The HNRNPDL Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the HNRNPDL gene in the HEK293T human embryonic kidney cell line. This product provides a loss-of-function model for investigating HNRNPDL’s roles in RNA metabolism. The polyclonal pool, generated by transient delivery of CRISPR/Cas9 components, contains a heterogeneous mix of edited alleles, enabling robust, population-level analyses without single-cell cloning. As a bulk knockout pool, it is well-suited for experiments requiring sufficient cell numbers for biochemical, transcriptomic, and functional assays, while minimizing clonal bias.
HEK293T cells are a widely used derivative of the HEK293 cell line, stably expressing the SV40 large T antigen. This antigen permits episomal replication of plasmids containing the SV40 origin of replication, resulting in high-level transient protein expression and efficient viral production. Originating from human embryonic kidney cells, HEK293T exhibits epithelial morphology and robust growth characteristics, making it a cornerstone for recombinant protein expression, lentivirus and retrovirus packaging, and functional genomics. Its genetic tractability and well-characterized proteome provide a reliable background for studying gene function.
HNRNPDL encodes an RNA-binding protein that participates in pre-mRNA alternative splicing, mRNA stability control, and nonsense-mediated mRNA decay. Under physiological conditions, HNRNPDL localizes predominantly to the nucleus, where it interacts with spliceosomal components and regulatory factors such as U2AF2 and SF1 to modulate splicing decisions. In response to cellular stress, including oxidative and heat shock, HNRNPDL translocates to cytoplasmic stress granules, forming complexes with TDP-43, FUS, and G3BP1, thereby contributing to the dynamic remodeling of these ribonucleoprotein condensates. HNRNPDL also auto-regulates its own mRNA levels. Its binding to muscle-specific transcripts and stress granule-associated mRNAs highlights its tissue-relevant and stress-responsive regulatory functions.
In the HEK293T host context, disruption of HNRNPDL allows dissection of its RNA regulatory roles independently of muscle or neuronal lineage-specific factors. The knockout cells serve as a platform to examine how loss of HNRNPDL affects global alternative splicing patterns, mRNA half-life, and nonsense-mediated decay efficiency in a genetically malleable system. Because HEK293T cells are non-muscle and non-neuronal, the model is particularly valuable for studying fundamental RNA-binding protein biology and stress granule dynamics without confounding tissue-specific differentiation programs. Furthermore, the polyclonal format mirrors the genetic heterogeneity of cell populations, which can be advantageous for assessing broad functional impacts and for applications such as CRISPR-based drug screens.
These polyclonal knockout cells are suitable for a range of experimental approaches. Researchers can employ western blotting and immunofluorescence to validate protein depletion and stress-induced granule localization. RT-qPCR and RNA-seq enable quantitative analysis of splicing isoform abundance and transcriptome-wide changes. Co-immunoprecipitation and minigene splicing reporter assays facilitate investigation of protein-RNA interactions and cis-regulatory elements. The model supports disease-relevant research into limb-girdle muscular dystrophy type 1G, amyotrophic lateral sclerosis, and frontotemporal dementia, where HNRNPDL dysfunction is implicated. For further technical details, please contact Ascent Research.
