HEK293 TLR5 NFkB-Luci Cell Line
Item | Cat# | Price |
Stable Cell Line | SNB-OT-0004 | $19,800 |
Compound Testing Services | CT-001 | $1,850 per 384w plate (Up To 16 cpds Dose) |
Product Description
Toll-like receptor 5 (TLR5) is a pattern-recognition receptor (PRR) of the innate immune system that specifically recognizes bacterial flagellin, a major structural protein of flagella. Expressed on the surface of various immune and epithelial cells, including macrophages, dendritic cells, and intestinal epithelial cells, TLR5 plays a crucial role in detecting motile bacteria and initiating early host defense responses. Upon binding to flagellin, TLR5 activates MyD88-dependent signaling, leading to NF-κB and MAPK pathway activation and inducing the production of pro-inflammatory cytokines, chemokines, and antimicrobial peptides. This response helps recruit immune cells to infection sites and shapes subsequent adaptive immunity. Beyond host defense, TLR5 also contributes to maintaining mucosal homeostasis and regulating interactions with commensal microbiota. Dysregulation of TLR5 signaling has been implicated in inflammatory disorders, metabolic diseases, and cancer, highlighting its importance as both a biological sensor and a potential therapeutic target.
Screeningbio’s HEK293/TLR5/NFkB-Luciferase reporter gene cell line stable expressed TLR5 protein and NFkB response element upstream of luciferase gene. Upon stimulated by TLR ligand, NFkB pathway was activated and induce luciferase expression.
Product Specifications
Target Type | TLR5 |
Species | Human |
HGNC Symbol | TLR5 |
Accession Number | NM_003268 |
Parental Line | HEK293 |
Lot# | See Vial |
Storage | Liquid Nitrogen |
Data
Target Background
Toll-like receptor 5 (TLR5) plays a central role in host defense by recognizing bacterial flagellin, but dysregulation of its signaling is increasingly linked to a wide spectrum of diseases. In infectious diseases, TLR5 activation is essential for mounting rapid inflammatory responses against flagellated pathogens such as Salmonella, Pseudomonas, and E. coli. However, excessive or prolonged TLR5 signaling can exacerbate tissue injury and sepsis. In the gastrointestinal tract, TLR5 is highly expressed on epithelial cells and helps maintain mucosal homeostasis. Loss-of-function polymorphisms in TLR5 have been associated with altered gut microbiota composition, increased susceptibility to inflammatory bowel disease (IBD), and dysregulated intestinal inflammation.
Beyond infectious and inflammatory disorders, TLR5 is implicated in metabolic diseases. Animal studies show that TLR5 deficiency can drive metabolic syndrome–like phenotypes, including obesity, insulin resistance, and hepatic inflammation, partly through microbiome-driven mechanisms. In cancer, TLR5 activation has context-dependent effects: it can promote antitumor immunity by stimulating cytokine production and dendritic cell activation, yet chronic inflammation driven by TLR5 may support tumor progression in certain tissues. Additionally, aberrant TLR5 signaling has been linked to respiratory diseases, such as asthma and chronic obstructive pulmonary disease, where heightened flagellin sensitivity contributes to airway inflammation.
Overall, TLR5 serves as both a protective immune sensor and a potential driver of pathology, making it a significant therapeutic target across multiple disease areas.