The HNRNPH1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal human cell population with targeted disruption of the HNRNPH1 gene. This heterogeneous knockout pool provides a loss-of-function model for studying HNRNPH1-dependent processes without clonal selection. The product is supplied as a population of HeLa cells bearing diverse editing events, enabling robust analysis of gene function in a mixed genetic background.
The host cell line, HeLa, is an immortalized epithelial cell line derived from a cervical adenocarcinoma of a 31-year-old female. HeLa cells are widely used in cancer research due to their robust growth, well-characterized genome, and amenability to genetic manipulation. They retain key features of epithelial tumor biology, including rapid proliferation and active signaling networks, making them a suitable platform for investigating RNA-binding proteins in cancer.
HNRNPH1 encodes an RNA-binding protein that preferentially binds G-rich sequences in pre-mRNA, regulating splice site selection and exon inclusion or skipping. It functions within the spliceosome complex, engaging with core spliceosomal snRNPs, SR proteins, and other hnRNP family members. Its activity is influenced by upstream transcriptional regulators such as MYC and cellular stress signals. Key downstream alternative splicing targets include the apoptosis regulators Bcl-x and Fas, as well as the adhesion molecule CD44. Through these interactions, HNRNPH1 integrates transcriptional cues with post-transcriptional mRNA processing, modulating mRNA metabolism and impacting cell fate decisions.
In HeLa cells, HNRNPH1 knockout disrupts normal alternative splicing, providing a model to dissect splicing dysregulation in cancer. The polyclonal background mirrors heterogeneous tumor populations, and loss of HNRNPH1 alters expression of key isoforms such as Bcl-x and Fas, thereby impacting apoptosis and proliferation. This tool helps elucidate HNRNPH1’s contribution to cervical adenocarcinoma progression and other cancers where splicing aberrations are prevalent.
This polyclonal knockout line is suitable for mechanistic studies of alternative splicing, target validation, and splicing modulator screening. Representative assays include RT-qPCR for isoform quantification, RNA immunoprecipitation, western blotting, RNA-seq, and cell viability or apoptosis analyses. For additional information, contact Ascent Research.
