CAPN15 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated via targeted disruption of the CAPN15 gene in the near-haploid HAP1 cell line. This product provides a robust loss-of-function model for investigating calpain-15 function, with the polyclonal format capturing a heterogeneous spectrum of edited alleles. The population is designed for researchers studying the molecular basis of cytoskeletal dynamics, cell adhesion, and programmed cell death, offering a versatile tool for genetic and pharmacological studies.
Derived from the KBM-7 chronic myeloid leukemia (CML) line, HAP1 is a near-haploid human cell line that maintains the Philadelphia chromosome (BCR-ABL fusion), making it a well-established model for malignant myeloid cell biology. Its haploid genome simplifies gene-editing experiments and reduces confounding background expression, enabling clean interpretation of knockout phenotypes. The cell line is widely used in genetic screens and pathway analyses due to its tractable growth characteristics and relevance to hematopoietic malignancies.
CAPN15 encodes a non-classical calpain family cysteine protease implicated in calcium-dependent proteolysis. Its activity is tightly regulated by upstream factors including calcium ions, the endogenous inhibitor calpastatin (CAST), and MAPK signaling cascades. Downstream, CAPN15-mediated cleavage modulates focal adhesion proteins such as talin and paxillin, cytoskeletal components including spectrin and filamin, and apoptotic regulators that serve as caspase substrates. The gene operates within a signaling network that integrates calcium channel flux, integrin engagement, and focal adhesion kinase (FAK) activity to control cell-matrix interactions and survival signals.
In the HAP1 CML background, disruption of CAPN15 is anticipated to impair calpain-dependent proteolysis, consequently altering focal adhesion turnover, actin remodeling, and apoptotic sensitivity. This knockout model is particularly useful for dissecting how calpain proteostasis contributes to the aberrant adhesive and migratory properties characteristic of leukemic cells. It also provides a platform to study crosstalk between BCR-ABL signaling and calpain-mediated pathways in a genetically defined context.
Typical research applications include mechanistic studies of cell adhesion and migration using modified Boyden chamber or scratch assays, evaluation of apoptotic responses via Annexin V staining and caspase activation profiling, and validation of calpain-15 as a therapeutic target in cancer metastasis and neurodegeneration. Complementary techniques such as Western blotting for proteolytic fragments and immunofluorescence imaging of focal adhesion complexes enable detailed phenotypic characterization. For additional product details or technical support, please contact Ascent Research.
