CD164 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HAP1 human cell line, carrying a targeted disruption of the CD164 gene. This heterogeneous knockout pool serves as a loss-of-function model for investigating the functions of CD164, a sialomucin adhesion receptor. The polyclonal format reduces clonal bias, allowing robust detection of phenotype. The CD164 gene disruption eliminates the full-length protein, providing a clean background for studying adhesion, migration, and downstream signaling.
HAP1 is a near-haploid chronic myeloid leukemia cell line established from a male patient, expressing the BCR-ABL1 fusion oncogene and possessing a deficient p53 pathway. The haploid karyotype simplifies genetic knockout, as disruption of a single allele can yield a complete loss-of-function phenotype. This characteristic makes HAP1 an exceptional host for functional genomic screens and studies requiring recessive phenotypic readouts. The leukemic origin of HAP1 further provides a disease-relevant context for exploring cancer-related adhesion and signaling pathways.
CD164 encodes a type I transmembrane sialomucin that functions as a cell adhesion receptor. It is activated by the chemokine CXCL12 and acts as a co-receptor for CXCR4, facilitating integrin-mediated adhesion and downstream signaling. CD164 interacts with integrin ??1, L-selectin, and galectin-3, and its engagement stimulates phosphorylation of FAK, SRC, PI3K/AKT, and ERK1/2, ultimately modulating ??-catenin activity. The receptor is transcriptionally regulated by Notch1 and Wnt3a, positioning it at the intersection of CXCL12/CXCR4 chemokine, Notch, and Wnt/??-catenin pathways. Through these interactions, CD164 orchestrates hematopoietic stem/progenitor cell homing, muscle satellite cell function, and metastatic dissemination.
In the HAP1 background, knockout of CD164 abolishes the receptor, markedly impairing CXCL12-induced chemotaxis and adhesion, and attenuating PI3K/AKT and ERK signaling cascades. The haploid nature of HAP1 ensures that the observed phenotypes are directly attributable to CD164 loss, without interference from a wild-type allele. The p53 deficiency and BCR-ABL1 oncogene create a milieu that mimics certain leukemic conditions, making this model particularly suited for dissecting how CD164 controls hematopoietic progenitor trafficking and contributes to leukemia cell migration.
This CD164 knockout polyclonal cell population is applicable to diverse research areas, including functional genomics, CRISPR screen controls, and hematopoietic stem cell biology. It enables investigation of cancer metastasis mechanisms in prostate, gastric, and acute myeloid leukemia, as well as the pathogenesis of DFNA66-related hearing loss. Typical assays include western blotting for signaling proteins, flow cytometry for surface marker analysis, cell adhesion and transwell migration assays, CXCL12 chemotaxis, RNA-seq for transcriptome profiling, and phospho-signaling analysis. For technical inquiries or to request a quotation, please contact Ascent Research.
