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Both HEK293 (human origin) and embryonic bovine lung cells transfected with bTLR5 responded to addition of H7 flagellin (show FliC Proteins). Responses were significantly reduced when mutations were introduced into the TLR5-binding regions of H7 flagellin (show FliC Proteins).
The results of this study demonstrated that TLR5 rs5744174 polymorphism may have no impact on the stroke risk, gene expression and inflammatory cytokines, but may influence the HDL-C serum level of IS patients in Chinese Han population.
Letter: TLR5 mRNA was not altered in peripheral mononuclear cells from patients with ankylosing spondylitis or rheumatoid arthritis.
These results indicate that in response to Pseudomonas aeruginosa or flagellin (show FliC Proteins), EGFR (show EGFR Proteins) associates with and tyrosine phosphorylates MUC1 (show MUC1 Proteins)-CT in primary normal human bronchial epithelial cells, leading to increased MUC1 (show MUC1 Proteins)-CT association with TLR5
Study elucidated the relationship between TLR5 and caveolin-1 (show CAV1 Proteins) at the transcriptional and translational levels using human cells, results suggest that caveolin-1 (show CAV1 Proteins) is a crucial regulator for maintaining and controlling TLR5 expression.
Study showed that MyD88 Toll/interleukin-1 receptor (TIR) domain interacted with TLR5TIR but not with TLR6TIR. The solubility of both TLR5TIR and TLR6TIR were influenced by its binding partner MyD88TIR. Moreover, TLR5TIR exhibited increased solubility.
TLR-5 was more abundant in OSCC than in CSCC (show CYP11A1 Proteins) samples.
p53 (show TP53 Proteins)-dependent amplification of transcriptional response to TLR5 activation required expression of NFkappaB (show NFKB1 Proteins) subunit p65 (show GORASP1 Proteins) and was mediated by several molecular mechanisms
MAMs MUC1 (show MUC1 Proteins) and MUC16 (show MUC16 Proteins) contribute to the maintenance of immune homeostasis at the ocular surface by limiting TLR-mediated innate immune responses.
TLR2 and 5 polymorphisms (rs5743708, rs3804099 and rs5744105) may not serve as the susceptible gene for sepsis in newborn infants.
Association of TLR5 Gene Polymorphisms in Ulcerative Colitis Patients of North India and Their Role in Cytokine Homeostasis.
TLR5 mediates CD172a (show SIRPA Proteins)(+) intestinal lamina propria dendritic cell induction of Th17 cells.
TLR5 activation plays an important role in the induction of podocyte apoptosis
TLR5 gene knockout impairs some effects of weight-reduction in diet-induced obesity (DIO). The glucose intolerance in DIO TLR5(-/-) mice was more significant than that in DIO C57BL/6 mice.
The results suggest that caveolin-1 (show CAV1 Proteins)/TLR5 signaling plays a key role in age-associated innate immune responses and that FlaB (show FliC Proteins)-PspA (show SFTPA1 Proteins) stimulation of TLR5 may be a new strategy for a mucosal vaccine adjuvant against pneumococcal infection in the elderly.
Over-activation of TLR5 signaling by high-dose flagellin (show FliC Proteins) induces liver injury in mice.
results define systemically administered TLR5 agonists as organ-specific immunoadjuvants, enabling efficient antitumor vaccination that does not depend on identification of tumor-specific antigens
an altered composition of the microbiota in a given environment can result in metabolic syndrome, but it is not a consequence of TLR5 deficiency per se
TLR5 deficiency mice after carbon tetrachloride administration reduced NF-kappaB (show NFKB1 Proteins) and MAPK (show MAPK1 Proteins) signaling pathways activation, which down regulated hepatic stellate cells activation.
Normal prostate tissue from WT mice showed strong expression of TLR4 (show TLR4 Proteins) and TLR5. However, TLR4 (show TLR4 Proteins) expression in the prostate tissue from TRAMP (show DPT Proteins) mice gradually decreased as pathologic grade became more aggressive.
aa 89-96 of flagellin (show FliC Proteins) is not only the crucial site responsible for TLR5 recognition, but is also important for humoral immune adjuvanticity through a TLR5-independent pathway.
This study identified variations in the promoter that resulted in changes in TLR5 gene expression.
TLR5 takes part in the airway mucosal defense systems as a unique endogenous potentiator of airway serous secretions.
The results indicated that TLR5 SNPs were associated with the transcript abundance of cytokines.
This gene encodes a member of the toll-like receptor (TLR) family, which plays a fundamental role in pathogen recognition and activation of innate immune responses. These receptors recognize distinct pathogen-associated molecular patterns that are expressed on infectious agents. The protein encoded by this gene recognizes bacterial flagellin, the principal component of bacterial flagella and a virulence factor. The activation of this receptor mobilizes the nuclear factor NF-kappaB, which in turn activates a host of inflammatory-related target genes. Mutations in this gene have been associated with both resistance and susceptibility to systemic lupus erythematosus, and susceptibility to Legionnaire disease.
toll-like receptor 5
, toll/interleukin-1 receptor-like protein 3