The ANXA10 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the HAP1 human chronic myeloid leukemia (CML) cell line, engineered to disrupt the ANXA10 gene. This heterogeneous knockout pool provides a loss-of-function model for annexin A10 biology in a near-haploid genetic background. The polyclonal format ensures a diverse array of gene-disruption events, enabling robust functional genomic analyses without clonal selection biases.
The HAP1 parental line is an adherent male CML cell line characterized by a near-haploid karyotype and constitutive expression of the BCR-ABL fusion oncoprotein. Its haploid genome facilitates direct genotype-phenotype correlations, making it an optimal host for CRISPR-mediated gene knockout studies. The BCR-ABL-positive status provides a disease-relevant setting for exploring kinase-driven signaling networks.
ANXA10 encodes an annexin family calcium-dependent phospholipid-binding protein that regulates endosomal trafficking, cell cycle progression, and apoptosis. ANXA10 functions downstream of TGF-?? signaling, under transcriptional control by SP1 and miR-224, and modulates MAPK/ERK and NF-??B pathways. It interacts with S100A10, S100A11, ANXA2, F-actin, and Rab proteins, influencing the expression of cyclin D1, Bcl-2, and MMP9. Consequently, ANXA10 disruption can perturb cell proliferation, survival, and invasive capacity, offering a tool to dissect these interconnected signaling cascades.
In the near-haploid HAP1 context, ANXA10 knockout yields unambiguous loss-of-function phenotypes due to single-copy gene disruption. Combined with BCR-ABL kinase activity, this model allows investigation of crosstalk between calcium-responsive annexin functions and oncogenic MAPK/ERK signaling. It is particularly suited to uncovering synthetic lethal interactions or compensatory mechanisms that may be exploited for therapeutic intervention in CML and other ANXA10-associated malignancies.
This knockout product is applicable to diverse research areas, including cancer cell biology, drug sensitivity profiling, and signal transduction. Recommended assays include RT-qPCR and western blotting for expression analysis, immunofluorescence and flow cytometry for phenotypic characterization, MTT and Annexin V apoptosis assays for functional readouts, and wound healing or migration assays. Co-immunoprecipitation and calcium imaging enable investigation of ANXA10 molecular interactions and calcium dynamics, while xenograft models support in vivo tumorigenicity studies. For more information, custom requests, or technical assistance, contact Ascent Research.
