The HNRNPH2 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HEK293T human embryonic kidney cell line, designed for investigation of heterogeneous nuclear ribonucleoprotein H2 (HNRNPH2) function. This product consists of a heterogeneous pool of cells carrying targeted disruptions of the HNRNPH2 gene, providing a versatile loss-of-function model without the clonal bias introduced by single-cell isolation. The polyclonal format is particularly suitable for studies where population-level effects of gene disruption are analyzed, minimizing artifacts associated with monoclonal selection while maintaining robust knockout across the culture.
The host cell line, HEK293T, is a widely used derivative of HEK293 cells that stably expresses the SV40 large T antigen, conferring exceptional transfectability and facilitating high-level protein expression and viral packaging. These adherent epithelial cells grow reliably in standard culture conditions and are a preferred platform for generating knockout models due to their ease of genetic manipulation and well-characterized transcriptome. The robust proliferative capacity and consistent performance in a broad range of molecular assays make HEK293T an ideal background for studying the fundamental aspects of RNA processing and splicing regulation.
HNRNPH2 encodes an RNA-binding protein that functions as a critical regulator of pre-mRNA processing, alternative splicing, and mRNA transport. Within the spliceosome, HNRNPH2 interacts with core components such as U1 and U2 snRNPs and SR proteins like SRSF1, as well as with other hnRNP family members including HNRNPA1 and HNRNPA2B1. It also associates with RNA polymerase II, linking transcription to splicing. Upstream regulators such as the transcription factors MYC and E2F modulate HNRNPH2 expression, while downstream, the protein controls the splicing of neuronal genes (e.g., GRIN1, SHANK3, SYNGAP1), thereby influencing mRNA isoform diversity and neuronal gene expression programs. Disruption of HNRNPH2 leads to widespread aberrant splicing and altered expression of genes essential for neurodevelopment.
In the HEK293T context, HNRNPH2 knockout provides a tractable system to dissect the fundamental mechanisms of splicing regulation without the complexity of neuronal cultures. Despite the non-neuronal origin of HEK293T cells, the core splicing machinery and RNA-binding protein networks are conserved, allowing mechanistic studies and high-throughput screening approaches. The polyclonal population captures the full spectrum of editing events, offering a more representative model for analyzing transcriptome-wide splicing changes and the cellular response to HNRNPH2 loss, and can serve as a baseline for comparative studies with disease-relevant cell types.
This knockout cell product is well-suited for modeling HNRNPH2-related neurodevelopmental disorders, investigating mRNA splicing regulation, and screening for splicing-modifying therapies. Researchers can validate HNRNPH2 depletion via Western blotting, characterize splicing isoform changes through RT-PCR, perform transcriptome-wide analysis using RNA-seq, examine subcellular localization by immunofluorescence, and map protein interaction networks with co-immunoprecipitation. The polyclonal HEK293T HNRNPH2 knockout cells thus provide a reliable and accessible tool for advancing the understanding of RNA processing in health and disease. For further technical details, please contact Ascent Research.
