The ALB Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ALB gene in the HAP1 human cell line. This product provides a genetically heterogeneous loss-of-function model for albumin research, generated by CRISPR/Cas9-mediated disruption of the ALB locus. The polyclonal format ensures a mixed population of cells carrying diverse editing events, enabling the study of gene function without clonal selection bias. Suitable for pooled knockout screens and population-level functional assays, this model serves as a versatile tool for investigating ALB-dependent processes.
The HAP1 cell line is a near-haploid, fibroblast-like cell line derived from a male patient with chronic myeloid leukemia. With its adherent growth and near-haploid karyotype, HAP1 is widely used in CRISPR-based functional genomics due to the ease of genetic manipulation and the simplified genotype-to-phenotype correlation. These cells lack the functional copies that complicate diploid models, making them particularly suitable for loss-of-function studies. HAP1’s fibroblast-like morphology and origin from the hematopoietic lineage offer a unique platform for studying hepatic genes in a non-hepatic context.
The ALB gene encodes albumin, the most abundant plasma protein, primarily produced by hepatocytes. Albumin is critical for maintaining oncotic pressure and serves as a major carrier for hydrophobic molecules, including fatty acids, bilirubin, steroid hormones, and drugs like warfarin. The protein interacts with the endothelial receptor gp60, facilitating transcytosis and tissue distribution. ALB expression is transcriptionally regulated by factors such as HNF1A, HNF4A, CEBPA, and glucocorticoids, and is induced during the acute phase response by IL-6. The downstream roles of albumin extend to antioxidant defense and modulation of inflammation, positioning ALB at a nexus of metabolic and vascular homeostasis.
In the HAP1 background, ALB disruption creates an albumin-null model that is not constrained by liver-specific expression patterns. Although HAP1 is not a hepatic cell line, its use allows direct assessment of ALB-dependent cellular processes, including ligand binding and intracellular trafficking, without the confounding influence of endogenous albumin. This model enables the dissection of albumin??s cell-autonomous roles, such as its interaction with calcium signaling and its potential involvement in pathways beyond its classical secretory function. The near-haploid nature of HAP1 ensures that the knockout phenotype is fully penetrant at the population level, providing a robust system for genetic interaction studies and high-throughput screenings.
Researchers can employ these polyclonal knockout cells for a range of applications, including drug-protein binding studies to evaluate pharmacokinetic interactions using drug binding assays, or analbuminemia disease modeling by analyzing fatty acid transport defects with fatty acid binding assays. They serve as effective controls in CRISPR screens due to the well-characterized HAP1 system, and are suitable for hepatic function research when combined with hepatocyte differentiation models. Validation of the knockout can be performed via Sanger sequencing of the targeted locus, RT-qPCR to confirm transcript reduction, western blot to assess protein loss, or ELISA for albumin quantification. These cells are invaluable for investigating albumin-related pathologies such as hypoalbuminemia, liver cirrhosis, and nephrotic syndrome. For further information, please contact Ascent Research.
