The HNRNPR Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from HEK293T cells, engineered for disruption of the HNRNPR gene. This heterogeneous pool of edited cells harbors CRISPR-mediated loss-of-function modifications, enabling functional studies without clonal isolation. The polyclonal format maintains genetic diversity while ablating endogenous hnRNP R expression, creating a versatile model for investigating RNA processing, mRNA transport, and translational control.
The HEK293T host cell line is an immortalized human embryonic kidney epithelial line expressing SV40 large T-antigen, which ensures exceptionally high transfectability and robust protein production. Commonly employed for recombinant protein expression and viral vector generation, this cell line provides a well-characterized, simplified system for molecular biology research. Its amenability to genetic manipulation makes it an ideal platform for generating CRISPR knockouts to dissect gene function in a controlled environment.
HNRNPR encodes hnRNP R, a multifaceted RNA-binding protein that regulates pre-mRNA alternative splicing, nucleocytoplasmic mRNA export, and translation. It directly interacts with the SMN protein and is integrated into the SMN complex, which is essential for spliceosomal snRNP assembly. Among its key downstream targets are SMN2 pre-mRNA, where hnRNP R enhances exon 7 inclusion, and tau mRNA, which it modulates for transport and local translation. Additional binding partners include other hnRNP proteins and spliceosomal components. Its activity is influenced by upstream transcriptional regulation and cellular stress, linking hnRNP R to adaptive responses and disease pathways including spinal muscular atrophy and neurodegeneration.
Knockout of HNRNPR in HEK293T cells disrupts normal RNA processing, even though these cells are non-neuronal. Core machinery and interaction partners like SMN remain present, enabling analysis of hnRNP R-dependent regulation of SMN2 splicing and tau mRNA metabolism. This loss-of-function model is particularly useful for studying molecular mechanisms relevant to spinal muscular atrophy and tau-related neurological disorders, as well as for examining the broader role of hnRNP R in cancer-related RNA dysregulation.
This knockout cell population supports diverse applications, including RNA processing studies, spinal muscular atrophy research, and cancer biology. Standard assays such as western blotting, immunofluorescence, and RT-qPCR can confirm knockout effects and target gene changes, while RNA-seq, RIP-seq, and CLIP-seq allow transcriptome-wide and interaction profiling. The model thus serves as a robust platform for dissecting hnRNP R-mediated regulatory networks. For further details, please contact Ascent Research.
