The EFCAB7 Knockout K-562 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the EFCAB7 gene in the K-562 human myelogenous leukemia cell line. This product provides a heterogeneous pool of cells harboring targeted gene disruption, enabling loss-of-function studies without clonal selection. EFCAB7 (EF-hand calcium-binding domain 7) is a predicted calcium sensor protein containing EF-hand domains, implicated in calcium-mediated signal transduction. The polyclonal format allows researchers to analyze gene function in a mixed genetic background, capturing a range of knockout efficiencies suitable for population-level phenotypic assays.
K-562 cells were originally established from the pleural effusion of a 53-year-old female patient with chronic myeloid leukemia (CML) in blast crisis. These suspension-adapted lymphoblasts exhibit an undifferentiated blast phenotype and carry the Philadelphia chromosome, resulting in expression of the BCR-ABL1 fusion oncoprotein. Additionally, K-562 cells are p53 null and possess a triploid karyotype, contributing to their robust proliferative capacity and genetic instability. As a well-characterized CML model, K-562 cells are widely employed for investigating leukemogenic signaling, drug responses, and hematopoietic differentiation.
EFCAB7 belongs to the EF-hand superfamily of calcium-binding proteins, which function as intracellular calcium sensors and signal transducers. It is predicted to interact with calmodulin and other EF-hand proteins, potentially participating in calcium-dependent signaling pathways that involve key mediators such as calcineurin and Ca2+/calmodulin-dependent protein kinases (CaMK). The mechanistic role of EFCAB7 remains largely uncharacterized, but its EF-hand domains suggest involvement in decoding transient calcium fluxes to regulate downstream cellular processes. Knockout of EFCAB7 in K-562 cells is expected to perturb calcium signaling networks, providing a valuable tool to dissect its molecular contributions.
In the K-562 leukemia context, disruption of EFCAB7-mediated calcium sensing may impact critical cellular functions including proliferation, survival, and myeloid differentiation. Given the absence of p53 and the constitutive BCR-ABL1 kinase activity, K-562 cells rely on alternative signaling networks that may intersect with calcium pathways. The undifferentiated blast phenotype of K-562 cells offers a reproducible backdrop to evaluate whether EFCAB7 loss alters differentiation markers (e.g., CD41, CD71) under various stimuli. This model thus allows investigation of calcium signaling in a leukemic background without the confounding effects of p53-dependent apoptosis.
EFCAB7 Knockout K-562 Polyclonal Cells are well-suited for a range of experimental applications including western blotting and RT-qPCR to confirm gene disruption, calcium flux assays to measure intracellular calcium dynamics, and cell proliferation assays to assess growth phenotypes. Flow cytometry-based analysis of myeloid differentiation markers such as CD41 and CD71 enables evaluation of differentiation states. These cells support functional studies of EF-hand proteins, screening for calcium pathway modulators, and broader investigations into calcium signaling in leukemia. For additional information, please contact Ascent Research.
