anti-TLR5 (TLR5) Antikörper

Human Toll-Like Receptor 5 (TLR5) Interaktionspartner

1. TLR5 has potential association with the development of eczema

2. High TLR5 expression is associated with the pathogenesis of rheumatoid arthritis.

3. SNPs associated with genetically determined high activity of TLR5 among patients with CD and genetically determined high IL-12 and IL-18 levels among patients with UC.

4. results suggest that Hsp90 inhibitors suppress TLR5 surface expression and activation of NF-kappaB in THP-1 cells in response to TLR5 ligand, and these inhibitory effects may be associated with the possible mechanisms by which Hsp90 inhibitors suppress myeloid leukemia.

5. this study signifies that TLR5 adaptor molecules are necessary for the proper production of cytokines, chemokines and pro-labour mediators after TLR ligation

6. the newly found long TLR5 transcripts may be involved in the negative regulation of TLR5 expression and function.

7. It was observed that the TLR5 polymorphisms rs5744168, rs2072493, and rs5744174 are less frequent in Indian Tamils, suggesting that the TLR5 gene remains conserved, which may be due to the genetic selection pressure to withstand prevailing endemic infectious diseases. We observed that these polymorphisms also failed to confer significant risk to develop chronic H. pylori infections and its associated clinical phenotypes

8. we identified significant interactions between TLR5 rs1640827, rs17163737 and Helicobacter pylori infection. This results provide valuable insights into the TLR5 and Helicobacter pylori infection involved in gastric carcinogenesis, and this may have important implications in personalized prevention of GC.

9. TLR 5, 7, and 9 expression patterns differed between HPV-positive and -negative oropharyngeal squamous cell carcinoma patients. In HPV-positive tumors the expression of TLR 5 and 7 correlated with tumor recurrence.

10. These results suggest that HMGB1-modulated TLR5 signaling is responsible for pain hypersensitivity.

11. data show that TLR-5 and TLR-9 are susceptible genes to lupus nephritis (LN) and that their expression is dysregulated in LN patients' kidneys, supporting a role of these mediators in the pathogenesis of LN.

12. These results indicate that in Chinese genetic variation of TLR5 may be not a determinant of susceptibility to hepatitis B virus-related diseases but may play a role in development of hepatitis B virus-related severe liver diseases.

13. Distinctive Recognition of Flagellin by Human and Mouse Toll-Like Receptor 5

14. This study independently confirms the association of TLR5 c.1174C>T with protection against death in melioidosis, identifies lower bacteremia, IL-10 and TNF-alpha production in carriers of the variant with melioidosis.

15. Study demonstrated that toll-like receptor 5 expression and functional activity as measured by interleukin 6 are modulated by hormones

16. findings suggest that TLR5 is functionally expressed in the SG and responds to its cognate ligand flagellin

17. Upregulation of TLR4, TLR5, and TLR9 suggests the involvement of bacteria or dysregulation of the immune response to commensal flora in small bowel mucosa in irritable bowel syndrome patients.

18. that TLR5 is involved in the pathogenesis and dissemination of esophageal adenocarcinoma through as-yet-uncharacterized mechanisms

19. Ligands for TLR1/2 or TLR5 may provide critical stimuli able to sustain the growth and the malignant phenotype of MCL cells.

20. The distribution of the TLR 5 genotypes did not differ significantly between bronchopulmonary dysplasia patients and controls.

Mouse (Murine) Toll-Like Receptor 5 (TLR5) Interaktionspartner

1. hematopoietic TLR5 deficiency inhibits atherosclerotic lesion formation by attenuated macrophage accumulation and defective T-cell responsiveness.

2. Denatured flagellin suppressed the production of the pro-inflammatory cytokines induced by intact flagellin or Pseudomonas aeruginosa both in vitro and in vivo, probably by blocking TLR5.

3. Data show that Toll-like receptor 5 (TLR5) plays a role in radiation-induced apoptosis, and CBLB502 pre-treatment could reduce the apoptosis.

4. These results suggest that HMGB1-modulated TLR5 signaling is responsible for pain hypersensitivity.

5. data directly demonstrate that nasal epithelial GM-CSF contributes to TLR5-mediated modulation of airway DCs and a subsequent IgA response.

6. Distinctive Recognition of Flagellin by Human and Mouse Toll-Like Receptor 5

7. The activation of NLRC4 by flagellin downregulated the flagellin-induced and TLR5-mediated immune responses against flagellin.

8. TLR5 but not NLRC4 is required for S. pneumoniae FliC-induced protection.

9. This resulted in Sp1 displacement from the promoter and binding of Sp3 to it, leading to p300 recruitment and histone acetylation, activating transcription. This is the first study addressing the mechanisms of physiological TLR5 expression in the intestine. Additionally, a novel insight is gained into Sp1/Sp3-mediated gene regulation that may apply to other genes

10. TLR5 mediates CD172a(+) intestinal lamina propria dendritic cell induction of Th17 cells.

11. The results provide novel insights into the mechanisms underlying the epididymal innate immune responses to uropathogenic Escherichia coli infection.

12. TLR5 activation plays an important role in the induction of podocyte apoptosis

13. 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.

14. The results suggest that caveolin-1/TLR5 signaling plays a key role in age-associated innate immune responses and that FlaB-PspA stimulation of TLR5 may be a new strategy for a mucosal vaccine adjuvant against pneumococcal infection in the elderly.

15. Over-activation of TLR5 signaling by high-dose flagellin induces liver injury in mice.

16. results define systemically administered TLR5 agonists as organ-specific immunoadjuvants, enabling efficient antitumor vaccination that does not depend on identification of tumor-specific antigens

17. 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

18. TLR5 deficiency mice after carbon tetrachloride administration reduced NF-kappaB and MAPK signaling pathways activation, which down regulated hepatic stellate cells activation.

19. Normal prostate tissue from WT mice showed strong expression of TLR4 and TLR5. However, TLR4 expression in the prostate tissue from TRAMP mice gradually decreased as pathologic grade became more aggressive.

20. aa 89-96 of flagellin is not only the crucial site responsible for TLR5 recognition, but is also important for humoral immune adjuvanticity through a TLR5-independent pathway.

Cow (Bovine) Toll-Like Receptor 5 (TLR5) Interaktionspartner

1. Both HEK293 (human origin) and embryonic bovine lung cells transfected with bTLR5 responded to addition of H7 flagellin. Responses were significantly reduced when mutations were introduced into the TLR5-binding regions of H7 flagellin.

2. Prediction and comparison of TLR protein domain architectures for multiple species revealed seven conserved regions of LRR patterning associated with the three genes investigated.

Pig (Porcine) Toll-Like Receptor 5 (TLR5) Interaktionspartner

1. This study identified variations in the promoter that resulted in changes in TLR5 gene expression.

2. TLR5 takes part in the airway mucosal defense systems as a unique endogenous potentiator of airway serous secretions.

3. The results indicated that TLR5 SNPs were associated with the transcript abundance of cytokines.

Goat Toll-Like Receptor 5 (TLR5) Interaktionspartner

1. Although being highly conserved among the ruminants, comparatively high variations in goat TLR5 might give an opportunity to host for recognizing the wider spectrum of pathogens.

Zebrafish Toll-Like Receptor 5 (TLR5) Interaktionspartner

1. Targeted exchange of drTLR5b and drTLR5a regions revealed that TLR5 activation needs a heterodimeric configuration of the receptor ectodomain and cytoplasmic domain, consistent with ligand-induced changes in receptor conformation

2. Our studies show that Pam3CSK4 and flagellin can stimulate the Tlr2 and Tlr5 signaling pathways leading to common and specific responses in the zebrafish embryo system.

3. Data suggest that the structure-based modeling study on paFliC, the paFliC-TLR5 complex, and the paFliC filament could contribute to the improvement of vaccine design to control P. aeruginosa infection.

4. the structural basis and mechanistic implications of TLR5-flagellin recognition