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Tir8/SIGIRR acts anti-inflammatory on different immune responses,its function in allergic asthma is a controversial issue, since anti- as well as pro-inflammatory effects have been reported
SIGIRR plays an important role in the negative regulation of LPS (show IRF6 ELISA Kits) response and tolerance in human bladder epithelial cells, possibly through its impact on TLR-mediated signaling.
Levels of SIGIRR are lower in human colorectal tumors, compared with nontumor tissues; tumors contain the dominant-negative isoform SIGIRR(DeltaE8).
SIGIRR predicts biochemical recurrence in patients with low Gleason score and low pathological stage prostate cancer.
decreased numbers of SIGIRR-positive CD4 (show CD4 ELISA Kits)+ T cells in SLE patients and its correlation with SLEDAI score as well as the clinical data suggest that SIGIRR may be involved in the pathogenesis of SLE.
To the best of our knowledge, this is one of the first reports of a phenotype associated with SIGIRR in humans. Our data provide novel mechanistic insight into the probable causation of necrotizing enterocolitis
An association was found in the SIGIRR rs7396562 polymorphism and systemic lupus erythematosus susceptibility in a Chinese population.
IL-37 acts as an extracellular cytokine by binding to the IL-18 (show IL18 ELISA Kits) receptor but using the IL-1R8 for its anti-inflammatory properties.
Lipopolysaccharide decreases SIGIRR expression by suppressing specificity protein 1 Sp1 (show SP1 ELISA Kits) via the TLR4 (show TLR4 ELISA Kits)-p38 (show CRK ELISA Kits) pathway in monocytes and neutrophils.
The present study was undertaken to characterize responses of B cells from systemic lupus erythematosus patients to TLR7 (show TLR7 ELISA Kits) and TLR9 (show TLR9 ELISA Kits) stimulation and to explore the potential role of SIGIRR.
Expression of SIGIRR(N86/102S) in the colonic epithelium of mice increases expression of inflammatory cytokines and formation and size of colitis-associated tumors.
IL-37 requires IL-18Ralpha and SIGIRR/IL-1R8 to diminish allergic airway inflammation in mice
Thus, SIGIRR expression by IEC reflects a strategy that sacrifices maximal innate responsiveness by IEC in order to promote commensal microbe based colonization resistance against bacterial pathogens.
This study identifies TIR8/SIGIRR as a novel intrinsic negative regulator of innate IL-17A (show IL17A ELISA Kits) expression
Absence of TIR8 reduces house dust mite-induced allergic airway inflammation in mice.
data suggest that TIR8 is an important negative regulator of an LPS (show TLR4 ELISA Kits)-mediated inflammatory response in tubular epithelial cells and dampens an effective antibacterial host response during pyelonephritis
TIR8 has a nonredundant effect in modulating the inflammation caused by Pseudomonas aeruginosa, in particular, by negatively regulating IL-1RI signaling, which plays a major role in the pathogenesis of bacterial pneumonia.
TIR8 was found in the GI tract and kidney. Expression of TIR8 mRNA was detected in lymph nodes, thymus and thyroid gland. Several isoforms of TIR8 were detected in the same organs, suggesting the occurrence of different post-translational processings.
Acts as a negative regulator of the Toll-like and IL-1R receptor signaling pathways. Attenuates the recruitment of receptor-proximal signaling components to the TLR4 receptor, probably through an TIR-TIR domain interaction with TLR4. Through its extracellular domain interferes with the heterodimerization of Il1R1 and IL1RAP (By similarity).
single Ig IL-1-related receptor
, single Ig IL-1R-related molecule
, single immunoglobulin domain IL1R1 related
, single immunoglobulin domain-containing IL1R-related protein
, toll/interleukin-1 receptor 8
, single Ig IL-1 receptor related protein
, single Ig IL-1R-related protein