The ABHD17B Knockout Jurkat Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from Jurkat human T lymphocytes, with targeted disruption of the ABHD17B gene. This loss-of-function model enables investigation of ABHD17B in T-cell signaling and leukemia biology without residual protein activity. The polyclonal population comprises a heterogeneous pool of edited alleles, suitable for functional studies where clonal homogeneity is not required.
The Jurkat cell line, an immortalized human T lymphocyte line from acute T-cell leukemia, is a standard model for TCR signaling and leukemia research. Jurkat cells exhibit well-defined signaling cascades downstream of the TCR?CCD3 complex, involving ZAP70, LAT, and PLC??1. Their genetic tractability and characterized background make them ideal for generating ABHD17B knockout cells and studying T-cell signaling dynamics.
ABHD17B encodes a protein depalmitoylase that removes palmitate from substrates such as N-Ras, regulating their membrane localization and signaling. In Jurkat cells, ABHD17B expression is regulated downstream of TCR activation and transcription factors NFAT and AP-1. Depalmitoylation of N-Ras by ABHD17B normally attenuates Ras membrane association and limits MAPK pathway activation, including ERK1/2 phosphorylation and ELK1-driven transcription. In the knockout model, loss of ABHD17B activity increases N-Ras palmitoylation, enhancing membrane tethering and potentiating signaling through BRAF?CMEK1/2?CERK1/2, which may promote T-cell proliferation and survival. This hyperactivation mirrors oncogenic Ras signaling relevant to T-ALL.
In Jurkat T lymphocytes, ABHD17B knockout creates a system with constitutively amplified Ras-driven MAPK signaling. This serves as a model for studying how dysregulated palmitoylation contributes to leukemogenesis and aberrant T-cell responses. Comparative studies between wild-type and ABHD17B-deficient cells allow dissection of depalmitoylation??s role in temporal control of Ras localization and signal termination after TCR engagement.
Research applications include functional studies of ABHD17B in TCR signaling, investigation of Ras palmitoylation dynamics, and screening for inhibitors of Ras membrane association. Typical assays are Western blotting for phospho-ERK, Ras activity pull-down, immunofluorescence for N-Ras localization, flow cytometry for proliferation and apoptosis, and RT-qPCR for target gene expression. These ABHD17B polyclonal knockout Jurkat cells provide a versatile platform for exploring protein depalmitoylation and oncogenic signaling. For more information, please contact Ascent Research.
