DNAJC19 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line. This product features targeted disruption of the DNAJC19 gene using CRISPR/Cas9 technology, creating a heterogeneous pool of cells with loss-of-function mutations. These cells provide a versatile model for studying mitochondrial protein import and associated pathways.
The Jurkat cell line is an immortalized human T lymphocyte line originally established from a patient with acute T cell leukemia. Jurkat cells are widely used in immunology research for their capacity to model T cell signaling, activation, and apoptosis. Their derivation from a leukemic background adds relevance to cancer biology studies, while their well-characterized signaling pathways make them a robust model for investigating gene functions in immune cells.
DNAJC19 encodes a mitochondrial co-chaperone that localizes to the inner mitochondrial membrane and stimulates the ATPase activity of mitochondrial Hsp70 (mortalin/HSPA9). As part of the TIM23 complex, which includes MAGMAS (PAM16), TIMM44, TIMM23, and TIMM17A, DNAJC19 facilitates the translocation of nuclear-encoded proteins into the mitochondrial matrix. It also interacts with cardiolipin and contributes to cardiolipin metabolism, thereby influencing mitochondrial membrane potential and the mitochondrial unfolded protein response. DNAJC19 activity is regulated by HSPA9 and the mitochondrial membrane potential, and it acts upstream of OXPHOS complex subunits, cardiolipin remodeling enzymes, and other mitochondrial matrix proteins. Disruption of DNAJC19 impairs protein import and cardiolipin homeostasis, leading to compromised oxidative phosphorylation and mitochondrial dysfunction.
In Jurkat T cells, mitochondrial dynamics are integral to immune signaling, metabolic reprogramming during activation, and the maintenance of cellular fitness. Knockout of DNAJC19 disrupts these mitochondrial processes, offering a tool to dissect how mitochondrial protein import and cardiolipin metabolism intersect with T cell function. This model is particularly relevant for studying dilated cardiomyopathy with ataxia (DCMA), a disease linked to DNAJC19 mutations, and for exploring mitochondrial contributions to T cell malignancies. By introducing DNAJC19 loss in a T lymphocyte context, researchers can investigate the tissue-specific consequences of mitochondrial impairment on immune cell behavior.
The DNAJC19 Knockout Jurkat Polyclonal Cells are suited for a range of downstream analyses, including western blotting, RT-qPCR, and immunofluorescence to assess protein expression and localization. Co-immunoprecipitation can probe interactions with MAGMAS, HSPA9, or TIMM23, while flow cytometry with mitochondrial membrane potential dyes enables functional readouts. Metabolic phenotyping via Seahorse analysis and cardiolipin quantification can reveal impacts on respiration and lipid composition. These cells are useful for DCMA disease modeling, studies of T cell metabolic reprogramming, and cardiolipin metabolism research. For further information, please contact Ascent Research.
