The Tmem176b Knockout EL4 Cell Line is a CRISPR/Cas9-mediated gene-disrupted cell line derived from the mouse T-cell lymphoma line EL4. This product provides a stable loss-of-function model for Tmem176b, enabling detailed investigation of its role in immune signaling without the need for transient silencing approaches. The knockout cell line is delivered as a ready-to-use culture, facilitating immediate employment in functional assays and gene perturbation studies relevant to immunology and cancer biology. The gene disruption is achieved through CRISPR/Cas9 technology, ensuring efficient targeting of the Tmem176b locus, though the exact editing pattern is not specified.
The parental EL4 cell line originates from a C57BL/6 mouse and represents a widely used model for T-cell activation, signal transduction, and lymphoma biology. EL4 cells recapitulate key aspects of T-lymphocyte function, including responsiveness to mitogens, cytokine secretion, and surface marker expression changes upon stimulation. Their malignant phenotype also renders them valuable for studying mechanisms of T-cell lymphomagenesis and immune evasion. The introduction of a Tmem176b knockout allows researchers to dissect gene-specific contributions within this well-characterized background, offering a controlled system for comparative analyses.
Tmem176b acts as a modulator of the NF-??B pathway and inflammasome assembly, functions critical for innate and adaptive immunity. The protein is induced by upstream stimuli such as TNF-??, IL-1??, and Toll-like receptor ligands, and it operates at a junction influencing both NF-??B activation and inflammasome component expression. Downstream, it regulates production of cytokines including IL-6 and IL-12, and controls expression of co-stimulatory molecules CD80 and CD86. Tmem176b interacts with MS4A family members and Fc receptor-like proteins, and it affects the assembly of the NLRP3/ASC/caspase-1 complex. Its disruption is known to attenuate NF-??B signaling, dampen inflammatory cytokine output, and impair dendritic cell maturation and T-cell activation.
In the context of EL4 T-lymphoma cells, loss of Tmem176b profoundly alters cellular responses central to immune function and malignant growth. Knockout cells exhibit diminished NF-??B activation, reduced pro-inflammatory cytokine secretion, and altered expression of T-cell activation markers such as CD69 and CD25. These changes make the line particularly suitable for dissecting TLR- and cytokine-driven signaling networks, as well as for investigating how inflammasome regulation intersects with T-cell biology. The model thus supports studies into the molecular underpinnings of autoimmune diseases, chronic inflammation, and immune evasion by lymphoma cells, where dysregulated NF-??B and inflammasome activity are prominent.
This knockout cell line is applied in diverse experimental workflows, including Western blotting for pathway component analysis, RT-qPCR for transcriptional profiling, and flow cytometry for activation marker measurement. Functional assays such as NF-??B luciferase reporter systems, CFSE-based proliferation tests, and Annexin V apoptosis detection provide quantitative insights into signaling dynamics. Researchers employ the line for screening immunomodulatory compounds, investigating T-cell receptor-proximal events, and exploring the regulatory interplay between Tmem176b and its interacting partners. For further details or technical support, please contact Ascent Research.
