GULP1 Knockout HT29 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma line. This product contains a genetically heterogeneous mixture of cells carrying CRISPR/Cas9-mediated disruptions at the GULP1 locus, creating a robust loss-of-function model for studying engulfment adaptor protein biology. The polyclonal format avoids clonal selection biases while providing reliable target-gene inactivation for downstream functional assays.
The HT29 cell line is a well-characterized human female-derived colon adenocarcinoma model extensively used in intestinal epithelial and oncology research. These adherent epithelial cells display oncogenic features, including constitutive activation of proliferation pathways, and serve as a physiologically relevant platform for investigating colorectal cancer mechanisms. Their intestinal origin renders them suitable for examining tumor?Cimmune microenvironment interactions and therapeutic vulnerabilities in vitro.
GULP1 functions as a phosphotyrosine-binding (PTB) domain-containing adaptor that links phosphatidylserine-sensing engulfment receptors to the actin polymerization machinery. Upon apoptotic cell phosphatidylserine exposure, GULP1 binds the cytoplasmic tails of receptors such as MEGF10, JEDI-1, and JEDI-2, recruiting downstream effectors ABI-1 and ENA-2. This complex activates RAC1 and CDC42 small GTPases, driving localized actin cytoskeletal rearrangements essential for phagocytic cup formation and efferocytosis. The core signaling module MEGF10/JEDI ?? GULP1 ?? ABI-1/ENA-2 ?? actin remodeling underscores GULP1’s pivotal role in apoptotic cell clearance.
In HT29 colorectal adenocarcinoma cells, GULP1 disruption allows dissection of defective efferocytosis in tumor progression. Impaired engulfment leads to accumulation of apoptotic cells, fostering a pro-inflammatory and immunosuppressive milieu. Altered actin dynamics downstream of GULP1 deficiency may modulate HT29 cell migration and invasion, key features of metastatic dissemination. This model bridges phagocytosis biology and cancer pathology, enabling immune evasion and metastasis studies.
This polyclonal knockout product supports diverse experimental workflows, including quantitative phagocytosis and efferocytosis assays with fluorescently labeled apoptotic targets. Western blotting, RT-qPCR, and co-immunoprecipitation confirm signaling complex integrity. Immunofluorescence and flow cytometry visualize receptor localization and population-level responses, while migration and invasion assays explore GULP1-dependent motile phenotypes. For ordering information or technical inquiries, contact Ascent Research.
