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

Electronic Gene Ontology annotations created by ARBA machine learning models

Combined Automated Annotation using Multiple IEA Methods

Interaction and specificity of Rel-related proteins in regulating Drosophila immunity gene expression.

Relish, a central factor in the control of humoral but not cellular immunity in Drosophila.

Activation of the Drosophila NF-kappaB factor Relish by rapid endoproteolytic cleavage.

The Drosophila caspase Dredd is required to resist gram-negative bacterial infection.

Cactus-independent nuclear translocation of Drosophila RELISH.

The Drosophila homolog of NTF-2, the nuclear transport factor-2, is essential for immune response.

A ubiquitin-proteasome pathway represses the Drosophila immune deficiency signaling cascade.

Sequential activation of signaling pathways during innate immune responses in Drosophila.

Discrete functions of TRAF1 and TRAF2 in Drosophila melanogaster mediated by c-Jun N-terminal kinase and NF-kappaB-dependent signaling pathways.

Inhibitor of apoptosis 2 and TAK1-binding protein are components of the Drosophila Imd pathway.

Cooperative control of Drosophila immune responses by the JNK and NF-kappaB signaling pathways.

An essential complementary role of NF-kappaB pathway to microbicidal oxidants in Drosophila gut immunity.

The Drosophila inhibitor of apoptosis protein DIAP2 functions in innate immunity and is essential to resist gram-negative bacterial infection.

Trade-offs between longevity and pathogen resistance in Drosophila melanogaster are mediated by NFkappaB signaling.

ird1 is a Vps15 homologue important for antibacterial immune responses in Drosophila.

Isolation of regulators of Drosophila immune defense genes by a double interaction screen in yeast.

Iap2 is required for a sustained response in the Drosophila Imd pathway.

Functional conservation of Rel binding sites in drosophilid genomes.

NF-kappaB/Rel-mediated regulation of the neural fate in Drosophila.

Akirins are highly conserved nuclear proteins required for NF-kappaB-dependent gene expression in drosophila and mice.

Genetic analysis of Drosophila melanogaster susceptibility to intestinal Vibrio cholerae infection.

The N-terminal half of the Drosophila Rel/NF-kappaB factor Relish, REL-68, constitutively activates transcription of specific Relish target genes.

Short-term starvation of immune deficient Drosophila improves survival to gram-negative bacterial infections.

Infection induces a survival program and local remodeling in the airway epithelium of the fly.

Two roles for the Drosophila IKK complex in the activation of Relish and the induction of antimicrobial peptide genes.

A novel system for the launch of alphavirus RNA synthesis reveals a role for the Imd pathway in arthropod antiviral response.

The Imd pathway is involved in antiviral immune responses in Drosophila.

Heterodimers of NF-kappaB transcription factors DIF and Relish regulate antimicrobial peptide genes in Drosophila.

Dynamic coordination of innate immune signaling and insulin signaling regulates systemic responses to localized DNA damage.

Ubiquitylation of the initiator caspase DREDD is required for innate immune signalling.

Dnr1 mutations cause neurodegeneration in Drosophila by activating the innate immune response in the brain.

Mutations in the IMD pathway and mustard counter Vibrio cholerae suppression of intestinal stem cell division in Drosophila.

Functional genomic analyses of two morphologically distinct classes of Drosophila sensory neurons: post-mitotic roles of transcription factors in dendritic patterning.

The Oct1 homolog Nubbin is a repressor of NF-κB-dependent immune gene expression that increases the tolerance to gut microbiota.

Akirin specifies NF-κB selectivity of Drosophila innate immune response via chromatin remodeling.

Lysosomal Degradation Is Required for Sustained Phagocytosis of Bacteria by Macrophages.

Inflammation-Induced, STING-Dependent Autophagy Restricts Zika Virus Infection in the Drosophila Brain.

The Kinase IKKβ Regulates a STING- and NF-κB-Dependent Antiviral Response Pathway in Drosophila.

A Comprehensive Drosophila melanogaster Transcription Factor Interactome.

2'3'-cGAMP triggers a STING- and NF-κB-dependent broad antiviral response in Drosophila.

Constitutive immune activity promotes JNK- and FoxO-dependent remodeling of Drosophila airways.

cGAS-like receptors sense RNA and control 3'2'-cGAMP signalling in Drosophila.

Protein Phosphatase 4 Negatively Regulates the Immune Deficiency-NF-κB Pathway during the Drosophila Immune Response.

Orally acquired cyclic dinucleotides drive dSTING-dependent antiviral immunity in enterocytes.

Drosophila Relish Activating lncRNA-CR33942 Transcription Facilitates Antimicrobial Peptide Expression in Imd Innate Immune Response.

A dRASSF-STRIPAK-Imd-JAK/STAT axis controls antiviral immune response in Drosophila.

Drosophila Relish-mediated miR-317 expression facilitates immune homeostasis restoration via inhibiting PGRP-LC.

The NF-κB/Relish Activates miR-308 to Negatively Regulate Imd Pathway Immune Signaling in Drosophila.

The Relish/miR-275/Dredd mediated negative feedback loop is crucial to restoring immune homeostasis of Drosophila Imd pathway.

Relish-facilitated lncRNA-CR11538 suppresses Drosophila Imd immune response and maintains immune homeostasis via decoying Relish away from antimicrobial peptide promoters.

Relish-mediated C2H2 zinc finger protein IMZF restores Drosophila immune homeostasis via inhibiting the transcription of Imd/Tak1.

A cryptic homotypic interaction motif of insect STING is required for its antiviral signaling.

Origins of immunity: Relish, a compound Rel-like gene in the antibacterial defense of Drosophila.

Regulated nuclear import of Rel proteins in the Drosophila immune response.

Phosphorylated REL is cleaved by and dissociates from DREDD in the PGN:PGRP-LC oligomer receptor 'signalling complex'

Activated Phospho IRD5:KEY dimer phosphorylates REL in the PGN:PGRP-LC oligomer receptor 'signalling complex'

REL binds to DREDD in the PGN:PGRP-LC oligomer receptor 'signalling complex'

Phosphorylated REL-68 forms a complex with PCAF at its target gene and activates transcription

Phosphorylated REL-68 transports from the cytosol to the nucleus

Phosphorylated REL is cleaved by and dissociates from DREDD in the monomeric PGN:PGRP-LE oligomer receptor 'signalling complex'

Activated Phospho IRD5:KEY dimer phosphorylates REL in the monomeric PGN:PGRP-LE oligomer receptor 'signalling complex'

REL binds to monomeric PGN:PGRP-LE oligomer receptor 'signalling complex'

AP-1 transcription factor forms a complex with STAT92E and DSP1 which displaces REL-68 from its target gene

Falcon deep research report on Rel