In Stock Cell Lines
Homo sapiens (Human)
Bone
Adherent
The TRAF6 Knockout SW1353 Cell Line is a CRISPR/Cas9-edited human chondrosarcoma cell line with a disrupted TRAF6 gene. TRAF6 is an E3 ubiquitin ligase that mediates NF-??B and MAPK signaling downstream of receptors such as IL-1R, TLR4, and RANK. In SW1353 cells, TRAF6 is critical for IL-1??-induced inflammatory responses, making this model valuable for studying chondrosarcoma signaling and cartilage biology. Researchers can use this knockout cell line for investigating TRAF6-dependent pathways, including cytokine production, ubiquitination, and kinase activation. Typical applications include NF-??B reporter assays, phospho-signaling analysis, and cytokine profiling. It is also suitable for inhibitor screening and functional studies of TRAF6 in cancer and inflammation.
MMP8 Knockout TE1 Polyclonal Cells
Cat. No. ARG12201
ARFIP2 Knockout 786-O Polyclonal Cells
Cat. No. ARG24963
CCS Knockout Hela Polyclonal Cells
Cat. No. ARG43352
FoxM1 Knockout PATU8988T Polyclonal Cells
Cat. No. ARG11356
CHUK Knockout CaSki Polyclonal Cells
Cat. No. ARG9749
MDA-MB-435
Cat. No. ARC0500
The TRAF6 Knockout SW1353 Cell Line is a CRISPR/Cas9-edited human knockout cell line derived from the SW1353 chondrosarcoma cell line, in which the TRAF6 gene has been disrupted. This loss-of-function model enables precise investigation of TRAF6-mediated signaling pathways without off-target effects of pharmacological inhibitors. The knockout cell line serves as a powerful tool for dissecting the role of TRAF6 in chondrosarcoma biology and innate immune signaling.
The SW1353 cell line was established from a primary grade II chondrosarcoma of a 72-year-old female. It is widely used as a chondrosarcoma model for studying cartilage biology, cancer, and inflammatory responses. SW1353 cells express chondrocytic markers and respond to inflammatory stimuli such as IL-1??, making them suitable for exploring TRAF6-dependent signaling in a chondrosarcoma context.
TRAF6 is an E3 ubiquitin ligase and adaptor protein that mediates signal transduction from receptors including RANK, CD40, IL-1R, TLR4, and NOD-like receptors. Upon receptor activation, TRAF6 interacts with the Ubc13/Uev1A E2 complex to catalyze K63-linked polyubiquitination of itself and downstream targets. This leads to activation of the TAK1/TAB2/TAB3 complex, which subsequently phosphorylates IKK?? and MAP kinase kinases, culminating in NF-??B and AP-1 transcription factor activation. Key downstream targets include pro-inflammatory cytokines (IL-6, TNF??, IL-1??), MAP kinases (JNK, p38, ERK), and the osteoclastogenic factor NFATc1. Negative regulators such as CYLD and A20 deubiquitinate TRAF6, fine-tuning the response.
In the SW1353 chondrosarcoma background, TRAF6 knockout significantly impacts IL-1??-mediated signaling, as TRAF6 is a critical mediator of NF-??B and MAPK activation downstream of the IL-1 receptor. This model is particularly relevant for studying inflammatory pathways that contribute to chondrosarcoma progression and cartilage degradation, similar to mechanisms observed in rheumatoid arthritis and osteoarthritis. Ablation of TRAF6 disrupts the expression of matrix metalloproteinases and inflammatory mediators, providing insights into tumor microenvironment interactions.
This TRAF6 Knockout SW1353 cell line is ideal for a broad range of functional studies, including NF-??B luciferase reporter assays, phospho-signaling analysis of JNK and p65, cytokine profiling via ELISA or RT-qPCR, and co-immunoprecipitation of TRAF6 interaction partners. It can also serve as a screening platform for small-molecule TRAF6 inhibitors or for investigating ubiquitin ligase activity. Researchers can employ this model to elucidate TRAF6-dependent mechanisms in chondrosarcoma cell proliferation, invasion, and drug resistance. For further information or bulk orders, please contact Ascent Research.
