Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic Gene Ontology annotation based on Rhea mapping
Combined Automated Annotation using Multiple IEA Methods
IRAK-4: a novel member of the IRAK family with the properties of an IRAK-kinase.
Pellino 1 is required for interleukin-1 (IL-1)-mediated signaling through its interaction with the IL-1 receptor-associated kinase 4 (IRAK4)-IRAK-tumor necrosis factor receptor-associated factor 6 (TRAF6) complex.
Characterization of Pellino2, a substrate of IRAK1 and IRAK4.
Human TLR-7-, -8-, and -9-mediated induction of IFN-alpha/beta and -lambda Is IRAK-4 dependent and redundant for protective immunity to viruses.
Identification of the phosphorylation sites on the E3 ubiquitin ligase Pellino that are critical for activation by IRAK1 and IRAK4.
Impaired neutrophil migration and phagocytosis in IRAK-4 deficiency.
Helical assembly in the MyD88-IRAK4-IRAK2 complex in TLR/IL-1R signalling.
What the Myddosome structure tells us about the initiation of innate immunity.
Mapping a dynamic innate immunity protein interaction network regulating type I interferon production.
The death domain-containing protein Unc5CL is a novel MyD88-independent activator of the pro-inflammatory IRAK signaling cascade.
β-TrCP-mediated IRAK1 degradation releases TAK1-TRAF6 from the membrane to the cytosol for TAK1-dependent NF-κB activation.
IRAK-M mediates Toll-like receptor/IL-1R-induced NFκB activation and cytokine production.
Functional assessment of the mutational effects of human IRAK4 and MyD88 genes.
A massively parallel pipeline to clone DNA variants and examine molecular phenotypes of human disease mutations.
Widespread macromolecular interaction perturbations in human genetic disorders.
Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing.
Architecture of the human interactome defines protein communities and disease networks.
Understanding early TLR signaling through the Myddosome.
Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.
A reference map of the human binary protein interactome.
Dimeric Structure of the Pseudokinase IRAK3 Suggests an Allosteric Mechanism for Negative Regulation.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
The IRAK4 scaffold integrates TLR4-driven TRIF and MYD88 signaling pathways.
Regulation of innate immune signaling by IRAK proteins.
OTUD5 promotes the inflammatory immune response by enhancing MyD88 oligomerization and Myddosome formation.
Molecular definition of the endogenous Toll-like receptor signalling pathways.
MyD88:MAL(TIRAP) cascade initiated on plasma membrane
IRAK4 binds to the activated TLR receptor:TIRAP:MyD88 complex
IRAK1 or IRAK2 binds to the activated IRAK4 :activated TLR:MyD88:TIRAP complex
First phosphorylation of IRAK1 by IRAK4 bound to activated TLR:MyD88:Mal
Second phosphorylation of IRAK1 by IRAK4 bound to activated TLR:MyD88:TIRAP
Multiple IRAK1 autophosphorylation steps
Dissociation of hp-IRAK1:TRAF6 from the activated TLR:oligo-Myd88:TIRAP:p-IRAK4 complex
Toll Like Receptor 9 (TLR9) Cascade
Toll Like Receptor 7/8 (TLR7/8) Cascade
Dissociation of p-IRAK2:TRAF6 from the activated TLR:oligo-Myd88:TIRAP:p-IRAK4 complex
IRAK4 is activated by autophosphorylation
IL1R1:IL1:IL1RAP:MYD88 homodimer binds IRAK4
IRAK2 is phosphorylated downstream of IRAK4 following IL1 receptor activation
IRAK1 binds to MYD88 within the IL1R complex
IRAK4 phosphorylates IRAK1
IRAK4-activated IRAK1 autophosphorylates
Hyperphosphorylated IRAK1 associates with TRAF6
The Interleukin 1 receptor complex binds Tollip
TRAF6 binding leads to IRAK1:TRAF6 release
hp-IRAK1,hp-IRAK4 bind Pellino1,2,3
hp-IRAK1, hp-IRAK4 4 phosphorylate Pellino-1 and 2
Defective IRAK4 does not bind MyD88:MAL:BTK:activated TLR2/4
IRAK4 deficiency blocks formation of the MyD88-IRAK4 Myddosome in the TLR5 pathway
hp-IRAK1:p-Pellino, IRAK4:p-Pellino bind UBE2N:UBE2V1
IRAK4 autophosphorylation in the complex with activated TLR:MyD88:TIRAP
Phosphorylation of IRAK2 bound to the activated IRAK4:MyD88 oligomer:TIRAP:activated TLR complex
Dissociation of hp-IRAK1/or IRAK2:TRAF6-oligomer from the p-IRAK4 :oligo-Myd88:activated TLR7/8 or 9 complex
Phosphorylation and release of IRF7 upon TLR7/8 or 9 activation
TRAF6 binds to hp- IRAK1/or p-IRAK2:p-IRAK4:MyD88:activated TLR7/8 or 9
IRAK1/or IRAK2 binds to the activated IRAK4 :MyD88:activated TLR 7/8 or 9
TRAF6 ubiquitinqtes IRF7 within the activated TLR7/8 or 9 complex
Multiple IRAK1 autophosphorylation steps within the complex pIRAK4:MyD88:activated TLR7/8 or 9
Second phosphorylation of IRAK1 by IRAK4 bound to MyD88: activated TLR 7/8 or 9
IRAK4 binds to the activated TLR7/8 or 9 receptor:MyD88 complex
Phosphorylation of IRAK2 bound to the activated IRAK4:MyD88 oligomer:activated TLR 7/8 or 9
IRAK4 autophosphorylation in the complex with MyD88:activated TLR 7/8 or 9
First phosphorylation of IRAK1 by IRAK4 bound to MyD88:activated TLR 7/8 or 9
TRAF6 interacts with IRF7 upon TLR7/8 or 9 activation
IRAK1/or IRAK2 binds to the activated IRAK4 :oligo MyD88:activated TLR5 or 10 complex
Multiple IRAK1 autophosphorylation within the complex p-IRAK4:oligo MyD88:activated TLR
TRAF6 binds to hp- IRAK1 or p-IRAK2
Phosphorylation of IRAK2 bound to the activated IRAK4:MyD88 oligomerl:activated TLR5 or 10 complex
IRAK4 autophosphorylation within the complex activated TLR:MyD88
MyD88 cascade initiated on plasma membrane
IRAK4 binds to MyD88 bound to the activated TLR5 or 10 receptor
Second phosphorylation of IRAK1 by IRAK4 bound to MyD88:activated TLR complex
First phosphorylation of IRAK1 by IRAK4 bound to MyD88:activated TLR
Dissociation of hp-IRAK1:TRAF6 or IRAK2:TRAF6-oligomer from the activated TLR5 or 10:oligo-Myd88:p-IRAK4 complex
Falcon deep research report on IRAK4
The pro-atherogenic cytokine interleukin-18 induces CXCL16 expression in rat aortic smooth muscle cells via MyD88, interleukin-1 receptor-associated kinase, tumor necrosis factor receptor-associated factor 6, c-Src, phosphatidylinositol 3-kinase, Akt, c-Jun N-terminal kinase, and activator protein-1 signaling.