The CASP7 knockout K-562 polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for disruption of the CASP7 gene in the human CML K-562 cell line. This polyclonal product provides a heterogeneous pool of gene-edited cells, avoiding clonal selection biases and enabling functional studies of caspase-7 loss. The CRISPR/Cas9-mediated gene disruption generates a loss-of-function model for the executioner caspase-7, facilitating investigation of apoptosis and related pathways. This model is particularly suited for studying apoptosis regulation, drug resistance, and non-apoptotic roles in hematopoietic cells.
K-562 is a human cell line isolated from the pleural effusion of a patient with chronic myelogenous leukemia and carries the Philadelphia chromosome, resulting in the BCR-ABL1 fusion oncoprotein. As a suspension cell line with erythroleukemia characteristics, K-562 is a well-established model for hematopoietic differentiation and leukemogenesis. The cells can be induced to undergo megakaryocytic and erythroid differentiation, making them valuable for studying lineage commitment. The BCR-ABL1 tyrosine kinase provides prosurvival signals that intersect with apoptotic pathways, underscoring the relevance of this background for apoptosis research.
Caspase-7, encoded by CASP7, is an executioner caspase activated by initiator caspases (caspase-8, -9, -10) in the intrinsic and extrinsic apoptotic pathways. Active caspase-7 cleaves substrates such as PARP1, lamin A, DFFA/ICAD, and ROCK1, triggering DNA fragmentation and nuclear lamina disassembly. Its regulation involves IAP family members including XIAP, cIAP1/2, and survivin, and it operates downstream of the cytochrome c/Apaf-1 apoptosome. Additionally, caspase-7 contributes to non-apoptotic processes, engaging inflammasome components NLRP3 and ASC during pyroptosis and inflammatory responses.
In K-562 cells, CASP7 knockout is expected to impair the execution phase of apoptosis, potentially leading to resistance to chemotherapeutic agents like etoposide and doxorubicin. Given the prosurvival signaling driven by BCR-ABL1, the loss of caspase-7 may exacerbate the anti-apoptotic phenotype, providing a relevant model to study drug resistance in CML. This knockout system also enables dissection of caspase-7??s role in differentiation and inflammation within a leukemia background, offering insights into non-apoptotic functions that may influence disease progression.
This polyclonal knockout product supports diverse applications including apoptosis signaling studies, drug resistance screening, and evaluation of pro-apoptotic compounds. Standard assays such as Western blotting and RT-qPCR for CASP7, flow cytometry for caspase-7 activity and Annexin V binding, TUNEL assays, and drug sensitivity profiling can be employed to characterize the cells. The model is also suitable for studying caspase-7??s involvement in pyroptosis and inflammatory signaling. For further information and technical support, please contact Ascent Research.
