The ITGAL Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ITGAL gene in HAP1 cells. ITGAL encodes integrin alpha L (CD11A), which pairs with integrin beta 2 to form the LFA-1 adhesion receptor. This polyclonal model enables loss-of-function studies of LFA-1-mediated adhesion and signaling, providing a powerful tool for investigating leukocyte integrin biology.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line. With a fibroblastoid adherent morphology and hematopoietic origin, HAP1 cells serve as a robust model for hematological and immunological research. The near-haploid genome facilitates unambiguous gene disruption, minimizing functional redundancy.
LFA-1 is activated by inside-out signals from T cell receptors, chemokine receptors such as CXCR4, and the small GTPase Rap1, which recruit talin and kindlin-3 to the ??2 cytoplasmic tail. Upon binding to ICAM-1, -2, or -3, LFA-1 triggers outside-in signaling through FAK, Src family kinases, and MAPK cascades, ultimately activating NF-??B and AP-1 transcription factors. ITGAL knockout therefore abolishes LFA-1?CICAM interactions and downstream cascades, impairing leukocyte adhesion, spreading, and immune synapse function.
In the HAP1 background, ITGAL disruption provides a simplified system to study LFA-1-dependent processes without competing signals from other leukocyte receptors. The hematopoietic lineage retains relevant signaling networks, while the near-haploid state ensures efficient gene inactivation. This model is ideal for dissecting integrin mechanobiology, adhesion dynamics, and signaling in a tractable, adherent cell format.
Applications include quantitative adhesion assays on ICAM-1-coated surfaces, Transwell migration experiments, flow cytometry for CD11A expression, and Western blotting for phospho-FAK (Y397). The cells are suitable for high-content screening of leukocyte adhesion modulators, co-culture studies modeling transendothelial migration, and investigation of autoimmune disease mechanisms. For further information, please contact Ascent Research.
