The DYNC1LI1 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population specifically designed for targeted disruption of the DYNC1LI1 gene in a human ovarian carcinoma background. This product provides a loss-of-function model to interrogate the role of cytoplasmic dynein light intermediate chain 1, a critical non-catalytic subunit of the cytoplasmic dynein motor complex. The polyclonal nature of the knockout pool ensures a heterogeneous collection of edited alleles, enabling robust functional studies without the bottleneck effects of clonal selection. Researchers are supplied with a ready-to-use polyclonal knockout cell population suitable for downstream molecular and cellular assays within the A2780 host cell context.
The A2780 cell line is a well-characterized human ovarian carcinoma model derived from an untreated patient. It is widely employed in cancer biology to investigate mechanisms of tumorigenesis, metastasis, and drug response. Endogenous expression of dynein complex components makes A2780 cells particularly suited for studying retrograde microtubule-based transport, organelle positioning, and mitotic events. The host cell line provides a clinically relevant platform for examining the impact of DYNC1LI1 loss in ovarian cancer pathophysiology, where dynein-dependent processes are often deregulated.
DYNC1LI1 encodes a light intermediate chain that facilitates cargo binding and processive motility of the dynein complex. It interacts with core dynein heavy chain DYNC1H1 and intermediate chain DYNC1I1, as well as regulatory factors including dynactin (DCTN1), Ndel1 (NDEL1), BICD2, and LIS1 (PAFAH1B1). Mechanistically, DYNC1LI1 is activated by mitotic kinases such as CDK1 and functions downstream of cell cycle regulators like FOXM1 to coordinate mitotic spindle orientation and Golgi positioning. Disruption of DYNC1LI1 impairs dynein-mediated retrograde transport, leading to mislocalization of organelles and mitotic defects, processes critically mediated through these interacting partners.
In the A2780 ovarian carcinoma model, knockout of DYNC1LI1 disrupts dynein-dependent functions including organelle distribution and mitotic spindle assembly, potentially influencing cell division fidelity and drug sensitivity. The loss-of-function model enables dissection of how dynein dysregulation contributes to ovarian cancer phenotypes, such as resistance to chemotherapeutic agents or altered metastatic potential. By perturbing the dynein complex in a disease-relevant context, researchers can explore the interplay between intracellular trafficking and oncogenic signaling pathways often driven by FOXM1 and CDK1 activity.
This polyclonal knockout product is optimized for diverse applications, including cancer cell biology, intracellular trafficking studies, and mitosis research. Representative assays include western blotting for DYNC1LI1 to confirm target disruption, immunofluorescence to visualize Golgi or endosome mislocalization, live-cell imaging of microtubule-based transport, and mitotic index analysis. Additionally, drug sensitivity assays can assess the role of dynein function in therapeutic response. For further technical specifications, please contact Ascent Research.
