The ITGB1 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-mediated loss-of-function model in which the ITGB1 gene is disrupted across a polyclonal population of HAP1 cells. This cell pool is designed for researchers investigating integrin beta-1 function without the confounding effects of monoclonal selection, thereby preserving physiological heterogeneity encountered in disease-relevant studies. The product provides a robust system for dissecting integrin-dependent adhesion, migration, and signaling in a well-characterized genetic background.
The host cell line, HAP1, is a near-haploid fibroblast-like line derived from the KBM-7 chronic myeloid leukemia patient. Its near-haploid karyotype simplifies genetic analysis and enables high-efficiency mutagenesis screens, making it a preferred model for unbiased functional genomics. The fibroblast-like morphology and adhesive properties of HAP1 cells render them particularly suitable for studying cell-matrix interactions and cytoskeletal dynamics.
ITGB1 encodes the integrin beta-1 subunit, a critical component of heterodimeric receptors for extracellular matrix (ECM) proteins such as fibronectin, collagen, and laminin. Upon ligand binding, integrin beta-1 is activated by intracellular adaptors talin and kindlin, and signals bidirectionally to regulate focal adhesion assembly. Downstream, integrin beta-1 activation engages focal adhesion kinase (FAK) and Src family kinases, which propagate signals through ILK, AKT, ERK, JNK, and transcription factors including beta-catenin, NF-kB, and AP-1. This signaling network couples ECM adhesion to cell survival, proliferation, and migration, with crosstalk to PI3K/AKT, MAPK/ERK, and Wnt pathways. ITGB1 also interacts with alpha integrin subunits ITGA1, ITGA2, ITGA5, and ITGAV, as well as focal adhesion constituents paxillin and vinculin.
In the HAP1 background, disruption of ITGB1 abolishes integrin beta-1-mediated adhesion and downstream signaling, providing a clean platform for structure-function studies and rescue experiments. The near-haploid genome eliminates confounding allelic compensation, enabling precise interrogation of ITGB1-dependent phenotypes. This model is highly relevant to pathologies such as cancer metastasis and fibrosis, where aberrant integrin signaling drives disease progression.
Researchers can deploy these polyclonal ITGB1 knockout HAP1 cells in a variety of assays, including cell adhesion to ECM substrates, transwell migration, immunofluorescence staining of focal adhesion proteins, western blotting for phosphorylated FAK, AKT, and ERK, and flow cytometry for surface integrin expression. The cells are applicable to studies of drug resistance, leukocyte adhesion deficiency, inflammatory bowel disease, and developmental disorders. For additional technical details or bulk ordering, please contact Ascent Research.
