The ABHD10 Knockout Jurkat Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in the Jurkat T lymphocyte background, enabling functional studies of the ABHD10 gene. This polyclonal pool contains a heterogeneous mixture of edited alleles, offering a robust model for loss-of-function analyses without clonal selection biases. The targeted gene disruption abrogates ABHD10 expression, facilitating investigation of its role in mitochondrial lipid metabolism and apoptotic signaling. These cells are supplied as a ready-to-use polyclonal population suitable for immediate expansion and experimentation.
The Jurkat host cell line is an immortalized human T lymphocyte derived from the peripheral blood of a patient with acute T cell leukemia. Jurkat cells serve as a well-established model for T cell activation, signal transduction, and apoptosis, particularly in studies of T cell receptor signaling and downstream pathways. Their human origin and T cell phenotype make them highly relevant for immunological and cancer research, and they have been extensively characterized for mitochondrial function and oxidative stress responses.
ABHD10 encodes a lysophosphatidylserine lipase localized to mitochondria, where it catalyzes the degradation of lysophosphatidylserine to glycerophosphoserine and free fatty acid. This enzymatic activity is critical for maintaining mitochondrial membrane integrity and modulating cellular reactive oxygen species (ROS) levels. Disruption of ABHD10 leads to accumulation of lysophosphatidylserine and oxidized phospholipids, resulting in increased ROS production, loss of mitochondrial membrane potential, and aberrant activation of apoptosis via caspase-3. ABHD10 therefore acts as a key regulator downstream of phospholipid catabolism, with effects on oxidative stress and programmed cell death. Representative pathway components include ABHD10, lysophosphatidylserine, phosphatidylserine, ROS, and caspase-3, although upstream regulatory inputs remain poorly defined.
In the Jurkat T cell context, ABHD10 knockout provides a physiologically relevant system to dissect the interplay between mitochondrial lipid metabolism and T cell function. Given the importance of mitochondrial health for lymphocyte activation, proliferation, and apoptosis, this model enables dissection of how ABHD10 deficiency perturbs mitochondrial integrity and ROS homeostasis in a human immune cell type. It allows researchers to explore connections between phospholipid dysregulation, mitochondrial dysfunction, and T cell fate decisions, offering insights into diseases such as ABHD10 deficiency-related cardiomyopathy and retinopathy, as well as broader mitochondrial disorders.
These polyclonal ABHD10 knockout cells are suitable for a range of experimental techniques including Western blotting, RT-qPCR, flow cytometry for apoptosis (Annexin V staining), mitochondrial membrane potential assays (JC-1), ROS detection with DCFDA, caspase activity measurements, MTT viability assays, and immunofluorescence for mitochondrial morphology. Specific research applications include T cell apoptosis studies, oxidative stress signaling, mitochondrial dysfunction analysis, and immune cell metabolism. For technical inquiries or additional product information, please contact Ascent Research.
