The ADARB1 Knockout HAP1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout population targeting the ADARB1 gene in the near-haploid HAP1 human cell line. This heterogeneous pool of loss-of-function alleles enables robust genetic perturbation of ADARB1-dependent RNA editing, avoiding clonal biases and supporting both focused and screening applications.
HAP1 is a human haploid cell model derived from the KBM-7 chronic myeloid leukemia line, expressing BCR-ABL. Its haploid state simplifies knockout generation, as perturbation of a single allele yields functional gene inactivation. Widely used for functional genomics, HAP1 cells offer efficient transfection, consistent growth, and high-throughput assay compatibility. The BCR-ABL-positive background further permits studies intersecting oncogenic signaling with RNA modification pathways.
ADARB1 encodes ADAR2, a double-stranded RNA-specific adenosine deaminase that catalyzes A-to-I editing. ADAR2 activity is regulated by calcium influx and CREB-dependent transcription, and it edits critical neuronal transcripts including the GRIA2 Q/R site, GRIK2, KCNA1, and HTR2C. GRIA2 editing at the Q/R site renders AMPA receptors impermeable to calcium, a modification essential for synaptic transmission and plasticity. ADAR2 interacts with ADAR1, DHX9, and RNA-binding proteins within the epitranscriptomic machinery.
In HAP1 cells, ADARB1 knockout creates a simplified platform for dissecting editing mechanisms. The haploid genotype ensures clear genotype-phenotype linkage. The polyclonal nature provides a range of editing disruptions suitable for synthetic lethality or modifier screens. Given ADAR2??s roles in ALS, epilepsy, and neurodevelopment, this model allows investigation of disease-associated editing events and evaluation of pharmacological interventions targeting ADAR2 activity.
Key applications include RT-qPCR and western blot for expression analysis, Sanger sequencing or RNA-seq for editing quantification at GRIA2 and other targets, calcium imaging and patch-clamp electrophysiology for functional readouts, and immunofluorescence for localization. The model supports epitranscriptomics, neurological disease research, and synaptic plasticity studies. For detailed protocol guidance and technical specifications, please contact Ascent Research.
