The HNRNPUL2 Knockout HEK293T Polyclonal Cells are a polyclonal knockout cell population generated by CRISPR/Cas9-mediated disruption of the HNRNPUL2 gene, providing a loss-of-function model for studying its roles in RNA processing and DNA repair. The polyclonal format avoids clonal selection biases and maintains genetic heterogeneity, enabling robust population-level analyses. This product is suitable for researchers investigating HNRNPUL2 function in a highly transfectable human cell background.
The host cell line, HEK293T, is an adherent epithelial cell line derived from female human embryonic kidney. It was originally transformed with sheared adenovirus 5 DNA and further modified to stably express the SV40 large T antigen. HEK293T is renowned for its high transfection efficiency and protein expression, making it a preferred system for transient expression, viral packaging, and biochemical studies. The SV40 T antigen allows episomal replication of plasmids containing the SV40 origin, facilitating amplified protein production.
HNRNPUL2 encodes an RNA-binding protein of the hnRNP family that is essential for pre-mRNA splicing, mRNA stability, and transcriptional regulation. In the DNA damage response (DDR), it is activated by ATM and ATR kinases and recruited to damage sites, where it interacts with the BRCA1/BARD1 complex to promote repair. HNRNPUL2 regulates alternative splicing of critical DDR genes such as BRCA1 and RAD51, thereby influencing homologous recombination. It also associates with PARP1, RNA polymerase II, and other hnRNP proteins, forming a nexus between RNA processing and DNA repair. Representative pathway components include ATM, ATR, BRCA1, BARD1, RAD51, and 53BP1.
In HEK293T cells, HNRNPUL2 knockout provides a powerful model to dissect its functions in a transformed epithelial context relevant to cancer biology. The expression of SV40 large T antigen inactivates p53 and Rb, mimicking checkpoint defects found in many cancers and allowing researchers to study HNRNPUL2-dependent DDR and splicing pathways independently of these tumor suppressors. This system is valuable for assessing how loss of HNRNPUL2 affects genomic stability and cellular responses to DNA-damaging agents or splicing inhibitors.
These polyclonal knockout cells enable a broad range of applications, including RNA-seq and RT-qPCR to profile splicing changes, minigene splicing reporter assays for mechanistic studies of splice site selection, co-immunoprecipitation to validate protein interactions (e.g., with BRCA1/BARD1), and ??H2AX immunofluorescence to quantify DNA damage foci. Cell cycle analysis by flow cytometry and western blotting of DDR markers are also supported. This product is ideal for functional genomics, cancer biology research, and spliceopathy investigations. For further details, please contact Ascent Research.
