The HNRNPH2 Knockout HeLa Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population originating from HeLa cells, designed to disrupt the HNRNPH2 gene. This loss-of-function model permits the study of HNRNPH2-dependent RNA processing events in the absence of endogenous wild-type protein expression. Owing to the polyclonal format, the cell population retains genetic heterogeneity, offering a robust system to examine variable cellular outcomes following targeted gene disruption.
HeLa cells are an immortalized human cervical adenocarcinoma cell line first derived in 1951, now a cornerstone of biomedical research. Their extensive characterization??including comprehensive genomic, transcriptomic, and proteomic data??along with dependable growth kinetics and amenability to genetic engineering, make them an ideal host for gene knockout studies. This cell line is particularly suited for investigating cancer-associated pathways and gene regulatory mechanisms.
HNRNPH2 encodes a heterogeneous nuclear ribonucleoprotein that binds RNA and regulates pre-mRNA processing, alternative splicing, and mRNA metabolism. It associates with intronic splicing enhancers and silencers, modulating splice site selection by interacting with spliceosome components including U1 snRNP, U2 snRNP, U2AF, and other hnRNP proteins. Its activity is controlled by upstream MAPK kinases and transcription factors, and it in turn determines the alternative splicing of transcripts critical for cell proliferation and apoptosis. HNRNPH2 also cooperates with SR proteins and RNA polymerase II, coupling transcription to post-transcriptional processing.
In HeLa cells, HNRNPH2 knockout enables dissection of splicing-dependent gene expression changes relevant to cancers such as glioblastoma and breast cancer. This model helps define how HNRNPH2 alternative splicing contributes to oncogenic phenotypes like proliferation, apoptosis evasion, and invasion within a well-characterized cervical cancer background.
This knockout cell population is optimized for diverse experimental workflows, including RNA-seq to map global splicing changes, RT-PCR splicing assays for isoform validation, CLIP-seq to identify genome-wide RNA?Cprotein interaction sites, and western blotting or immunofluorescence to verify HNRNPH2 protein depletion. Applications span cancer biology, RNA splicing mechanism studies, drug target validation, and functional genomics. For technical inquiries and ordering, please contact Ascent Research.
