The KHDRBS2 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-mediated gene disruption model targeting KHDRBS2 in a polyclonal HeLa cell population. This pooled knockout format provides a heterogeneous loss-of-function system, enabling the study of KHDRBS2-dependent cellular processes without clonal selection artifacts. The polyclonal design preserves the genetic diversity inherent to the HeLa background, making it suitable for population-level assessments of signaling and splicing alterations following KHDRBS2 ablation.
The HeLa cell line, derived from a cervical adenocarcinoma of Henrietta Lacks, is an immortalized, HPV18-positive, highly aneuploid human epithelial model extensively used in cancer research. Its robust growth, well-characterized signaling networks??including active MAPK/ERK and PI3K/AKT pathways??and widespread use in functional genomics establish it as an ideal host for investigating KHDRBS2 function. HeLa cells?? high transfection efficiency and responsiveness to growth factors facilitate precise dissection of KHDRBS2-mediated splicing regulation.
KHDRBS2 encodes an RNA-binding protein that couples extracellular signals to alternative pre-mRNA splicing. Upon stimulation, upstream regulators such as EGF activate SRC family kinases (including SRC and FYN), which phosphorylate KHDRBS2. This phosphorylation modulates KHDRBS2??s interaction with RNA polymerase II CTD and spliceosomal components like SF1 and U2AF, thereby altering the splicing of downstream targets including CD44, BCL2L1 (BCL-x), and FGFR2. KHDRBS2 also interacts with PLC??1 and integrates signals from the PI3K/AKT pathway, positioning it at a convergence point between growth factor signaling and alternative splicing decisions that govern cell proliferation and survival.
In HeLa cells, KHDRBS2 regulates oncogenic splicing isoforms of CD44 and BCL2L1, thereby influencing apoptosis resistance, migration, and proliferation??phenotypes central to cervical and other cancers. The polyclonal knockout HeLa model allows researchers to examine the collective impact of KHDRBS2 loss on signal-dependent splicing without clonal bias, revealing pathway-level consequences. Given HeLa cells?? endogenous activation of SRC and MAPK/ERK signaling, this system is particularly suited for dissecting how KHDRBS2 phosphorylation status controls splice site selection of targets linked to glioblastoma, breast, lung, and hepatocellular carcinoma pathogenesis.
This product is designed for a wide range of applications, including western blotting and RT-qPCR-based quantification of KHDRBS2 and splice variant changes, transcriptome-wide RNA-seq for identifying KHDRBS2-dependent splicing events, and functional assays such as proliferation, migration/invasion, and apoptosis analyses. Co-immunoprecipitation studies can probe altered protein interactions with SRC, FYN, and spliceosomal factors, while phospho-protein analysis reveals signaling dynamics. The polyclonal knockout cells are an essential tool for drug screening targeting splicing modulators and for validating KHDRBS2 as a therapeutic vulnerability in cancers with dysregulated alternative splicing. For further details, please contact Ascent Research.
