The ITFG1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in which the ITFG1 gene has been disrupted in Jurkat human T lymphocytes. This loss-of-function model is engineered to facilitate detailed analysis of integrin alpha FG-GAP repeat-containing protein 1 function. As a polyclonal pool, these cells maintain genetic diversity, offering a robust experimental system free from clonal artifacts. By eliminating ITFG1 expression, the cells provide a powerful platform for dissecting integrin-mediated adhesion, migration, and signaling pathways critical for T-cell activation.
The Jurkat cell line, derived from a 14-year-old male with acute T-cell leukemia, is an immortalized T lymphocyte model widely employed in immunology research. These cells are extensively characterized for studies of TCR signal transduction, proliferation, apoptosis, and HIV infection. Upon TCR/CD3 engagement, Jurkat cells elicit robust signaling cascades, making them an ideal host for examining the crosstalk between integrin function and T-cell activation, while their leukemic background further enables investigation of malignant T-cell adhesion and dissemination.
ITFG1 encodes an adaptor protein linking integrin alpha-4 (ITGA4) to downstream effectors. Upon TCR stimulation, RAP1 GTPase, activated via the CXCL12/CXCR4 axis, cooperates with ITFG1, talin-1, and kindlin-3 to induce inside-out activation of ??4??1 integrin. This triggers FAK and SRC phosphorylation, activating PI3K/AKT and NF-kappaB pathways. ITFG1 interacts with ITGA4, ITGB1, vinculin, and actin, functioning downstream of RAP1GEF to organize focal adhesions and transduce signals that drive NF-kappaB nuclear entry and IL-2 transcription.
In Jurkat cells, ITFG1 knockout abolishes integrin-dependent adhesion to ICAM-1/VCAM-1, impedes migration, and disrupts immune synapse formation. Biochemically, it blunts TCR-induced FAK and AKT phosphorylation, attenuates NF-kappaB activation, and markedly reduces IL-2 secretion. This model enables precise dissection of how integrin outside-in signals couple to transcriptional programs controlling T-cell activation and effector function. It holds significance for autoimmune and chronic inflammatory conditions where integrin dysregulation promotes T-cell hyperactivity, and for studying T-cell leukemia adhesion and tissue infiltration.
These polyclonal knockout cells support diverse assays including adhesion to ICAM-1/VCAM-1, flow cytometric detection of active integrin ??1, western blot for phospho-FAK/phospho-AKT, NF-kappaB luciferase reporter, IL-2 ELISA following TCR crosslinking, transwell migration, and immunofluorescence of focal adhesions. Researchers can explore integrin signaling in T cells, immune synapse dynamics, screen checkpoint regulators of T-cell activation, or develop preclinical autoimmune and leukemia dissemination models. For additional information, please contact Ascent Research.
