The KHDRBS3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population designed for loss-of-function analysis of the KHDRBS3 gene. This heterogeneous pool of HeLa cells carries targeted disruptions of the KHDRBS3 locus, enabling investigation of its roles in alternative splicing and signaling without clonal isolation.
HeLa cells are an HPV18-positive cervical adenocarcinoma epithelial line widely used in cancer research. Their transformed phenotype, driven by HPV oncoproteins E6/E7, provides a relevant background for studying oncogenic pathways. This established model supports robust experimental manipulation, making it ideal for dissecting gene functions in tumor biology.
KHDRBS3 encodes an RNA-binding protein that regulates alternative splicing of pre-mRNAs. It is activated by SRC family kinases (SRC, FYN) in response to signals such as TCR activation or INSR. Phosphorylated KHDRBS3 modulates splicing of targets including CD44, BCL2L1, FGFR2, and CCND1. It interacts with SAM68, SF1, and U2AF to control exon usage, thereby linking kinase signaling to transcript isoform selection and impacting proliferation and apoptosis.
In HPV18-positive cervical adenocarcinoma cells, KHDRBS3 knockout enables dissection of its contribution to cancer-relevant splicing decisions. Aberrant alternative splicing is implicated in cervical, breast, and glioblastoma malignancies. Ablating KHDRBS3 in HeLa cells allows researchers to examine how it coordinates pro-proliferative or anti-apoptotic isoform switches, offering a model to test SRC pathway inhibitors or splicing-targeted therapies.
Applications include RT-PCR isoform analysis and RNA-seq to map splicing alterations, western blotting and phospho-tyrosine assays to assess SRC signaling, and co-immunoprecipitation to probe KHDRBS3 complexes. Phenotypic assays such as MTS proliferation and Annexin V apoptosis measurements quantify functional outcomes. This polyclonal knockout tool serves functional genomics, drug screening, and cancer signaling studies. For further details, contact Ascent Research.
