The GOLM1 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population of human Jurkat T-lymphoblastoid cells, engineered to disrupt the GOLM1 gene (Golgi membrane protein 1). This pooled format provides a heterogeneous loss-of-function model, avoiding clonal selection biases, and is suitable for functional genomic screens and signaling pathway analysis. CRISPR-mediated gene disruption eliminates GOLM1 protein function, which is critical for Golgi-based protein trafficking and post-translational modifications. The polyclonal nature of these cells ensures robust reproducibility in population-level assays.
Jurkat cells, derived from the peripheral blood of a patient with acute T cell leukemia, are an immortalized T cell line widely employed to study TCR signaling, apoptosis, and cytokine responses. Their transformed phenotype supports rapid suspension growth and sensitivity to extrinsic and intrinsic apoptotic stimuli, making them an ideal model for examining immune cell signaling and oncogenic mechanisms. This cellular background enables precise dissection of GOLM1??s contributions to lymphocyte biology and Golgi-dependent trafficking processes relevant to T cell function.
GOLM1 is a type II Golgi-resident protein that regulates secretory trafficking and Golgi architecture through interactions with GRASP55, GRASP65, GM130, p115, SORT1, and Rab GTPases. It is activated by upstream signals including EGF, TNF-??, IL-6, HGF, and androgen receptor, and functions to enhance AKT/mTOR and NF-??B signaling via PI3K and IKK, respectively. GOLM1 also transduces signals to the Wnt/??-catenin pathway, promoting expression of cyclin D1, MMPs, and ??-catenin. Thus, GOLM1 integrates proliferative and survival signals at the Golgi, linking extracellular stimuli to downstream oncogenic cascades.
In Jurkat cells, loss of GOLM1 is expected to impair anterograde transport of immunoreceptors and cytokine receptors, reducing surface expression and dampening TCR-triggered activation. This disruption attenuates PI3K/AKT/mTOR survival signals and NF-??B transcriptional responses, altering cytokine secretion and apoptotic sensitivity. Golgi morphology may be compromised, as reflected by mislocalization of GRASP65 and GM130. Consequently, this knockout model provides a unique tool to probe the Golgi-dependent regulation of T cell activation, proliferation, and apoptosis, and to evaluate GOLM1 as a therapeutic target in lymphoid malignancies.
This knockout polyclonal pool enables diverse applications: from dissecting Golgi-mediated protein trafficking in immune cells by immunofluorescence and surface receptor flow cytometry, to investigating GOLM1??s role in T cell activation via phospho-AKT/NF-??B western blotting and cytokine multiplexing. The model supports cancer target validation by screening for regulators of AKT/mTOR and Wnt pathways, with readouts such as RT-qPCR for cyclin D1 and MMPs, and migration assays. These cells are valuable for studies in hepatocellular carcinoma, prostate cancer, breast cancer, and glioblastoma. For further inquiries or custom requirements, please contact Ascent Research.
