The ABHD16A Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T-lymphocyte cell line, designed for loss-of-function studies of ABHD16A. This product disrupts the ABHD16A gene, encoding a serine hydrolase that acts as a phosphatidylserine lipase, thereby preventing generation of the bioactive lipid mediator lysophosphatidylserine (LysoPS). The polyclonal pool provides a heterogeneous knockout background, suitable for investigating ABHD16A-dependent signaling without clone-specific biases.
Jurkat cells are an immortalized human T-cell line originally established from the peripheral blood of a 14-year-old male with acute T-cell leukemia. They serve as a widely used model for T-cell receptor signaling, apoptosis, and immune response mechanisms. The CD4+ Jurkat line retains key aspects of T-cell physiology, including responsiveness to lipid mediators, making it a relevant host for dissecting ABHD16A function in immune regulation.
ABHD16A participates in phospholipid metabolism and lipid mediator signaling by hydrolyzing phosphatidylserine to LysoPS. LysoPS activates the G protein-coupled receptors GPR34 and P2Y10, triggering downstream calcium signaling and modulating cytokine production. This axis is regulated by upstream inflammatory stimuli and transcriptional programs in immune cells. ABHD16A interacts directly with its phosphatidylserine substrate and is functionally linked to LysoPS-responsive GPCRs, placing it at a critical lipid?Cprotein interface that influences immune cell behavior.
In Jurkat T cells, ABHD16A-mediated LysoPS signaling contributes to T-cell activation and migration. Disruption of ABHD16A alters the availability of LysoPS, potentially dampening GPR34/P2Y10-driven pathways and affecting calcium flux, CD69 and CD25 expression, and cytokine secretion profiles. This polyclonal knockout model allows researchers to evaluate how loss of ABHD16A reshapes lipid-mediated immune responses, providing insights into the intersection of phospholipid metabolism and adaptive immunity.
These ABHD16A knockout Jurkat polyclonal cells support diverse experimental applications, including immunology and lipid signaling research. Typical assays include Western blotting and RT-qPCR to confirm target disruption, LC-MS/MS for LysoPS quantification, flow cytometry for activation markers (CD69, CD25), cytokine ELISA, cell migration assays, and calcium flux or GPCR activation studies. The model is valuable for autoimmune disease modeling and studies of inflammatory and neurodegenerative conditions where LysoPS signaling is implicated. For further information, please contact Ascent Research.
