NLRX1
NLRX1 (NLR family member X1, also known as NOD9 and CLR11.3) is a member of the NLR family that localises to the outer mitochondrial membrane. It regulates mitochondrial antiviral responses and also influences autophagy, inflammasome activation and reactive oxygen species-dependent signalling. Browse Assay Genie's current range of NLRX1 research reagents below, or read on for the biology behind the target.
NLRX1 participates in antiviral signalling at the mitochondrion. It acts as a negative regulator of MAVS-mediated antiviral responses by inhibiting the virus-induced interaction between RLH (RIG-like helicase) proteins and MAVS. In a separate role, it promotes autophagy by interacting with TUFM and subsequently recruiting the autophagy-related proteins ATG5 and ATG12. It also regulates MAVS-dependent NLRP3 inflammasome activation, which attenuates apoptosis.
NLRX1 has no inhibitory effect on the NF-kappa-B signalling pathway. Instead, it enhances NF-kappa-B and JUN N-terminal kinase dependent signalling through the production of reactive oxygen species. It also regulates virus-mediated inflammation and energy metabolism in a sex-dependent manner. In females, it prevents uncontrolled inflammation and dysregulated energy metabolism, and may therefore contribute to the sex differences seen in infectious and inflammatory diseases.
The NLRX1 gene encodes a protein of the NLR family that sits on the outer mitochondrial membrane, and RefSeq reports three transcript variants that encode the same protein. UniProt places it in the NLRP group, while HGNC lists it in the NLR family under the names NOD9 and CLR11.3. Orthologous genes, both named Nlrx1, are annotated in mouse and rat, which allows its mitochondrial immune functions to be studied in rodent models.
NLRX1 inhibits the virus-induced RLH-MAVS interaction, making it a key regulator for studying how mitochondria control antiviral responses.
NLRX1 interacts with TUFM and recruits ATG5 and ATG12, linking a mitochondrial NLR protein to the promotion of autophagy.
NLRX1 regulates MAVS-dependent NLRP3 inflammasome activation to attenuate apoptosis, a link relevant to inflammatory signalling studies.
NLRX1 regulates viral inflammation and energy metabolism in a sex-dependent manner, which may help explain sex differences in infectious and inflammatory disease.
NLRX1 is a mitochondrial regulator of antiviral signalling. It inhibits the RLH-MAVS interaction, promotes autophagy through TUFM, ATG5 and ATG12, and regulates MAVS-dependent NLRP3 inflammasome activation. It also enhances NF-kappa-B and JUN N-terminal kinase signalling through reactive oxygen species production.
NLRX1 is the NLR family member X1 gene and protein. Its aliases are NOD9 and CLR11.3. RefSeq reports three transcript variants for the NLRX1 gene, and all three encode the same protein, so there are no distinct protein isoforms from these variants.
Mouse and rat both have an ortholog named Nlrx1. The human protein localises to the outer mitochondrial membrane. Its function in females, where it limits uncontrolled inflammation and energy metabolism, may contribute to sex differences in disease; check the datasheet of any product for its validated reactivity.
Other NLR family members, mitochondrial antiviral signalling proteins and autophagy regulators linked to NLRX1 biology.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q86UT6; product specifications from Assay Genie datasheets.