In Stock Cell Lines
Homo sapiens (Human)
Esophagus
Adherent
The TOLLIP Knockout KYSE-150 Cell Line is a CRISPR/Cas9-edited knockout cell line based on the human esophageal squamous cell carcinoma line KYSE-150. This model disrupts the TOLLIP gene, which encodes an adaptor protein that negatively regulates TLR and IL-1R signaling by promoting IRAK1 degradation and inhibiting NF-??B, while also facilitating autophagy via LC3 and modulating TGF-?? signaling through Smad7. Ideal for investigating innate immunity, autophagy, and drug sensitivity in esophageal cancer, this knockout line supports assays such as NF-??B reporter analysis, LC3-II flux measurements, and xenograft tumor models. For more information, contact Ascent Research.
CETN3 Knockout K562 Polyclonal Cells
Cat. No. ARG19343
GATA6 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16795
MBIP Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG15543
DDX5 Knockout TE1 Polyclonal Cells
Cat. No. ARG12207
NEDD4L Knockout 786-O Polyclonal Cells
Cat. No. ARG5720
Nqo1, Nqo2 Knockout C2C12 Cell Line
Cat. No. ARG0181
The TOLLIP Knockout KYSE-150 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human esophageal squamous cell carcinoma line KYSE-150. This product provides a stable loss-of-function model through CRISPR/Cas9-mediated disruption of the TOLLIP gene, enabling functional studies of TOLLIP in its native cellular context without introducing exogenous expression constructs.
KYSE-150 is an established human esophageal squamous cell carcinoma cell line originally derived from the well-differentiated esophageal carcinoma of a 49-year-old Japanese female. It retains characteristic features of esophageal cancer, including malignant growth properties and responsiveness to relevant growth factors and cytokines, making it a robust platform for investigating oncogenic mechanisms and therapeutic targets.
TOLLIP encodes an adaptor protein that serves as a critical negative regulator of innate immune signaling downstream of Toll-like receptors (TLRs) and the interleukin-1 receptor (IL-1R). Upon stimulation by upstream regulators such as lipopolysaccharide (LPS), IL-1??, or TGF-??, TOLLIP interacts with IRAK1, promoting its degradation and thereby attenuating TRAF6-dependent IKK complex activation and subsequent NF-??B transcriptional responses. Additionally, TOLLIP facilitates autophagic clearance of protein aggregates by binding to LC3, and it modulates TGF-?? signaling through direct association with Smad7, influencing the activity of Smad2/3 transcription factors. Molecular interactions extend to TLR2, TLR4, TOM1, and the TGF-?? type I receptor, positioning TOLLIP at a nexus of inflammatory, autophagic, and fibrogenic pathways.
In esophageal squamous cell carcinoma, TOLLIP may influence tumor behavior by balancing pro-inflammatory and cytoprotective signals. Disruption of TOLLIP could alter NF-??B?Cdriven gene expression, autophagy flux, and cellular responses to chemotherapeutic agents, thereby affecting tumor growth, invasion, and drug sensitivity. This knockout cell line thus offers a physiologically relevant model to dissect TOLLIP’s context-dependent roles in cancer progression and innate immunity within the esophageal microenvironment.
Researchers can employ this cell line in a wide range of mechanistic and functional assays. NF-??B reporter assays and co-immunoprecipitation of IRAK1-containing complexes allow examination of TLR/IL-1R signaling nodes. Autophagic flux can be monitored by LC3-II turnover analysis, while cell viability and wound healing migration assays evaluate the impact on cancer cell proliferation and motility. In vivo xenograft tumor growth assays further enable assessment of tumorigenic potential and drug responsiveness. The model is also suited for genetic or pharmacological screening to identify synthetic lethal interactions or signaling crosstalk with TGF-?? cascades. For further technical details, please contact Ascent Research.
