The DYNC1LI1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the DYNC1LI1 gene in a human B lymphocyte background. This product provides a loss-of-function model for investigating cytoplasmic dynein-based processes without the need for transient knockdown or inhibitors. The polyclonal nature of the edited cell pool ensures a heterogeneous population with gene disruption across the target locus, suitable for robust functional genomic studies.
The host Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt’s lymphoma-derived B lymphocyte model, extensively characterized for its rapid growth and ease of genetic manipulation. Originating from a patient with Burkitt’s lymphoma, these cells retain key features of B-cell malignancy, including constitutive activation of MYC and NF-??B signaling pathways, making them a relevant system for hematological cancer research and immunological studies.
DYNC1LI1 encodes a light intermediate chain subunit that is integral to the cytoplasmic dynein motor complex, where it directly interacts with the dynein heavy chain DYNC1H1 and bridges the complex to the dynactin activator via DCTN1 (p150Glued). This interaction is critical for microtubule minus-end-directed transport of diverse cargoes, including endosomes, lysosomes, Golgi-derived vesicles, and mRNA ribonucleoprotein complexes. DYNC1LI1 function is dynamically regulated by upstream factors such as LIS1 (PAFAH1B1) and NDEL1, which modulate dynein processivity and force generation. In mitotic cells, DYNC1LI1 facilitates spindle pole focusing and chromosome alignment by anchoring dynein at the spindle poles, while in interphase, it maintains organelle positioning and autophagic flux through retrograde transport.
In the Raji B-cell lymphoma context, disruption of DYNC1LI1 is anticipated to severely impair retrograde trafficking and mitotic fidelity, potentially leading to cytokinesis failure, genomic instability, or apoptosis. Given the reliance of rapidly dividing lymphoma cells on precise mitotic machinery, this knockout model provides a valuable platform to dissect dynein??s contribution to lymphoma cell proliferation and survival. Moreover, altered organelle positioning may affect B-cell receptor signaling and intracellular protein sorting, offering insights into dynein-dependent mechanisms underlying lymphomagenesis.
Researchers can employ this polyclonal knockout population in a wide array of experimental workflows. Standard validation by western blotting and RT-qPCR confirms DYNC1LI1 disruption, while immunofluorescence microscopy reveals changes in dynein localization and organelle distribution. Functional assays such as live-cell imaging of fluorescently tagged lysosomes or endosomes quantify trafficking defects, and flow cytometry enables high-content analysis of cell cycle perturbations and Annexin V-based apoptosis detection. Co-immunoprecipitation experiments can assess the integrity of the dynein-dynactin complex. Key applications include screening novel anti-mitotic agents in lymphoma, studying the role of dynein in immune synapse formation, and investigating ciliogenesis defects in B-cell lineages. For pricing and availability, please contact Ascent Research.
