The HNRNPR Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the HNRNPR gene in human near-haploid HAP1 cells. This heterogeneous pool of edited cells carries targeted disruptions of HNRNPR, enabling robust functional investigation of this RNA-binding protein without the need for single-cell cloning. The product is well suited for experiments requiring a polyclonal knockout model that maintains genetic diversity while abrogating HNRNPR expression across the population.
The HAP1 cell line is a human near-haploid, fibroblast-like cell line derived from the KBM-7 chronic myeloid leukemia cell line. Its adherent growth and near-haploid karyotype simplify genetic manipulation and interpretation of knockout phenotypes, as the presence of a single gene copy per cell minimizes confounding effects from genetic redundancy. These characteristics establish HAP1 as a versatile platform for functional genomics, high-throughput genetic screens, and mechanistic studies in a human cell context.
HNRNPR encodes a heterogeneous nuclear ribonucleoprotein that functions as an RNA-binding protein, playing a critical role in mRNA processing, axonal transport, and local translation regulation, particularly in neurons. HNRNPR interacts with SMN, FMRP, STAU1, and the motor protein KIF5A to assemble neuronal RNA transport granules that mediate the trafficking of specific mRNA targets, including ACTB and GAP43, along microtubules. Its activity is regulated by cellular stress signals such as oxidative stress, and it contributes to translational control at synapses, thereby influencing neuronal development and plasticity. Disruption of HNRNPR perturbs these complexes and downstream pathways, offering a direct route to dissect its mechanistic contributions.
Although HAP1 cells are not of neuronal origin, their near-haploid background and robust growth make them an ideal reductionist model to dissect the fundamental cell biology of HNRNPR, including its roles in RNA granule assembly, mRNA transport, and translation regulation. This polyclonal knockout pool enables researchers to investigate loss-of-function effects in a simplified genetic system, facilitating studies of RNA?Cprotein interactions, stress granule dynamics, and global transcriptomic changes without the complexity of diploid or neuronal systems. The knockout model is especially valuable for linking HNRNPR-dependent mechanisms to broader cellular RNA processing pathways.
This cell population supports a diverse range of applications, including functional genomics screens to identify modulators of mRNA trafficking, mechanistic studies of RNA granule composition using immunoprecipitation and CLIP-seq, and transcriptome-wide analysis via RNA-seq. Routine assays such as western blotting and RT-qPCR confirm knockout efficiency, while immunofluorescence and live-cell imaging can assess perturbations in RNA granule localization and dynamics. The cells also enable functional rescue experiments to validate HNRNPR-dependent phenotypes, providing a comprehensive toolkit for research into diseases such as spinal muscular atrophy, amyotrophic lateral sclerosis, and neurodevelopmental disorders. For further information or to discuss custom applications, please contact Ascent Research.
