KRTCAP2 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the KRTCAP2 gene, enabling detailed loss-of-function studies in a near-haploid human background. The polyclonal nature of this product provides a heterogeneous pool of cells carrying a variety of CRISPR/Cas9-mediated gene disruptions, offering a robust model for analyzing the functional consequences of KRTCAP2 ablation without the selection biases inherent to monoclonal lines. This product is an essential tool for investigating integrin-mediated cell adhesion and migration, drug sensitivity, and cancer cell signaling.
The HAP1 host cell line is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line, exhibiting an adherent fibroblast-like morphology. Its near-haploid karyotype minimizes the genetic redundancy associated with diploid genomes, making it an exceptionally powerful model for targeted gene knockout and high-throughput functional genomic screens. HAP1 cells retain key characteristics of CML and have become a widely adopted platform for exploring cancer biology, including signaling pathway dissection and drug resistance mechanisms.
KRTCAP2 is a protein implicated in the regulation of integrin beta1 (ITGB1)-mediated adhesion and migration, acting as a potential tumor suppressor. Mechanistically, KRTCAP2 interacts with ITGB1 and the tetraspanin CD151, and its expression is transcriptionally regulated by the p63 transcription factor TP63. Loss of KRTCAP2 disrupts ITGB1 activation and downstream signaling, affecting the focal adhesion kinase PTK2 (FAK), SRC kinase, and the MAPK/ERK cascade (MAPK3/1), as well as AKT1. These alterations impair the ITGB1/ITGA2?CPTK2?CSRC?CMAPK/AKT signaling axis and involve the small GTPases RAC1 and RHOA, ultimately compromising cell adhesion strength and migratory capacity.
In the HAP1 CML context, KRTCAP2 knockout provides a physiologically relevant system to dissect adhesion-dependent signaling pathways that contribute to leukemic cell homing, niche interactions, and stroma-mediated drug resistance. The disruption of KRTCAP2 may attenuate key survival and motility signals, highlighting its role in integrin-driven oncogenic processes. This haploid model amplifies phenotypes, facilitating the identification of signaling dependencies that might otherwise be obscured in diploid cells, and offering a unique platform for mechanistic studies in leukemia biology.
These polyclonal knockout cells are ideally suited for a range of functional assays, including cell migration (e.g., transwell or wound healing assays), adhesion to extracellular matrix components, and co-immunoprecipitation to analyze ITGB1-containing complexes. They also support phospho-signaling analysis by Western blot or flow cytometry (e.g., phospho-FAK, phospho-ERK1/2), RT-qPCR validation of downstream transcriptional targets, and immunofluorescence for focal adhesion dynamics. Moreover, they serve as a valuable model for drug sensitivity screening in CML and for investigating KRTCAP2’s broader role in cancer cell signaling. For additional information on this product, please contact Ascent Research.
