This product comprises a population of ITFG1 knockout A-549 polyclonal cells generated by CRISPR/Cas9-mediated gene disruption. The polyclonal pool contains a heterogeneous mixture of cells with targeted disruption of the ITFG1 locus, providing a versatile loss-of-function model that avoids clonal artifacts. These ready-to-use polyclonal knockout cells are suitable for functional studies where ITFG1 protein expression is ablated, enabling investigation of its roles in cellular adhesion, immune modulation, and signal transduction. The knockout population is derived from the widely used A-549 lung adenocarcinoma cell line and is quality controlled for viability and robust expansion post-editing.
The parental A-549 cell line is a human alveolar basal epithelial adenocarcinoma line established from a 58-year-old male, serving as a key in vitro model for non-small cell lung cancer. A-549 cells exhibit adherent, epithelial morphology and retain features relevant to lung tumor biology, such as KRAS mutation and p53 pathway alterations, making them a staple in oncology drug discovery and mechanistic studies. This genetic background provides a physiologically relevant context for dissecting how ITFG1 loss influences tumor cell behavior, particularly in matrix adhesion and migration, and for exploring the intersection of integrin signaling and cancer progression.
ITFG1 (Integrin Alpha FG-GAP Repeat Containing 1), also known as TIP (T-cell immunomodulatory protein), functions as a negative regulator of T-cell receptor (TCR) signaling by binding CD4 and disrupting Lck recruitment to the TCR/CD3 complex, thereby attenuating pro-inflammatory cytokines such as IL-2. In T-cells, ITFG1 expression is induced by TCR stimulation and IL-2 through NFAT-dependent transcription, feeding back to dampen T-cell activation and proliferation. Beyond immune cells, ITFG1 interacts with integrin subunits and modulates integrin-mediated adhesion and signaling, suggesting a broader role in cell?Cextracellular matrix dynamics. Thus, ITFG1 knockout can simultaneously impact immune regulatory checkpoints and integrin-dependent adhesive functions, linking TCR signaling (LCK, ZAP70) with adhesion complex components.
In the A-549 adenocarcinoma background, ITFG1 knockout provides a powerful system to evaluate the gene??s contribution to integrin-mediated processes such as attachment, spreading, migration, and invasion??hallmarks of metastatic potential. Because ITFG1 has been implicated in cancer immune evasion through its immunomodulatory domain, this knockout model also facilitates co-culture experiments with T-cells to examine how lung tumor cell ITFG1 deficiency alters T-cell activation, immune synapse formation, and cytokine secretion. The polyclonal nature captures diverse editing events, enabling physiologically averaged phenotypic assessments that avoid single-clone bias and better represent therapeutic populations.
Researchers can employ these ITFG1 knockout A-549 polyclonal cells in a range of experimental workflows. Western blotting and RT-qPCR confirm ITFG1 ablation at the protein and mRNA levels, respectively. Cell adhesion and migration/invasion assays with extracellular matrix components quantify changes in integrin-dependent behavior. T-cell co-culture and activation assays, coupled with flow cytometry for surface markers such as CD69 or cytokine production, reveal the functional impact on immune modulation. The cells are also suited for high-content imaging and drug response studies to probe integrin signaling dependency in lung cancer. For further technical information and customization options, please contact Ascent Research.
