The DYNC1LI1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to model loss of function of the DYNC1LI1 gene. This product provides a heterogeneous pool of Jurkat T lymphocytes carrying targeted disruptions in DYNC1LI1, enabling researchers to interrogate the roles of cytoplasmic dynein light intermediate chain 1 (DYNC1LI1) in cellular processes. The polyclonal format avoids clonal selection bias and captures a range of gene-edited allelic variants, offering a robust system for functional genomics studies without the assumption of complete knockout at the cellular level.
The host cell line, Jurkat, is an immortalized human T?lymphocyte line originally derived from a T?cell leukemia patient. Jurkat cells are extensively employed as a model for T?cell receptor (TCR) signaling, immune synapse formation, and downstream immune effector mechanisms. Their well-characterized signaling networks, coupled with rapid proliferation and ease of genetic manipulation, make them particularly suitable for investigating genes implicated in lymphocyte function, cancer biology, and intracellular trafficking pathways.
DYNC1LI1 encodes a light intermediate chain of the cytoplasmic dynein 1 motor complex, which is responsible for minus?end?directed transport along microtubules. DYNC1LI1 interacts with multiple dynein and dynactin subunits, including DCTN1 (p150 glued), DCTN2, DYNC1H1, and DYNC1I2, and associates with regulatory proteins such as LIS1 and NDE1. This complex is regulated by upstream factors including RAB7 and Cyclin B/CDK1, and it facilitates the retrograde movement of diverse cargoes??endosomes, lysosomes, mitochondria, and mRNAs??thereby governing organelle positioning, mitotic spindle assembly, and cell cycle progression. DYNC1LI1 also contributes to neuronal migration during development, and its dysfunction is linked to neurodevelopmental disorders like microcephaly and intellectual disability, as well as cancer progression.
In the Jurkat T?cell context, DYNC1LI1 knockout disrupts dynein?dependent transport processes that are critical for TCR signaling and immune function. Given that Jurkat cells rely on endosomal recycling, lysosomal exocytosis, and polarized vesicle trafficking for receptor activation and signal transduction, loss of DYNC1LI1 is expected to impair these pathways, providing insights into how dynein machinery supports lymphocyte responses. Moreover, the immortalized leukemic background highlights the gene??s relevance to cancer cell division, making this knockout model a valuable tool for exploring mitotic vulnerabilities and potential therapeutic targeting of the dynein complex in hematological malignancies.
This polyclonal knockout population is suited for a wide array of experimental applications, including validation of DYNC1LI1 disruption via western blotting and RT?qPCR, assessment of dynein localization by immunofluorescence, and functional assays such as live?cell imaging of organelle motility, flow cytometric cell cycle analysis, co?immunoprecipitation to probe dynein?dynactin interactions, and mitotic index determination. Researchers can employ these cells to screen dynein inhibitors, dissect mechanisms of intracellular trafficking in T?cells, model dynein?related pathologies, and investigate the role of DYNC1LI1 in cancer cell proliferation. For additional information and technical support, please contact Ascent Research.
