The AIP Knockout HAP1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 near-haploid cell line. This model introduces targeted gene disruption in the AIP locus, leading to loss of functional AIP protein expression across the cell population. As a polyclonal pool, it captures a spectrum of editing events, offering a practical approach for pooled functional genomics screens and pathway analysis.
HAP1 cells are a near-haploid, fibroblast-like cell line originally derived from a male patient with chronic myeloid leukemia. Their near-haploid karyotype simplifies genetic manipulation and phenotypic analysis, as most genes are present in a single copy, minimizing confounding effects from additional alleles. HAP1 cells are widely adopted for CRISPR-based knockout and knock-in studies, protein interaction mapping, and high-content screening campaigns. The adherent morphology and robust growth characteristics make them suitable for a broad range of cell-based assays.
AIP functions as a co-chaperone that stabilizes the cytoplasmic aryl hydrocarbon receptor (AhR) complex, which also includes HSP90 and other cofactors. Upon binding of ligands such as TCDD or kynurenine, AhR translocates to the nucleus, dimerizes with ARNT, and activates transcription of target genes including CYP1A1 and CYP1B1. AIP is also implicated in mitochondrial regulation through interactions with Tom20 and modulation of cAMP degradation via PDE4A. Knockout of AIP disrupts AhR protein stability, attenuating ligand-induced transcription and potentially impairing mitochondrial respiration and metabolic adaptation.
The HAP1 background is particularly advantageous for studying AIP loss-of-function because the near-haploid genome ensures that single-allele disruptions result in a complete knockout phenotype across the population. This isogenic context allows clear dissection of AhR signaling dynamics, mitochondrial function, and stress responses without the compensatory effects common in diploid lines. Moreover, the polyclonal nature of the product reflects the inherent diversity of CRISPR editing outcomes, which can be leveraged to study gene dosage effects or to identify critical functional domains through variant analysis.
This AIP knockout model is suited for a wide array of biomedical research applications, including mechanistic studies of AhR-mediated dioxin toxicity, pituitary adenoma pathogenesis, and cancer metabolism. It can be employed in AhR-dependent luciferase reporter assays, quantitative PCR for CYP1A1/CYP1B1 induction, immunofluorescence tracking of AhR nuclear translocation, and co-immunoprecipitation of the AIP-HSP90-AhR complex. Additional uses include mitochondrial respiration profiling via Seahorse analysis and drug screening for AhR modulators targeting the chaperone interface. For detailed product specifications and ordering information, please contact Ascent Research.
