The APOL2 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphoblast cell line, designed for constitutive disruption of the APOL2 gene. This pool of edited cells provides a heterogeneous population with loss-of-function mutations in APOL2, enabling robust investigation of its roles in apoptosis and immune signaling without clonal selection.
Jurkat cells are an immortalized T lymphocyte line originally isolated from the peripheral blood of a 14-year-old male with acute T cell leukemia. Widely utilized as a model system, Jurkat cells recapitulate key aspects of T cell signaling, activation-induced cell death, and gene expression regulation, making them an ideal host for studying apoptosis-related genes such as APOL2.
APOL2 encodes a pro-apoptotic BH3-only protein that functions as a critical regulator of the intrinsic apoptosis pathway. Upon induction by upstream regulators including TP53, IFNG, TNF, STAT1, and IRF1, APOL2 binds and neutralizes anti-apoptotic BCL-2 family members such as BCL2 and BCL2L1, thereby releasing BAX and BAK to mediate mitochondrial outer membrane permeabilization and subsequent cytochrome c (CYCS) release. This cascade leads to activation of CASP9 and the effector caspase CASP3, driving programmed cell death. APOL2 also interacts with BCL2L11 and BECN1, suggesting additional roles in autophagy modulation and innate immune responses.
Disruption of APOL2 in Jurkat cells impairs the intrinsic apoptotic machinery, resulting in resistance to diverse cell death stimuli such as cytokine withdrawal, DNA damage, and chemotherapeutic agents. This knockout model thus provides a valuable tool for dissecting the contribution of BH3-only proteins to T cell apoptosis and for evaluating mechanisms of drug sensitivity and resistance in leukemia and other malignancies.
Typical applications include assessing apoptosis induction by flow cytometric Annexin V staining, measuring caspase-3/7 activity, and monitoring mitochondrial membrane potential with JC-1 dye. Researchers can validate APOL2 disruption via RT-qPCR and Western blotting, and explore protein interactions through co-immunoprecipitation with BCL-2 family members. The knockout cells are also suitable for viability assays (e.g., MTS) following treatment with apoptotic stimuli, facilitating studies in cancer biology, immunology, and drug discovery. For further information, please contact Ascent Research.
