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
NLRX1 is a regulator of mitochondrial antiviral immunity.
Mapping a dynamic innate immunity protein interaction network regulating type I interferon production.
NLRX1 attenuates apoptosis and inflammatory responses in myocardial ischemia by inhibiting MAVS-dependent NLRP3 inflammasome activation.
Inhibition of Avian Influenza A Virus Replication in Human Cells by Host Restriction Factor TUFM Is Correlated with Autophagy.
The mitochondrial proteins NLRX1 and TUFM form a complex that regulates type I interferon and autophagy.
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NLRX1 interacts with the mitochondrial elongation factor TUFM, which recruits the autophagy proteins ATG5-ATG12 (and ATG16L1); the NLRX1-TUFM complex promotes autophagy and dampens type I interferon, linking NLRX1 to autophagy/mitophagy.
NLRX1 is a mitochondrial NOD-like receptor that amplifies NF-kappaB and JNK pathways by inducing reactive oxygen species production.
Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context.
NLRX1 inhibits MAVS-DDX58 interaction
NLRX1 binds CHUK:IKBKB:IKBKG
Falcon deep research report for NLRX1
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LLM-synthesized review of NLRX1 emphasizing an emerging "unifying" mitophagy-receptor model (direct LC3 binding, acetyl-CoA metabolite sensing), multi-compartment mitochondrial localization (matrix, inner membrane, outer membrane), and negative regulation of RIG-I/MAVS, cGAS-STING and NF-kappaB, while explicitly noting context-/cell-type-dependence of the antiviral effects.