The ABHD14B Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat T lymphoblast line, featuring CRISPR-mediated disruption of the ABHD14B gene. This product provides a mixed population of cells with heterogeneous editing events, enabling loss-of-function studies without clonal selection. The knockout model is designed for investigating ABHD14B’s role in protein palmitoylation and mitochondrial regulation.
Jurkat cells are an immortalized human T lymphocyte line derived from the peripheral blood of a 14-year-old patient with acute T cell leukemia. These suspension cells are widely used as a model for T cell antigen receptor (TCR) signaling, calcium flux, and downstream mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-??B) pathways. Their leukemic origin and rapid growth make them ideal for studying oncogenic signaling and apoptosis in T cell malignancies.
ABHD14B encodes a putative ??/?? hydrolase domain-containing protein implicated in the regulation of protein S-palmitoylation, a reversible lipid modification catalyzed by ZDHHC palmitoyltransferases and removed by palmitoyl-protein thioesterases. Though its direct substrates are unknown, ABHD14B likely interacts with the palmitoylation machinery to influence the localization and function of mitochondrial and signaling proteins. In Jurkat cells, ABHD14B disruption may alter the palmitoylation status of proteins involved in mitochondrial fatty acid metabolism, thereby impacting mitochondrial enzyme activity and membrane potential. The mechanistic link between ABHD14B and T cell signaling remains unclear, but palmitoylation is known to regulate key TCR-associated kinases and adaptor proteins.
In the Jurkat leukemic background, loss of ABHD14B provides a unique tool to dissect how protein palmitoylation contributes to mitochondrial dysfunction and T cell signaling abnormalities. Given the emerging role of S-palmitoylation in oncogenic signaling and metabolic reprogramming, this polyclonal knockout model enables researchers to explore ABHD14B’s potential involvement in leukemia cell survival, proliferation, and metabolic adaptation. The polyclonal nature preserves cellular heterogeneity, making it suitable for bulk functional assays that reflect population-level responses.
This knockout product supports a broad range of applications, including investigation of protein palmitoylation dynamics via Western blotting with palmitoyl-specific antibodies or acyl-biotin exchange, assessment of mitochondrial function by flow cytometry for mitochondrial membrane potential (e.g., using TMRM or JC-1), quantification of mitochondrial gene expression by RT-qPCR, and metabolic profiling with Seahorse analyzers. Additionally, it can be used for co-immunoprecipitation studies to identify ABHD14B-interacting proteins and for apoptosis assays under palmitoylation-modulating conditions. For further details or custom inquiries, please contact Ascent Research.
