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Zebrafish Tirap adaptor lacks the phosphatidylinositol 4,5-bisphosphate binding motif, which could partially explain zebrafish insensitivity to lipopolysaccharide, hence its resulting inability to activate downstream Toll (show TLR4 ELISA Kits)-like receptor signaling.
Epistatic interaction between MyD88 (show MYD88 ELISA Kits) and TIRAP against Helicobacter pylori.
Presence of at least one copy of the TIRAP (2054C > T) variant may be associated with severity of bronchopulmonary dysplasia among preterm neonates.
TIRAP polymorphisms are associated with progression and survival of patients with symptomatic myeloma.
This present meta-analysis suggests TIRAP C539T polymorphism is significantly correlated with reduced risk of TB infection, with stronger effect in European.
The TIRAP S180L and TLR9 (show TLR9 ELISA Kits) -1486 T>C polymorphism showed no association with systemic lupus erythematosus (SLE) risk, but they influenced SLE phenotype.
Evaluated the possible association between TIRAP rs1893352 and rs8177374 (S180L) gene polymorphisms and pulmonary tuberculosis in a sample of Iranian population.
TIRAP rs81777374 is associated with resistance to pulmonary tuberculosis.
Data indicate that TcpB (NP_540591) may mimic the function of TIRAP through their similar TIR domain structures.
PSP (show MSMB ELISA Kits) has an immunoregulatory effect through regulation of the TLR4 (show TLR4 ELISA Kits)-TIRAP/MAL-MyD88 (show MYD88 ELISA Kits) signaling pathway.
the results of our study suggest that there is a defect of TIRAP and MyD88 (show MYD88 ELISA Kits) proteins in B-CLL lymphocytes.
TIRAP plays a functional role in transducing LPS (show IRF6 ELISA Kits) signaling from TLR-4 (show TLR4 ELISA Kits) to downstream effector molecules involved in NF-kappaB (show NFKB1 ELISA Kits) activation, and TIRAP promotes apoptotic signaling
genetic polymorphism is associated with interferon-gamma (show IFNG ELISA Kits) signaling and susceptibility to infections
TIRAP/Mal deficiency significantly inhibited the activity of titanium particles with adherent bacterial debris to stimulate in vivo osteolysis and in vitro cytokine mRNAs and secretion.
A critical role for the TLR signaling adapter Mal in alveolar macrophage-mediated protection against Bordetella pertussis.
The D-helix peptide, 2R9, also potently inhibited TLR4 (show TLR4 ELISA Kits), TLR7 (show TLR7 ELISA Kits), and TLR9 (show TLR9 ELISA Kits), but not TLR3 (show TLR3 ELISA Kits) or TNF-alpha (show TNF ELISA Kits) signaling. Cell imaging, co-immunoprecipitation, and in vitro studies demonstrated that 2R9 preferentially targets TIRAP.
MyD88 adaptor (show MYD88 ELISA Kits)-like (Mal) functions in the epithelial barrier and contributes to intestinal integrity via protein kinase C (show PKC ELISA Kits).
our data reveal a differential, but inflammation-independent, requirement for Mal and MyD88 (show MYD88 ELISA Kits) during TLR2 (show TLR2 ELISA Kits)-promoted gastric tumourigenesis.
Mal is essential for the maintenance of intestinal homeostasis and expression of Mal in nonhematopoietic cells prevents chronic intestinal inflammation that may predispose to colon neoplasia.
Study reports that, in response to natural activators of innate immunity, the sorting adaptor TIRAP regulates TLR signaling from the plasma membrane and endosomes.
TIRAP plays a central role in regulating the effects of lipopolysaccharides or lipoteichoic acid on chlorpromazine-induced hepatotoxicity.
PIP5Kalpha promotes TLR4 (show TLR4 ELISA Kits)-associated microglial inflammation by mediating PIP(2)-dependent recruitment of TIRAP to the plasma membrane
The innate immune system recognizes microbial pathogens through Toll-like receptors (TLRs), which identify pathogen-associated molecular patterns. Different TLRs recognize different pathogen-associated molecular patterns and all TLRs have a Toll-interleukin 1 receptor (TIR) domain, which is responsible for signal transduction. The protein encoded by this gene is a TIR adaptor protein involved in the TLR4 signaling pathway of the immune system. It activates NF-kappa-B, MAPK1, MAPK3 and JNK, which then results in cytokine secretion and the inflammatory response. Alternative splicing of this gene results in several transcript variants\; however, not all variants have been fully described.
MyD88 adapter-like protein
, Toll-interleukin 1 receptor domain-containing adaptor protein
, toll/interleukin-1 receptor domain-containing adapter protein
, TIR domain-containing adaptor protein
, Toll-like receptor adaptor protein
, adapter protein wyatt
, adaptor protein Wyatt
, toll-interleukin 1 receptor domain-containing adaptor protein
, TIR domain-containing adapter protein
, Toll-like receptor 4 adaptor protein
, myD88 adapter-like protein