In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The TNFAIP3 Knockout THP-1 Cell Line is a CRISPR/Cas9-edited knockout of the TNFAIP3 gene in THP-1 monocytic cells. A20 is a ubiquitin-editing enzyme that terminates NF-??B signaling by deubiquitinating RIPK1 and TRAF6, functioning as a critical anti-inflammatory regulator. This loss-of-function model enables study of dysregulated NF-??B activation, cytokine overproduction, and inflammatory disease mechanisms. It is suitable for NF-??B pathway analysis, drug screening, and interaction studies, with THP-1 providing a human monocyte/macrophage platform for innate immune research.
NSUN6 Knockout HT29 Polyclonal Cells
Cat. No. ARG13850
PCYOX1L Knockout Hela Polyclonal Cells
Cat. No. ARG8353
ALAS1 Knockout huh-7 Polyclonal Cells
Cat. No. ARG27864
CASP1 Knockout CAL27 Polyclonal Cells
Cat. No. ARG42394
PCGF1 Knockout Raji Polyclonal Cells
Cat. No. ARG1674
YUMM1.7
Cat. No. ARC1027
The TNFAIP3 Knockout THP-1 Cell Line is a CRISPR/Cas9-edited knockout cell line engineered to disrupt the TNFAIP3 gene in human THP-1 monocytic cells. This loss-of-function model enables precise genetic ablation of A20, a critical negative regulator of NF-??B signaling, providing a definitive tool to study inflammatory feedback mechanisms without pharmacological interference. It is particularly suited for dissecting ubiquitin-dependent control of innate immune responses.
THP-1 is a human acute monocytic leukemia cell line derived from the peripheral blood of a 1-year-old male. Widely used as a monocyte/macrophage model, THP-1 cells can be differentiated into macrophage-like cells and respond robustly to inflammatory agonists such as TNF-?? and LPS. Their human origin and amenability to genetic manipulation make them a physiologically relevant platform for studying signal transduction in innate immunity and inflammation.
TNFAIP3 encodes A20, a dual-function ubiquitin-editing enzyme with N-terminal deubiquitinase activity and C-terminal E3 ubiquitin ligase activity. A20 is recruited to activated receptor complexes, including TNFR1 and TLR4, where it deubiquitinates RIPK1 and TRAF6 to terminate pro-inflammatory signaling. By dismantling K63-linked polyubiquitin chains, A20 prevents sustained activation of the IKK complex, thereby blocking I??B?? phosphorylation and NF-??B p65/p50 nuclear translocation. A20 also interacts with adaptors such as TRAF1, TRAF2, ABIN-1, and TAX1BP1, and restricts NLRP3 inflammasome priming and necroptosis by modulating RIPK1 ubiquitination. Collectively, these mechanisms position A20 as a master brake on inflammatory and cell death pathways.
In the THP-1 background, TNFAIP3 knockout leads to hyperactivation of NF-??B and exaggerated secretion of IL-6, TNF, and IL-1?? upon stimulation with LPS or TNF-??. This phenotype mirrors features of chronic inflammatory diseases associated with A20 deficiency, including rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, and psoriasis. Additionally, loss of A20??s anti-apoptotic and necroptosis-suppressive functions makes this model valuable for examining cell death decisions under inflammatory stress and for investigating A20??s tumor-suppressive role in B-cell lymphomas.
This knockout cell line supports multiple experimental readouts, including western blotting for phospho-IKK and I??B??, ELISA for cytokine secretion, and RT-qPCR for pro-inflammatory transcripts. It is also suited for NF-??B luciferase assays, co-immunoprecipitation of A20 interactors, and flow cytometric analysis of apoptosis or necroptosis upon TNF-?? stimulation. The line facilitates high-throughput drug screening and transcriptomic profiling by RNA-seq. For customized services or bulk orders, contact Ascent Research.
