The ABCF2 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population specifically engineered for loss-of-function investigations of the ABCF2 gene. Derived from the widely utilized HEK293T human embryonic kidney cell line, this polyclonal knockout model enables robust interrogation of ABCF2-mediated translation regulation and drug resistance mechanisms. The polyclonal nature of the knockout pool provides a genetically heterogeneous population with targeted disruptions, supporting experimental designs where monoclonal isolation is not required.
The HEK293T parental cell line is an immortalized human embryonic kidney epithelial derivative that stably expresses the SV40 large T antigen, enhancing episomal replication of plasmids containing the SV40 origin of replication. Originally derived from HEK293 cells through adenovirus type 5 transformation, HEK293T cells are a staple in molecular and cellular biology for their high transfectability and robust protein production. Their embryonic kidney origin makes them a pertinent model for studying renal cell biology, developmental signaling, and epithelial homeostasis, while their genetic tractability facilitates CRISPR-based genomic editing approaches.
ABCF2 is a non-transporter ABC protein that functions as a translation regulator, selectively enhancing the synthesis of anti-apoptotic (BCL2, XIAP) and drug resistance (ABCB1) proteins to mediate cisplatin resistance. It interacts with ribosomal subunits and translation initiation factors such as eIF3, eIF4F, and ABCE1. Upstream, DNA damage signals from cisplatin activate ATF4 and p53, which may regulate ABCF2 expression, coupling genotoxic stress to translation of survival factors. This positions ABCF2 at the intersection of translation control, apoptosis inhibition, and drug resistance, with links to mTOR signaling.
The HEK293T background provides a clean genetic platform to dissect ABCF2 function, as these cells retain functional translation and apoptosis machinery without the confounding mutations of cancer lines. ABCF2 knockout in this context allows precise measurement of cisplatin-induced translation changes via polysome profiling and protein synthesis assays. As an epithelial line, HEK293T also models how ABCF2 may promote survival of carcinoma cells from kidney, ovary, breast, and lung under chemotoxic stress. The polyclonal knockout pool, with its allelic diversity, avoids clonal artifacts and is well-suited for population-level drug sensitivity screens and functional genomics.
This product supports diverse research applications, including mechanistic studies of drug resistance, cisplatin sensitivity profiling, and ABCF2 target validation. Standard assays such as Western blotting and RT-qPCR can monitor ABCF2 depletion and downstream effector expression (e.g., BCL2, XIAP, ABCB1). Cisplatin cytotoxicity and apoptosis assays (cleaved caspase-3) directly assess chemosensitivity. For translation-level analysis, polysome profiling and co-immunoprecipitation of initiation factors (eIF3, eIF4F) can be performed. RNA-seq of knockout versus parental cells provides transcriptome-wide insights. For inquiries, please contact Ascent Research.
