC1 signaling, which are critical for sustaining rapid proliferation and survival under stress. Disruption of DENND4C may impair Rab10-dependent processes, providing a tool to dissect how endocytic trafficking and autophagy contribute to lymphomagenesis and drug resistance. This model is particularly valuable given the frequent dysregulation of PI3K/AKT/mTORC1 signaling in B-cell malignancies.
Researchers can employ DENND4C Knockout Raji Polyclonal Cells in a variety of assays, including flow cytometry with dextran uptake to quantify macropinocytosis, immunofluorescence for Rab10 subcellular localization, autophagy flux analyses via LC3 turnover, and phospho-signaling profiling of mTORC1 and AMPK pathways. Further, co-immunoprecipitation studies can probe DENND4C interactions with DENND4A, Rab10, and endosomal proteins. These tools are ideal for elucidating DENND4C’s role in B-cell lymphoma biology, mTOR signaling, and mechanisms underlying drug sensitivity. For further technical inquiries, please contact Ascent Research.
