The ITGA1 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human ITGA1 gene in the near-haploid HAP1 cell line. This product provides a heterogeneous pool of cells with disrupted ITGA1, enabling the study of integrin alpha-1 loss-of-function in a defined genetic background without the selective pressures of single-cell cloning. The polyclonal format maintains population-level representation, reducing clonal artifacts and facilitating large-scale functional genomics applications.
HAP1 is a fibroblast-like, near-haploid human cell line originally derived from the KBM-7 chronic myeloid leukemia (CML) line. Its near-haploid karyotype simplifies knockout generation and genetic screening, as a single allele typically needs to be targeted for phenotypic expression. Widely used in functional genomics, HAP1 cells provide a robust platform for investigating gene function in adhesion, migration, and signal transduction, retaining key pathways relevant to cancer and extracellular matrix biology.
ITGA1 encodes the alpha-1 subunit of integrin, which heterodimerizes with integrin beta-1 (ITGB1) to form a major receptor for collagens (COL1A1, COL2A1) and laminins. Ligand binding triggers activation of focal adhesion kinase (FAK/PTK2) and SRC family kinases, leading to downstream phosphorylation of ERK1/2 (MAPK1/3) and AKT1, thereby regulating cell adhesion, migration, proliferation, and survival. Upstream, ITGA1 expression is induced by cytokines such as TGFB1, IL1B, TNF, and EGF. Key intracellular adaptors like talin-1 (TLN1) and vinculin (VCL) link the integrin complex to the actin cytoskeleton, reinforcing focal adhesion dynamics. This signaling axis positions ITGA1 at the nexus of mechanical and biochemical cues from the microenvironment.
Disrupting ITGA1 in HAP1 cells creates a powerful loss-of-function model to dissect integrin-dependent phenotypes in a haploid background. The absence of a second functional allele ensures robust phenotypic penetrance, making this polyclonal population ideal for genetic screens and high-content assays. Researchers can interrogate how loss of ITGA1 impacts adhesion to collagen matrices, alters migration velocity and directionality, or rewires downstream kinase networks. Given the role of ITGA1 in fibrosis, cancer metastasis, and inflammation, this model is particularly valuable for testing anti-fibrotic or anti-metastatic compounds.
Typical applications include adhesion assays on collagen-coated surfaces, wound healing migration studies, and evaluation of phospho-FAK and phospho-AKT by western blotting. The polyclonal nature supports population-level analyses by flow cytometry and RNA-seq, while co-immunoprecipitation can confirm disrupted ITGA1-ITGB1 heterodimerization. This product is suited for drug screening, siRNA rescue experiments, and synthetic lethality studies in haploid cells. For additional information, please contact Ascent Research.
