BCAR1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 cell line, featuring targeted disruption of the BCAR1 gene. This mixed knockout pool enables loss-of-function studies without clonal selection artifacts, providing a versatile tool for investigating integrin-mediated signaling in a near-haploid human hematopoietic progenitor background.
The HAP1 cell line is near-haploid, derived from the KBM-7 chronic myeloid leukemia line, and displays adherent, fibroblast-like morphology with a stable hematopoietic progenitor phenotype. Its reduced genome complexity facilitates efficient gene disruption and minimizes functional redundancy, making it an ideal host for generating knockout models to dissect signaling networks with low genetic background interference.
BCAR1 (p130Cas) serves as a scaffold protein in focal adhesions, phosphorylated by SRC family kinases upon integrin engagement by ligands such as fibronectin and collagen. This phosphorylation recruits CRK and other SH2 domain proteins, activating downstream effectors including RAC1, PAK, MAPK1/ERK2, and AKT1 to regulate actin dynamics, cell migration, proliferation, and survival. BCAR1 also interacts with FAK, SRC, BCAR3, and PTPN12, and is modulated by growth factors such as EGF and PDGF, positioning it as a central integrator of adhesive and mitogenic signals. Among its transcriptional targets are MMP9 and Cyclin D1, linking adhesion to matrix remodeling and cell cycle progression.
In the HAP1 hematopoietic progenitor model, BCAR1 disruption impairs integrin-dependent adhesion and migration, providing a system to study cancer cell dependency on focal adhesion signaling. Given BCAR1’s roles in breast cancer metastasis, anti-estrogen resistance, and progression of ovarian and lung adenocarcinomas, this polyclonal knockout population enables robust analysis of signaling rewiring and therapeutic resistance mechanisms without single-clone biases.
Researchers can utilize these cells in wound healing, Transwell migration/invasion, and adhesion assays, complemented by immunoprecipitation and Western blotting for phospho-BCAR1 (Tyr410), ERK, or AKT. Phospho-signaling arrays, live-cell imaging of actin dynamics, and RT-qPCR for MMP9 and CCND1 provide comprehensive characterization of pathway alterations. For additional technical inquiries or to discuss how this knockout model can accelerate your research, please contact Ascent Research.
