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anti-Human TLR5 Antikörper:
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Dog (Canine) Monoclonal TLR5 Primary Antibody für FACS, IHC - ABIN4360264
Smith, Varley, Eardley, Feather, Trejdosiewicz, Southgate: Toll-like receptor responses of normal human urothelial cells to bacterial flagellin and lipopolysaccharide. in The Journal of urology 2011
Show all 28 Pubmed References
Dog (Canine) Monoclonal TLR5 Primary Antibody für FACS, IHC (p) - ABIN4360253
Li, Younger, Gartenhaus, Joseph, Hu, Baer, Brown, Davila: Inhibition of IRAK1/4 sensitizes T cell acute lymphoblastic leukemia to chemotherapies. in The Journal of clinical investigation 2015
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Dog (Canine) Monoclonal TLR5 Primary Antibody für FACS - ABIN4360267
Crellin, Garcia, Hadisfar, Allan, Steiner, Levings: Human CD4+ T cells express TLR5 and its ligand flagellin enhances the suppressive capacity and expression of FOXP3 in CD4+CD25+ T regulatory cells. in Journal of immunology (Baltimore, Md. : 1950) 2005
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Dog (Canine) Monoclonal TLR5 Primary Antibody für FACS - ABIN4360261
Fukata, Breglio, Chen, Vamadevan, Goo, Hsu, Conduah, Xu, Abreu: The myeloid differentiation factor 88 (MyD88) is required for CD4+ T cell effector function in a murine model of inflammatory bowel disease. in Journal of immunology (Baltimore, Md. : 1950) 2008
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Human Polyclonal TLR5 Primary Antibody für FACS, IHC (p) - ABIN4360266
Brandon, Perez, Jennings, Cohen, Sindhava, Bondada, Kaplan, Bryson: Association between chronic liver and colon inflammation during the development of murine syngeneic graft-versus-host disease. in American journal of physiology. Gastrointestinal and liver physiology 2010
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Human Monoclonal TLR5 Primary Antibody für FACS, IHC (p) - ABIN532010
Wong, Cheung, Ip, Lam: Intracellular signaling mechanisms regulating toll-like receptor-mediated activation of eosinophils. in American journal of respiratory cell and molecular biology 2007
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Human Polyclonal TLR5 Primary Antibody für IF (p), IHC (p) - ABIN673239
Hao, Zhang, Liang, Song, Hou: rFliC prolongs allograft survival in association with the activation of recipient Tregs in a TLR5-dependent manner. in Cellular & molecular immunology 2014
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Human Polyclonal TLR5 Primary Antibody für WB - ABIN550253
Takeda, Kaisho, Akira: Toll-like receptors. in Annual review of immunology 2003
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Human Polyclonal TLR5 Primary Antibody für IF, WB - ABIN550252
Hayashi, Smith, Ozinsky, Hawn, Yi, Goodlett, Eng, Akira, Underhill, Aderem: The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5. in Nature 2001
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Human Polyclonal TLR5 Primary Antibody für WB - ABIN411612
Rolli, Rosenblatt-Velin, Li, Loukili, Levrand, Pacher, Waeber, Feihl, Ruchat, Liaudet: Bacterial flagellin triggers cardiac innate immune responses and acute contractile dysfunction. in PLoS ONE 2010
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TLR5 signalling has evolved differently in ruminants.
Clinically, vaginal-douche BD2 concentrations were reduced (p < 0.05) in women suffering recurrent urinary tract infections (rUTI), compared to age-matched healthy controls with concentrations further decreased (p < 0.05) in a TLR5(392Stop) single nucleotide polymorphism rUTI subgroup.
TLR5 polymorphisms were screened in 131 chronic hepatitis B patient and 168 individuals by polymerase chain reaction (PCR) - restriction fragment length polymorphism (RFLP) technique
In addition to previously identified binding sites at the N-terminal and central segment of the TLR5 ectodomain, we developed the TLR5'-D1 interaction interface on TLR5 and showed a species-specific recognition relevance of this extended region. Residues were identified that contribute to the interaction between two TLR5 ectodomains in an active signaling complex.
Proinflammatory signaling mediated by innate immunity engagement of flagellin-activated TLR5 in tumor cells results in antitumor effects through NME3 kinase, a positive downstream regulator of flagellin-mediated NFkappaB signaling, enhancing survival for several human cancers.
TLR5 has potential association with the development of eczema
High TLR5 expression is associated with the pathogenesis of rheumatoid arthritis.
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.
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.
this study signifies that TLR5 adaptor molecules are necessary for the proper production of cytokines, chemokines and pro-labour mediators after TLR ligation
the newly found long TLR5 transcripts may be involved in the negative regulation of TLR5 expression and function.
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
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.
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.
These results suggest that HMGB1-modulated TLR5 signaling is responsible for pain hypersensitivity.
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.
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.
Distinctive Recognition of Flagellin by Human and Mouse Toll-Like Receptor 5
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.
Study demonstrated that toll-like receptor 5 expression and functional activity as measured by interleukin 6 are modulated by hormones
High TLR5 expression is associated with postburn infection.
Mouse TLR5 ectodomain (aa 27-641) was modelled. Residues that differ between human TLR5 and mouse TLR5 in the region 377-425 were mutated and assessed for activation potential. A species-specific nature of the ligand-receptor interaction exists both on the ligand and the receptor side.
neonatal selection by Toll-like receptor 5 influences long-term gut microbiota composition
hematopoietic TLR5 deficiency inhibits atherosclerotic lesion formation by attenuated macrophage accumulation and defective T-cell responsiveness.
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.
Data show that Toll-like receptor 5 (TLR5) plays a role in radiation-induced apoptosis, and CBLB502 pre-treatment could reduce the apoptosis.
data directly demonstrate that nasal epithelial GM-CSF contributes to TLR5-mediated modulation of airway DCs and a subsequent IgA response.
The activation of NLRC4 by flagellin downregulated the flagellin-induced and TLR5-mediated immune responses against flagellin.
TLR5 but not NLRC4 is required for S. pneumoniae FliC-induced protection.
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
TLR5 mediates CD172a(+) intestinal lamina propria dendritic cell induction of Th17 cells.
The results provide novel insights into the mechanisms underlying the epididymal innate immune responses to uropathogenic Escherichia coli infection.
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/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.
Over-activation of TLR5 signaling by high-dose flagellin 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
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.
Prediction and comparison of TLR protein domain architectures for multiple species revealed seven conserved regions of LRR patterning associated with the three genes investigated.
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.
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.
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
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.
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.
the structural basis and mechanistic implications of TLR5-flagellin recognition
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/interleukin-1 receptor-like protein 3
, toll-like receptor 5
, TLR 5
, toll-like receptor 5b