Gene Ontology annotation through association of InterPro records with GO terms

Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity

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

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara

Electronic Gene Ontology annotations created by ARBA machine learning models

Combined Automated Annotation using Multiple IEA Methods

Human TLR7 or TLR8 independently confer responsiveness to the antiviral compound R-848.

Molecular basis for the immunostimulatory activity of guanine nucleoside analogs: activation of Toll-like receptor 7.

Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA.

Suppression of RNA recognition by Toll-like receptors: the impact of nucleoside modification and the evolutionary origin of RNA.

Activation of innate defense against a paramyxovirus is mediated by RIG-I and TLR7 and TLR8 in a cell-type-specific manner.

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.

Expression of the Bcl-2 protein BAD promotes prostate cancer growth.

Cultured human melanocytes express functional toll-like receptors 2-4, 7 and 9.

UNC93B1 physically associates with human TLR8 and regulates TLR8-mediated signaling.

Structural basis for endosomal trafficking of diverse transmembrane cargos by PX-FERM proteins.

Structural Analysis Reveals that Toll-like Receptor 7 Is a Dual Receptor for Guanosine and Single-Stranded RNA.

Deoxyguanosine is a TLR7 agonist.

Chikungunya virus infection induces differential inflammatory and antiviral responses in human monocytes and monocyte-derived macrophages.

Presence of Genetic Variants Among Young Men With Severe COVID-19.

Cryo-EM structures of Toll-like receptors in complex with UNC93B1.

TLR7 gain-of-function genetic variation causes human lupus.

Lysosomal endonuclease RNase T2 and PLD exonucleases cooperatively generate RNA ligands for TLR7 activation.

TLR processing at low pH

Full-length TLR3/7/8/9 binds to UNC93B1

TLR folding by chaperones GP96 and CNPY3

UNC93B1 delivers endosomal full-length TLRs to endolysosome

Folded full-length TLR7/8/9 dissociates from the GP96:CNPY3 complex

Endosomal TLRs pass through the Golgi

C-ter TLR7 dimer binds TLR7, TLR8 ligands

C-ter TLR7 dimer binds HCQ

C-ter TLR7 dimer binds imiquimod

MyD88 oligomerization within the complex of activated TLR 7/8 or 9 : MyD88

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

MyD88 interacts with the activated TLR receptor 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

C-ter TLR7 dimer binds SARS-CoV-2 GU-rich ssRNA

G or G analog binds C-ter TLR7 dimer

G or G analog binds C-ter TLR7 GoF variant

RSV ssRNA binds C-ter TLR7 dimer

Falcon deep research report on TLR7