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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 04 Mar 2015.

Toll-interleukin 1 receptor

Mal, TIRAP, BSAC, Wyatt
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: MyD88, TLR4, CAN, TLR2, TRAM
Papers on Mal
Preparation of novel (-)-gossypol nanoparticles and the effect on growth inhibition in human prostate cancer PC-3 cells in vitro.
New
Xu et al., Xinxiang, China. In Exp Ther Med, 31 Mar 2015
UNASSIGNED: The aim of the present study was to investigate the antitumor effects and possible mechanism of (-)-gossypol nanoparticles, loaded with vv polyethylene glycol-maleimide (mPEG-Mal), in vitro.
Genetic variation in pattern recognition receptors and adaptor proteins associated with development of chronic Q fever.
New
van de Vosse et al., Nijmegen, Netherlands. In J Infect Dis, 26 Mar 2015
METHODS:  Twenty-four single nucleotide polymorphisms (SNPs) in genes encoding TLRs, NOD-like receptor-2, αvβ3-integrin, CR3, and adaptors MyD88 and TIRAP were genotyped in 139 chronic Q fever patients and in 220 control individuals with cardiovascular risk-factors and previous exposure to C.burnetii.
CD14, TLR4 and TRAM show different trafficking dynamics during LPS stimulation.
New
Husebye et al., Trondheim, Norway. In Traffic, 24 Mar 2015
Mal-MyD88 is recruited to the plasma membrane to initiate the signaling cascade leading to production of pro-inflammatory cytokines while TRAM-TRIF is recruited to early endosomes to initiate the subsequent production of type I interferons.
Correlation of sensitizing capacity and T-cell recognition within the Bet v 1 family.
New
Bohle et al., Vienna, Austria. In J Allergy Clin Immunol, 07 Mar 2015
OBJECTIVE: We analyzed the T-cell epitopes of Mal d 1, the nonsensitizing Bet v 1 homolog in apple, and assessed possible differences in uptake and antigen processing of Bet v 1, Api g 1, and Mal d 1. METHODS: For epitope mapping, Mal d 1-specific T-cell lines were stimulated with overlapping synthetic 12-mer peptides.
Toll/interleukin-1 receptor (TIR) domain-mediated cellular signaling pathways.
New
Park et al., Kyŏngsan, South Korea. In Apoptosis, 28 Feb 2015
The Toll-like receptor/Interleukin (IL)-1 receptor (TLR/IL-1R) superfamily comprises proteins that contain the phylogenetically conserved Toll/IL-1 receptor (TIR) domain, which is responsible for the propagation of downstream signaling through recruitment of TIR domain containing cytosolic adaptor proteins such as MyD88, TIRAP/MAL, TRIF, TRAM and SARM.
A promiscuous lipid-binding protein diversifies the subcellular sites of toll-like receptor signal transduction.
New
Impact
Kagan et al., Boston, United States. In Cell, Mar 2014
Here, we report that, in response to natural activators of innate immunity, the sorting adaptor TIRAP regulates TLR signaling from the plasma membrane and endosomes.
High pressure effects on allergen food proteins.
Review
Smeller et al., Budapest, Hungary. In Biophys Chem, 2014
According to this criterion we selected the following allergen proteins: Mal d 1 and Mal d 3 (apple), Bos d 5 (milk), Dau c 1 (carrot), Gal d 2 (egg), Ara h 2 and Ara h 6 (peanut), and Gad m 1 (cod).
Toll-like receptors' pathway disturbances are associated with increased susceptibility to infections in humans.
Review
Condino-Neto et al., São Paulo, Brazil. In Arch Immunol Ther Exp (warsz), 2013
TLRs and IL-1R are a family of receptors related to the innate immune response that contain an intracellular domain known as the Toll-IL-1R (TIR) domain that recruits the TIR-containing cytosolic adapters MyD88, TRIF, TIRAP and TRAM.
Clinical relevance of mupirocin resistance in Staphylococcus aureus.
Review
Bonten et al., Utrecht, Netherlands. In J Hosp Infect, 2013
EUCAST and BSAC clinical thresholds for S. aureus are ≤1mg/L for susceptible and >256mg/L for resistant, placing the susceptible threshold at the epidemiological cut-off value (ECOFF).
Mal, more than a bridge to MyD88.
Review
O'Neill et al., Dublin, Ireland. In Iubmb Life, 2013
This review will focus on one of those adaptors, MyD88 adaptor-like (Mal), also known as TIRAP.
[Negative regulation of Toll-like receptor signalling].
Review
Choroszyńska et al., Lublin, Poland. In Postepy Hig Med Dosw (online), 2012
MyD88, TIRAP, TRIF, TRAM, and IPS-1, which participate in the cascade activation of kinases (IKK, MAP, RIP-1, TBK-1) as well as transcription factors (NF-κB, AP-1) and regulatory factor (IRF3).
The p110δ isoform of the kinase PI(3)K controls the subcellular compartmentalization of TLR4 signaling and protects from endotoxic shock.
Impact
Vanhaesebroeck et al., London, United Kingdom. In Nat Immunol, 2012
Lipopolysaccharide activates plasma-membrane signaling and endosomal signaling by Toll-like receptor 4 (TLR4) through the TIRAP-MyD88 and TRAM-TRIF adaptor complexes, respectively, but it is unclear how the signaling switch between these cell compartments is coordinated.
Bone morphogenetic protein signaling in vascular disease: anti-inflammatory action through myocardin-related transcription factor A.
GeneRIF
Lagna et al., Boston, United States. In J Biol Chem, 2012
molecular inhibitory pathway linking BMP4 signaling, activation of MRTF-A, and inhibition of NF-kappaB provides insights into the etiology of PAH and a potential focus of therapeutic intervention.
Poxviral protein A46 antagonizes Toll-like receptor 4 signaling by targeting BB loop motifs in Toll-IL-1 receptor adaptor proteins to disrupt receptor:adaptor interactions.
GeneRIF
Bowie et al., Dublin, Ireland. In J Biol Chem, 2012
Poxviral protein A46 inhibits TLR4 signaling and interacts with Toll-IL-1 receptor (TIR) domain-containing proteins of the receptor complex.
Toll-like receptor signal adaptor protein MyD88 is required for sustained endotoxin-induced acute hypoferremic response in mice.
GeneRIF
Santos et al., Montréal, Canada. In Am J Pathol, 2012
Toll-like receptor signal adaptor protein MyD88 is required for sustained endotoxin-induced acute hypoferremic response in mice.
Phosphoinositide binding by the Toll adaptor dMyD88 controls antibacterial responses in Drosophila.
Impact
Kagan et al., Boston, United States. In Immunity, 2012
These data are reminiscent of the interactions between the mammalian Toll adaptors MyD88 and TIRAP with one major exception.
MAL facilitates the incorporation of exocytic uroplakin-delivering vesicles into the apical membrane of urothelial umbrella cells.
GeneRIF
Sun et al., New York City, United States. In Mol Biol Cell, 2012
the exclusion of MAL from the expanding 2D crystals of uroplakins explains the selective association of MAL with the hinge areas in the uroplakin-delivering fusiform vesicles, as well as at the apical surface
The kinase Btk negatively regulates the production of reactive oxygen species and stimulation-induced apoptosis in human neutrophils.
Impact
Morio et al., Tokyo, Japan. In Nat Immunol, 2012
In the absence of Btk, the adaptor Mal was associated with PI(3)K and PTKs at the plasma membrane, whereas in control resting neutrophils, Btk interacted with and confined Mal in the cytoplasm.
Structural insights into TIR domain specificity of the bridging adaptor Mal in TLR4 signaling.
GeneRIF
Shen et al., Tianjin, China. In Plos One, 2011
The Mal-Toll/interleukin-1 receptor (TIR) domains AB loop is capable of mediating direct binding to the TIR domains of TLR4 and MyD88 simultaneously.
Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.
Impact
Karsan et al., Vancouver, Canada. In Nat Med, 2010
We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll-interleukin-1 receptor domain-containing adaptor protein (TIRAP) and tumor necrosis factor receptor-associated factor-6 (TRAF6) as respective targets of these miRNAs.
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