The HNRNPAB Knockout HeLa Polyclonal Cells represent a population of CRISPR/Cas9-edited HeLa cells with targeted disruption of the HNRNPAB gene. As a polyclonal knockout population, this product provides a genetically heterogeneous pool of cells with HNRNPAB loss-of-function, suitable for studying gene function without clonal artifacts. CRISPR/Cas9-mediated gene disruption was employed to ablate HNRNPAB expression, generating a versatile model for investigating RNA processing and cancer-related pathways.
HeLa cells are an immortalized cervical adenocarcinoma cell line derived from an HPV18-positive tumor. These epithelial cells are widely used in cancer biology due to their robust growth, easy transfectability, and well-characterized signaling networks. The HeLa background provides a relevant context for investigating HNRNPAB??s role in cervical cancer progression and RNA metabolism.
HNRNPAB encodes an RNA-binding protein that participates in pre-mRNA splicing, nucleocytoplasmic transport, and mRNA stability. It interacts with spliceosomal proteins, other hnRNP family members, and RNA polymerase II, and its activity is regulated by transcriptional control and cellular stress signals. HNRNPAB functions within mRNA splicing and transport pathways, associating with U1 snRNP, U2 snRNP, the SF3B complex, and mRNA export factors. Downstream, it modulates splicing targets such as SMN2 and influences mRNA stability, thereby shaping the cellular transcriptome.
In the context of HeLa cells, HNRNPAB knockout disrupts RNA processing mechanisms that are often dysregulated in cervical adenocarcinoma. Since HeLa cells are HPV18-positive and display altered splicing patterns, loss of HNRNPAB may reveal vulnerabilities in cancer cell survival and proliferation. This model enables dissection of how RNA-binding protein dysfunction contributes to oncogenic phenotypes, offering insights into both cervical cancer and broader RNA metabolism disorders.
Researchers can employ these polyclonal cells to study RNA processing mechanisms, screen for splicing-modulating compounds, and investigate cancer cell biology. Representative assays include RT-qPCR for alternative splicing isoforms, RNA-seq for global transcriptome analysis, western blotting and immunofluorescence for protein expression, and functional assays such as cell proliferation, migration, and invasion. This knockout model is a valuable tool for exploring HNRNPAB-dependent pathways in disease. For additional information or bulk orders, please contact Ascent Research.
