In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
CRISPR/Cas9-edited TSC22D3 knockout Jurkat E6.1 cell line from human acute T-cell leukemia disrupts the glucocorticoid-induced leucine zipper (GILZ) transcriptional repressor. GILZ normally binds NF-??B p65 and c-Jun to suppress inflammatory cytokines and modulate apoptosis via BCL2L11 (BIM). This loss-of-function cell line enables detailed interrogation of glucocorticoid receptor signaling, NF-??B/AP-1 transcription, and GILZ-mediated apoptosis in a T-cell context. Representative assays include luciferase reporter measurements, ELISA for IL-2 and IFN-?? quantification, and Annexin V apoptosis assessments following dexamethasone exposure, facilitating anti-leukemic drug screening.
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The TSC22D3 Knockout Jurkat E6.1 Cell Line is a genetically engineered human T lymphocyte product featuring CRISPR/Cas9-mediated disruption of the TSC22D3 gene. This knockout cell line enables loss-of-function studies of the glucocorticoid-induced leucine zipper (GILZ) transcriptional repressor in a well-characterized T-cell leukemia background. The TSC22D3 gene is targeted for disruption, abrogating GILZ expression and allowing investigation of its regulatory roles in immune signaling and apoptosis.
The parental Jurkat E6.1 cell line is a subclone of the classic Jurkat line, originally derived from an acute T-cell leukemia patient. These immortalized T lymphoblastoid cells serve as a principal model for studying T-cell receptor signaling, leukemia biology, and glucocorticoid-induced responses. The Jurkat E6.1 derivative maintains the core characteristics of antigen-independent growth and expression of T-lineage markers, providing a robust and physiologically relevant platform for dissecting T-cell signaling networks.
GILZ functions as a transcriptional repressor downstream of glucocorticoid receptor (NR3C1) activation, binding directly to NF-??B p65 (RelA) and AP-1 components such as c-Jun and c-Fos to inhibit their transactivation of pro-inflammatory genes. The glucocorticoid receptor?CGILZ axis modulates expression of cytokines IL-2 and IFN-??, and the pro-apoptotic factor BCL2L11 (BIM). GILZ also integrates signals from IL-10, IL-2, and TGF-??, and interacts with 14-3-3 scaffolds and mTORC1 components, linking metabolic sensing to immune regulation. TSC22D3 disruption therefore removes a critical brake on NF-??B and AP-1, leading to unchecked inflammatory gene expression and altered apoptosis.
In Jurkat cells, TSC22D3 knockout recapitulates a state of glucocorticoid resistance observed in certain leukemias and autoimmune disorders. Enhanced NF-??B and AP-1 activity drives overproduction of cytokines and promotes a pro-survival phenotype by modulating BCL2L11 expression. This model is particularly valuable for probing the tumor-suppressive functions of GILZ in T-cell acute lymphoblastic leukemia, as loss of GILZ may contribute to leukemogenesis by impairing glucocorticoid-mediated apoptosis.
Researchers utilize this knockout cell line to study glucocorticoid signaling mechanisms, screen for compounds that restore glucocorticoid sensitivity, and investigate the interplay between NR3C1, NF-??B, and AP-1 in T cells. Representative assays include Western blotting for GILZ and downstream effectors, quantitative PCR for target gene expression, NF-??B luciferase reporter measurements, ELISA for cytokine secretion, and Annexin V apoptosis assessment after dexamethasone treatment. This engineered cell line supports drug discovery efforts targeting inflammatory pathways and T-cell leukemia. For further information, please contact Ascent Research.
