The DYNLL2 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for studying human DYNLL2 loss-of-function. This model employs CRISPR/Cas9-mediated gene disruption to eliminate DYNLL2 expression, providing a controlled background for functional studies. As a polyclonal population, it avoids clonal artifacts and represents a robust knockout system.
HEK293T cells are human embryonic kidney epithelial cells that stably express adenoviral E1A and E1B proteins and SV40 large T antigen. Derived from HEK293 cells transformed with sheared adenovirus 5 DNA, this line is valued for its high transfectability and robust protein expression capability, making it ideal for recombinant protein production and mechanistic studies. The SV40 large T antigen enables episomal replication of plasmids containing the SV40 origin, further expanding experimental utility.
DYNLL2 encodes a dynein light chain that functions as a molecular hub in apoptosis inhibition, intracellular transport, and mitotic spindle assembly. As a homodimeric component of the cytoplasmic dynein complex, DYNLL2 directly interacts with the dynein intermediate chain and various cargo adaptors, facilitating minus-end-directed transport along microtubules. Its anti-apoptotic activity stems from binding and sequestering BH3-only proteins Bim and Bmf, thereby suppressing the intrinsic apoptotic cascade. Upstream, DYNLL2 is regulated by p53 signaling, which can induce its expression under stress. Additionally, DYNLL2 participates in mitotic spindle checkpoint control through interactions with Bub3 and the mitotic checkpoint complex, linking dynein motor function to chromosome segregation fidelity.
In HEK293T cells, which already express adenoviral proteins that perturb apoptosis and cell cycle, DYNLL2 knockout provides a sensitized system to dissect its role in apoptosis resistance and mitotic control. Ablation of DYNLL2 is expected to release sequestered BH3-only proteins, potentiating apoptotic responses, and may disrupt dynein-dependent transport and spindle assembly. This polyclonal knockout population enables rigorous interrogation of DYNLL2 functions in a genetically tractable epithelial background.
Key applications include apoptosis assays (caspase activity, Annexin V staining), co-immunoprecipitation of DYNLL2 with Bim, Bmf, and dynein intermediates, immunofluorescence for mitotic spindle analysis, and intracellular transport studies via live-cell imaging. RT-qPCR can assess transcriptional changes. This model is ideal for cancer biology, neurodegenerative disease research, and cell cycle checkpoint studies. For more information, contact Ascent Research.
