Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation based on Enzyme Commission mapping
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
Automatic transfer of annotations from Rhea to GO
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
mda-5: An interferon-inducible putative RNA helicase with double-stranded RNA-dependent ATPase activity and melanoma growth-suppressive properties.
The V proteins of paramyxoviruses bind the IFN-inducible RNA helicase, mda-5, and inhibit its activation of the IFN-beta promoter.
IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction.
Inhibition of retinoic acid-inducible gene I-mediated induction of beta interferon by the NS1 protein of influenza A virus.
Negative regulation of the RIG-I signaling by the ubiquitin ligase RNF125.
Negative regulation of MDA5- but not RIG-I-mediated innate antiviral signaling by the dihydroxyacetone kinase.
Regulation of signal transduction by enzymatically inactive antiviral RNA helicase proteins MDA5, RIG-I, and LGP2.
Solution structures of cytosolic RNA sensor MDA5 and LGP2 C-terminal domains: identification of the RNA recognition loop in RIG-I-like receptors.
A shared interface mediates paramyxovirus interference with antiviral RNA helicases MDA5 and LGP2.
ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response.
Structural basis of double-stranded RNA recognition by the RIG-I like receptor MDA5.
Activation of MDA5 requires higher-order RNA structures generated during virus infection.
PCBP2 mediates degradation of the adaptor MAVS via the HECT ubiquitin ligase AIP4.
NLRC5 negatively regulates the NF-kappaB and type I interferon signaling pathways.
MDA5 is SUMOylated by PIAS2β in the upregulation of type I interferon signaling.
Ribose 2'-O-methylation provides a molecular signature for the distinction of self and non-self mRNA dependent on the RNA sensor Mda5.
A diverse range of gene products are effectors of the type I interferon antiviral response.
Immune signaling by RIG-I-like receptors.
DDX60, a DEXD/H box helicase, is a novel antiviral factor promoting RIG-I-like receptor-mediated signaling.
Mapping a dynamic innate immunity protein interaction network regulating type I interferon production.
DHX9 pairs with IPS-1 to sense double-stranded RNA in myeloid dendritic cells.
Cooperative assembly and dynamic disassembly of MDA5 filaments for viral dsRNA recognition.
Herpes simplex virus 1 tegument protein US11 downmodulates the RLR signaling pathway via direct interaction with RIG-I and MDA-5.
Ankrd17 positively regulates RIG-I-like receptor (RLR)-mediated immune signaling.
Human respiratory syncytial virus nucleoprotein and inclusion bodies antagonize the innate immune response mediated by MDA5 and MAVS.
Tetraspanin 6 (TSPAN6) negatively regulates retinoic acid-inducible gene I-like receptor-mediated immune signaling in a ubiquitination-dependent manner.
MDA5 assembles into a polar helical filament on dsRNA.
Structural basis for dsRNA recognition, filament formation, and antiviral signal activation by MDA5.
Paramyxovirus V proteins disrupt the fold of the RNA sensor MDA5 to inhibit antiviral signaling.
RIOK3-mediated phosphorylation of MDA5 interferes with its assembly and attenuates the innate immune response.
TRIM65-catalized ubiquitination is essential for MDA5-mediated antiviral innate immunity.
Echovirus 6 Infects Human Exocrine and Endocrine Pancreatic Cells and Induces Pro-Inflammatory Innate Immune Response.
The nucleocapsid proteins of mouse hepatitis virus and severe acute respiratory syndrome coronavirus share the same IFN-β antagonizing mechanism: attenuation of PACT-mediated RIG-I/ MDA5 activation.
The Zinc-Finger Protein ZCCHC3 Binds RNA and Facilitates Viral RNA Sensing and Activation of the RIG-I-like Receptors.
Cryo-EM Structures of MDA5-dsRNA Filaments at Different Stages of ATP Hydrolysis.
Physical and functional interaction between A20 and ATG16L1-WD40 domain in the control of intestinal homeostasis.
NOD1 Promotes Antiviral Signaling by Binding Viral RNA and Regulating the Interaction of MDA5 and MAVS.
A reference map of the human binary protein interactome.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) membrane (M) protein inhibits type I and III interferon production by targeting RIG-I/MDA-5 signaling.
ISG15-dependent activation of the sensor MDA5 is antagonized by the SARS-CoV-2 papain-like protease to evade host innate immunity.
SARS-CoV-2 Membrane Protein Inhibits Type I Interferon Production Through Ubiquitin-Mediated Degradation of TBK1.
MDA5 ISGylation is crucial for immune signaling to control viral replication and pathogenesis.
viral dsRNA:IFIH1, viral dsRNA:K63polyUb-DDX58 bind MAVS
MAVS interacts with RIPK1 and FADD
USP17 deubiquitinates RCE1, CDC25A, DDX58, IFIH1
viral dsRNA binds IFIH1:TKFC
TBK1/IKK epsilon complex interacts with MAVS bound TRAF3
Recruitment of TRAF3 to MAVS
Phosphorylation and release of IRF3/IRF7
Recruitment of TRAF6/TRAF2 to MAVS
Dimerzation of procaspase-8, procaspase-10
Phosphorylation and release of IRF7
Recruitment of caspase-8 and -10 to FADD complex
Recruitment of TBK1/IKK epsilon complex to TANK:TRAF6
Activation of IKK by MEKK1
Recruitment of TANK to TRAF6
Recruitment of IRF7 to TRAF6
Recruitment of IKK complex
OTUD5 deubiquitinates TRAF3
Negative regulation of DDX58/IFIH1 signaling by RNF216
NLRC5 interacts with DDX58/IFIH1
TBK1 or IKBKE forms homodimers
TBK1, IKBKE form homodimers
TBK1, IKBKE are autophosphorylated at Ser172
Phosphorylation of TBK1/IKBKE
IFIH1:TKFC binds SARS-CoV-2 dsRNA intermediates
SARS-CoV-2 nsp3 deISGylates ISGylated IFIH1
Recruitment of ITCH and K48 ubiquitination of MAVS
Interaction of PCBP2 with MAVS
RNF125 mediated ubiquitination of RIG-I, MDA5 and IPS-1
Loss of cellular RNA homeostasis contributes to MDA5 activation during virus infection.
Gain-of-function mutations in IFIH1 cause a spectrum of human disease phenotypes associated with upregulated type I interferon signaling.
RNA editing by ADAR1 prevents MDA5 sensing of endogenous dsRNA as nonself.