The HNRNPA0 Knockout HEK293T Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HEK293T human embryonic kidney cell line, engineered to disrupt the HNRNPA0 gene. HNRNPA0 encodes an AU-rich element (ARE)-binding protein that post-transcriptionally regulates mRNA stability and translation. This polyclonal knockout pool offers a heterogeneous population with disrupted HNRNPA0 expression, providing a robust loss-of-function model without clonal selection artifacts. It serves as a valuable tool for dissecting the role of HNRNPA0 in mRNA metabolism and signaling.
The parental HEK293T cell line, derived from human embryonic kidney epithelium, stably expresses the SV40 large T antigen, enabling episomal replication of plasmids with the SV40 origin. This feature supports high-level protein expression and viral propagation, making HEK293T a preferred host for functional genomics and CRISPR-based knockout generation. Its well-characterized growth and epithelial morphology facilitate diverse downstream analyses, including high-throughput screening and imaging.
HNRNPA0 mediates ARE-directed mRNA decay and translational control by binding AU-rich elements in 3?? UTRs of targets like TNF-??, COX-2, and IL-6 mRNAs. Upon stimulation by cytokines or stress, p38 MAPK phosphorylates MAPKAPK2, which then phosphorylates HNRNPA0, altering its RNA-binding affinity and subcellular localization. This modulates the stability of ARE-containing transcripts, regulating inflammatory and stress responses. HNRNPA0 also interacts with HuR, AUF1, and TIA-1, integrating signals into post-transcriptional regulatory networks.
In the HEK293T background, HNRNPA0 knockout enables dissection of ARE-mediated regulatory mechanisms in a genetically tractable, well-characterized cell model. The polyclonal nature of the knockout pool recapitulates population-level heterogeneity, minimizing clonal bias while allowing robust assessment of gene function. Researchers can investigate how loss of HNRNPA0 affects basal and stimulus-induced expression of inflammatory mediators, or explore its role in splicing and nuclear export. The combination of SV40 large T antigen expression and HNRNPA0 disruption creates a versatile platform for studying RNA-protein interactions and signal-dependent mRNA turnover in epithelial cells.
This knockout model is suited for studying post-transcriptional gene regulation, ARE-mediated mRNA decay, and p38 MAPK signaling. Applications include western blotting, RT-qPCR for target mRNAs, RNA immunoprecipitation, actinomycin D chase assays, ARE-luciferase reporters, and cytokine ELISA. The cells also support RNA-seq for transcriptome-wide analyses. For further information or to request a quote, please contact Ascent Research.
