CD151 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-mediated gene-disrupted polyclonal population of the near-haploid HAP1 cell line, designed to abolish CD151 protein expression. This heterogeneous pool of knockout cells provides a robust, population-averaged readout for functional studies, removing the need for single-cell clone isolation while maintaining the power of a loss-of-function model. The polyclonal format is particularly suited for high-throughput screening, signal transduction analysis, and phenotypic assays where diverse genetic edits collectively inform CD151-dependent biology.
The HAP1 host cell line originates from the KBM-7 chronic myeloid leukemia background and retains a near-haploid karyotype. As an adherent hematopoietic progenitor line, it is widely used in CRISPR-based functional genomics due to its simplified genetic landscape, which facilitates straightforward knockout generation and phenotype interpretation. HAP1 cells exhibit robust adhesion and migration behaviors, making them an appropriate platform to investigate integrin-mediated processes and leukemogenesis-related pathways.
CD151, a tetraspanin, orchestrates integrin-mediated cell adhesion, migration, and signaling by integrating with laminin-binding ??3??1 and ??6??1 integrins and forming lateral interactions with related tetraspanins (CD9, CD81, CD63) and receptors such as EGFR and c-Met. Upstream factors including TGF-??, HIF-1??, and the transcription factor SP1 modulate CD151 expression. CD151-dependent signaling proceeds through focal adhesion kinase (FAK), Src, PI3K/AKT, ERK1/2, and Rho GTPases (Rac1, Cdc42), thereby regulating focal adhesion turnover, cytoskeletal dynamics, and matrix metalloproteinase production. Knockout of CD151 disrupts these complexes, attenuating integrin clustering and downstream pathway activation, which ultimately impairs cell motility and matrix remodeling.
In the HAP1 context, loss of CD151 significantly alters cell adhesion and migration, as the hematopoietic lineage relies heavily on integrin?Cextracellular matrix interactions. The haploid nature of HAP1 ensures that a single genetic disruption event abrogates CD151 function in activated cells, allowing unambiguous dissection of its role in focal adhesion assembly, hemidesmosome-related structures, and anchorage-dependent signaling. This model thus enables precise interrogation of CD151??s contribution to ERK/MAPK and PI3K/AKT pathway activation without interference from wild-type allele compensation.
CD151 Knockout HAP1 Polyclonal Cells support a range of cancer biology and cell signaling applications, including metastasis studies, integrin signaling research, and angiogenesis assays. Representative techniques include Transwell migration and invasion, wound healing, adhesion to laminin, immunofluorescence for focal adhesion markers, co-immunoprecipitation of CD151-integrin complexes, flow cytometry for integrin surface expression, and western blotting for phospho-FAK, phospho-AKT, and phospho-ERK1/2. The polyclonal population is also amenable to xenograft metastasis models. For further information, contact Ascent Research.
