The HNRNPUL1 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the HNRNPUL1 gene has been disrupted in human HEK293T cells. This loss-of-function model is designed for detailed investigation of HNRNPUL1-dependent processes, including DNA double-strand break (DSB) repair and RNA metabolism. The polyclonal mixture preserves genetic heterogeneity, enabling robust functional studies without clonal selection bias.
HEK293T cells, a derivative of the HEK293 line, stably express the SV40 large T antigen, which allows episomal replication of plasmids carrying the SV40 origin. This characteristic supports high-yield protein expression and lentiviral packaging, making HEK293T a preferred host for a wide range of biochemical and cell biological experiments. The cells exhibit fast growth, consistent transfection efficiency, and well-mapped signaling cascades, providing a reliable platform for studying HNRNPUL1 function in a human cellular context.
HNRNPUL1 encodes an RNA-binding protein that functions at the interface of DNA repair and RNA processing. Upon generation of DNA double-strand breaks, HNRNPUL1 is recruited to damage sites in an ATM kinase-dependent manner. At DSB foci, it interacts directly with BRCA1, RAP80, CtIP, and PARP1, facilitating the stable accumulation of BRCA1 and subsequent loading of RAD51. This interaction promotes homologous recombination repair, a high-fidelity pathway critical for genomic stability. In parallel, HNRNPUL1 participates in RNA splicing and transcriptional regulation, thereby linking DNA damage signaling to RNA metabolism. The ATM-HNRNPUL1-BRCA1 axis represents a key node in the DNA damage response network.
Given HEK293T’s widespread use in DNA repair research, this HNRNPUL1 knockout population is particularly valuable for dissecting repair pathway choice and the cellular response to genotoxic stress. Defects in homologous recombination are hallmarks of breast and ovarian cancers, and HNRNPUL1’s role in BRCA1 recruitment places it at the center of cancer-relevant signaling. The model supports direct testing of PARP inhibitor sensitivity and investigation of synthetic lethal relationships. Its rapid growth and facile transfection enable high-content screening and quantitative analysis of repair kinetics using standard immunofluorescence-based assays for ??H2AX and RAD51 foci formation.
Researchers can leverage this knockout system for a multitude of experimental applications, including detailed DNA damage signaling studies, cancer cell biology investigations, functional genomics screens, and drug sensitivity profiling. Compatible techniques range from Western blotting and co-immunoprecipitation to assess protein?Cprotein interactions, to HR reporter assays that directly measure homologous recombination efficiency. RNA-seq can be employed to pinpoint HNRNPUL1-dependent splicing changes. The polyclonal knockout cells offer reproducible phenotypic characterization and serve as a robust starting point for custom projects. For additional product information or technical support, please contact Ascent Research.
