The ARPC1B Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the ARPC1B gene in HEK293T cells. This product provides a heterogeneous loss-of-function model for studying ARPC1B-mediated actin dynamics, without clonal isolation, preserving population diversity for robust functional studies.
HEK293T is an adherent human embryonic kidney cell line expressing the SV40 large T antigen, which enhances plasmid amplification and transfection efficiency. Widely employed for protein expression, viral production, and signaling studies, its well-characterized biology and genetic tractability make it an ideal host for cytoskeletal research.
ARPC1B is a critical subunit of the Arp2/3 complex that nucleates branched actin polymerization. It is activated by nucleation-promoting factors such as the WAVE complex (including WASF1, ABI, NCKAP1) and WASp, downstream of RAC1, CDC42, and PIP2. The Arp2/3 complex interacts with other subunits (ARPC2-5, ARP2, ARP3) and regulators like Cortactin and Abi1 to generate branched actin networks driving lamellipodia formation, cell migration, endocytosis, and vesicular trafficking. Disruption of ARPC1B impairs these processes, compromising actin-dependent cellular functions and resulting in defective lamellipodia extension and reduced directional cell migration.
In HEK293T cells, ARPC1B knockout disturbs the intrinsic actin regulatory machinery, offering a platform to dissect Arp2/3-dependent roles in an epithelial cellular context. This model is valuable for investigating the molecular mechanisms underlying ARPC1B deficiency, a disorder marked by autoinflammation, thrombocytopenia, and recurrent infections, and for probing RAC1/CDC42-WAVE-Arp2/3 signaling. Additionally, the knockout cells can be used to study the impact of ARPC1B loss on receptor-mediated endocytosis and intracellular trafficking pathways.
These polyclonal knockout cells are suited for diverse assays: Western blotting of ARPC1B and actin, phalloidin-based F-actin staining, scratch migration assays, immunofluorescence for lamellipodia, co-immunoprecipitation of Arp2/3 complex components, flow cytometry for trafficking-dependent surface receptors, and RT-qPCR for actin remodeling genes. They support research into actin dynamics, host-pathogen interactions, and screening of cytoskeletal modulators. Moreover, they enable functional studies of immune cell-relevant processes such as phagocytosis and migration. For detailed specifications and ordering, contact Ascent Research.
