ARMC1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat immortalized human T lymphocyte cell line. This product features targeted disruption of the ARMC1 gene, producing a heterogeneous pool of edited cells suitable for studying the loss-of-function effects of ARMC1 in T cell biology. The polyclonal format retains genetic diversity among knockout alleles, offering a representative model for phenotypic analysis without clonal selection biases.
The Jurkat cell line originates from the peripheral blood of a 14-year-old male patient with acute T cell leukemia (T-ALL). This immortalized T lymphocyte line is a classical model for investigating T cell receptor signaling, cytokine production, and apoptosis. Jurkat cells harbor defective PTEN and constitutive NF-??B activity, which, together with their proliferative and apoptotic characteristics, provide a relevant background for studying leukemia-associated signaling dysregulation.
ARMC1 encodes a mitochondrial armadillo repeat-containing protein that functions as a scaffold modulating protein-protein interactions crucial for mitochondrial homeostasis and apoptosis. In Jurkat cells, ARMC1 acts downstream of TCR stimulation and the MYC oncogene. It interacts directly with the apoptosis regulators BCL2, BAX, and the mitochondrial channel VDAC, thereby influencing mitochondrial outer membrane permeabilization. This interaction regulates cytochrome c release, which subsequently triggers apoptosome formation, Caspase-9 activation, and executioner Caspase-3 cleavage. Consequently, ARMC1 serves as a molecular rheostat for the mitochondrial apoptotic threshold governed by the BCL2 family.
Disruption of ARMC1 in Jurkat cells yields a powerful model to examine its contribution to mitochondrial apoptosis in T-ALL. Loss of ARMC1 may impair cytochrome c mobilization and caspase cascade activation, potentially conferring apoptotic resistance??a hallmark of leukemia progression. The polyclonal composition mirrors tumor heterogeneity, enabling evaluation of heterogeneous responses to death-inducing agents and facilitating the identification of dominant functional consequences under physiological and therapeutic conditions.
These polyclonal knockout cells are optimized for a range of assays, including Western blotting for apoptosis-related proteins (BCL2, BAX, Caspase-3, cytochrome c), flow cytometry with Annexin V/PI for apoptosis quantification, JC-1 staining for mitochondrial membrane potential, and co-immunoprecipitation to validate ARMC1-containing complexes. Caspase activity assays and RT-qPCR profiling of MYC-responsive genes can further dissect ARMC1??s role at the signaling interface. This product supports preclinical studies on mitochondrial apoptosis regulation and the evaluation of ARMC1 as a therapeutic target in leukemia. For technical inquiries, please contact Ascent Research.
