The GPR107 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat CD4+ T-cell leukemia line, designed to eliminate functional expression of the GPR107 gene through targeted gene disruption. As a polyclonal pool of edited cells, this reagent ensures population-level diversity and reduces clonal artifacts, making it suitable for studies where uniform genetic background is not required. The knockout cells are provided ready for downstream applications, enabling direct interrogation of GPR107-dependent phenotypes without the need for clone isolation.
Jurkat cells are a well-established model for T-cell signaling and apoptosis, originally isolated from a patient with acute T-cell leukemia. They exhibit constitutive activation of growth-promoting pathways, including aberrant Notch signaling, which is frequently mutated in T-ALL. This leukemic background provides a disease-relevant context for examining the interplay between membrane trafficking and oncogenic transcription in malignant T lymphocytes.
GPR107 is a Golgi-resident GPCR-like protein that functions as a transcriptional target of the Notch pathway. Upon Notch activation, the CSL/RBP-J complex drives GPR107 expression, which in turn regulates endolysosomal trafficking through interactions with Rab GTPases, SNAREs, and sorting nexins. GPR107 loss-of-function attenuates the expression of Hes/Hey transcription factors, disrupting lysosomal biogenesis and impairing the intracellular sorting of signaling receptors.
In Jurkat cells, GPR107 knockout disrupts the Notch signaling axis that sustains leukemic growth and survival. Reduced Hes1 and Hey1 levels compromise anti-apoptotic programs, while defective lysosomal trafficking alters receptor turnover and signal termination. This model thus captures the bidirectional relationship between Golgi-endosome dynamics and Notch-driven oncogenicity, offering a valuable tool for dissecting how trafficking defects contribute to T-ALL pathogenesis.
Applications include transcriptomic profiling by RNA-seq, quantitative RT-PCR and Western blotting for Notch targets, flow cytometry for activation markers, and immunofluorescence to assess Golgi and lysosomal morphology. Notch reporter and lysosomal activity assays directly measure pathway functionality, while proliferation and apoptosis assays quantify GPR107-dependent survival signals. This polyclonal knockout population is ideal for pharmacological screens and mechanistic studies in T-cell leukemia. For further information, please contact Ascent Research.
