The GULP1 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited pool derived from HEK293T cells, designed to disrupt GULP1. This population provides a loss-of-function model for the engulfment adaptor GULP1, which links apoptotic cell recognition to cytoskeletal remodeling. As a polyclonal knockout product, it contains diverse editing events, supporting population-level assays without clonal selection.
The HEK293T cell line is an adherent human embryonic kidney epithelial line stably expressing SV40 large T-antigen, which enables episomal plasmid replication and yields high transfectability. These features make it a preferred host for protein expression, lentivirus production, and CRISPR genome editing. Its epithelial context is well-suited for examining non-phagocytic functions of engulfment machinery components such as GULP1.
GULP1 functions as a cytoplasmic adaptor that binds NPxY motifs in activated engulfment receptors like BAI1 and LRP1 via its PTB domain. It couples these receptors to ARF6-mediated cytoskeletal rearrangements and Rac1 activation, independent of Elmo/Dock180. GULP1 also interacts with integrin ??5 and modulates focal adhesion turnover, linking apoptotic cell clearance to cell motility. Key upstream regulators include phosphatidylserine and BAI1, while downstream effectors include Rac1 and ARF6, establishing GULP1 as a node connecting efferocytosis to epithelial migration and proliferation.
In HEK293T cells, GULP1 ablation disrupts both its established role in phagocytic signaling and its tumor-relevant contributions to migration and proliferation. Because these cells are non-professional phagocytes, the knockout reveals GULP1-dependent mechanisms in epithelial contexts, such as Rac1-driven lamellipodia formation and ARF6-regulated membrane trafficking. This polyclonal population mimics the heterogeneity of tumor cell pools, providing a valuable resource for studying processes like ovarian and colorectal cancer progression.
This GULP1 knockout polyclonal cell pool is suitable for diverse applications, including pHrodo phagocytosis assays, Boyden chamber migration studies, co-immunoprecipitation with BAI1/LRP1, and Rac1/ARF6 activity measurements. High-content screening for clearance modulators and migration inhibitors is also achievable. Researchers investigating Alzheimer??s disease, cancer, or age-related phagocytic decline can utilize this model to interrogate GULP1 function. Contact Ascent Research for more information.
