The HNRNPH1 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HEK293T cells, designed for loss-of-function studies of the HNRNPH1 gene. This heterogeneous pool of target-gene-disrupted cells provides a robust model for population-level assays without single-cell cloning.
HEK293T cells are human embryonic kidney cells transformed with adenovirus 5 DNA, constitutively expressing SV40 large T antigen. They are widely used for viral production, protein expression, and gene editing due to high transfection efficiency and rapid growth.
HNRNPH1 is a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family and an essential RNA-binding protein that preferentially binds G-tract sequences within pre-mRNAs. Through its interaction with core spliceosome components and regulatory factors, such as U2AF1, PTB, and SRSF proteins, HNRNPH1 modulates alternative exon inclusion or skipping, influencing mRNA isoform expression. This process is responsive to upstream signals transmitted by MYC and the MAPK pathway, which activate HNRNPH1-mediated splicing programs. Notably, HNRNPH1 directs the alternative splicing of MDM2 to produce isoforms that differentially regulate p53 activity, and it controls the splicing of FAS to modulate apoptotic signaling, thereby integrating proliferative and cell death cues.
In the HEK293T background, CRISPR/Cas9-mediated knockout of HNRNPH1 disrupts these splicing networks, leading to altered expression of MDM2 and FAS variants and consequent changes in cell cycle progression and sensitivity to apoptosis. This polyclonal population captures the variability expected in heterogeneous knockout contexts, making it ideal for studying the robustness of splicing-dependent phenotypes. The model is particularly relevant for investigating the molecular basis of glioblastoma and breast cancer, where HNRNPH1 overexpression correlates with oncogenic splicing patterns, and for exploring its roles in neurodevelopmental disorders linked to RNA processing defects.
Researchers can employ this product for high-throughput screening of splicing modulators, validation of HNRNPH1 as a therapeutic target, and detailed mechanistic dissection of RNA-protein interactions. Compatible assays include RNA sequencing to globally assess splicing changes, CLIP to define RNA-binding landscapes, co-immunoprecipitation to isolate HNRNPH1-containing complexes, and Western blotting or RT-qPCR to quantify downstream effector expression. Proliferation and apoptosis assays enable functional validation. For additional information or custom inquiries, please contact Ascent Research.
