The ARFGEF2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from human Jurkat T lymphocytes. This product features targeted disruption of the ARFGEF2 gene, which encodes the guanine nucleotide exchange factor BIG2. The polyclonal pool provides a heterogeneous loss-of-function model for analyzing ARFGEF2-dependent processes without clonal selection bias.
Jurkat cells originate from the peripheral blood of a 14-year-old male with acute T-cell leukemia and are widely utilized as a model for T-cell receptor (TCR) signaling, activation, and apoptosis. Their robust growth and well-characterized signaling pathways make them a standard host for studying membrane trafficking in the context of immune function and leukemogenesis.
ARFGEF2 (BIG2) is a guanine nucleotide exchange factor that activates ARF GTPases, mainly ARF1 and ARF3, at the Golgi. This activation promotes COPI coat assembly and retrograde intra-Golgi trafficking. Upstream regulators such as brefeldin A inhibit BIG2, while PKA-mediated phosphorylation provides additional control. Downstream, active ARF1 recruits COPI subunits (e.g., COPB1) and adaptors like AP-1 and GGAs to facilitate vesicle budding. BIG2 also interacts with ARFGAP1 and BIG1 within a network that coordinates Golgi organization and endosomal recycling. In T cells, this GTPase cascade intersects with TCR signaling through endomembrane reorganization required for signal transduction and cytokine secretion.
In Jurkat T cells, ARFGEF2-driven ARF activation governs membrane trafficking essential for TCR signaling and cytokine release. Loss of BIG2 may disrupt Golgi integrity and COPI-mediated transport, affecting surface receptor display and secretion. This knockout model thus dissects the interplay between vesicular traffic and T-cell function, with relevance to leukemia and neurodevelopmental pathologies linked to ARFGEF2 mutations.
These polyclonal knockout cells enable flow cytometry for surface markers, western blotting, RT-qPCR, immunofluorescence of Golgi structure, ELISA-based cytokine measurement, and co-immunoprecipitation of trafficking machinery. They also support Golgi fragmentation assays and secretion studies, enabling detailed investigation of retrograde transport and effector molecule release. Researchers can apply this model to T-cell signaling studies, drug target validation, and functional screens for neurodevelopmental disorders. For further information, please contact Ascent Research.
