The HNRNPDL Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, designed to disrupt HNRNPDL expression. This loss-of-function model enables investigation of post-transcriptional regulatory mechanisms without inhibitors or transient knockdowns. The polyclonal format preserves heterogeneity, offering a robust system for population-level gene function studies. Gene disruption was achieved by CRISPR/Cas9-mediated targeting, yielding a heterogeneous pool of cells with abrogated HNRNPDL protein.
The parental HeLa cell line is an immortalized cervical adenocarcinoma epithelial line from Henrietta Lacks, positive for HPV18. Widely used for gene expression, virology, and cancer research, HeLa cells display strong growth and are amenable to genetic manipulation. This cervical cancer origin provides a relevant context for studying HNRNPDL’s role in proliferation and malignant transformation, given its regulation of mRNAs controlling cell cycle and apoptosis.
hnRNPDL is an RNA-binding protein that binds AU-rich elements (AREs) in 3?? UTRs of target mRNAs, modulating stability and translation. It can promote mRNA decay via the CCR4-NOT complex or stabilize transcripts, depending on context. Upstream regulation involves kinases such as p38 MAPK, ERK, AKT, and transcription factor MYC, and it responds to stress stimuli. HNRNPDL interacts with hnRNPA1, hnRNPC, UPF1, eIF4E, and 14-3-3 proteins, positioning it within networks controlling alternative splicing, stress granule assembly, and mRNA fate. Key downstream targets include ARE-containing transcripts like p53, cyclin D1, and TNF-??, linking hnRNPDL to cell cycle, apoptosis, and inflammation.
Loss of HNRNPDL in HeLa cells is expected to disrupt post-transcriptional control of proliferation and survival genes, impacting cancer phenotypes. The HPV18-positive background adds complexity, as viral oncoproteins may intersect hnRNPDL pathways. This knockout model helps dissect hnRNPDL’s role in mRNA metabolism within cervical adenocarcinoma, potentially uncovering stress response vulnerabilities involving stress granules. Although HNRNPDL mutations are linked to muscular dystrophy and neurodegeneration, the HeLa context primarily supports oncogenic studies.
Researchers can apply these cells in diverse workflows, including RNA immunoprecipitation and CLIP to validate mRNA targets, and RNA-seq for transcriptome-wide analysis. Western blotting and RT-qPCR quantify downstream proteins and mRNAs (e.g., p53, cyclin D1). Immunofluorescence monitors stress granule dynamics, while reporter assays measure ARE-mediated regulation. Co-immunoprecipitation maps protein interactions. For specifications, contact Ascent Research.
