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NLRX1 Polyclonal Antibody
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- BACKGROUND
Application 
| WB, IHC-P |
|---|---|
| Primary Accession | Q86UT6 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 107616 Da |
| Gene ID | 79671 |
|---|---|
| Other Names | NLR family member X1 (Caterpiller protein 11.3) (CLR11.3) (Nucleotide-binding oligomerization domain protein 26) (Nucleotide-binding oligomerization domain protein 5) (Nucleotide-binding oligomerization domain protein 9) |
| Dilution | WB~~WB 1:500-2000, IHC-p 1:50-300, ELISA 1:10000-20000 |
| Format | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% (W/V) sodium azide. |
| Storage Conditions | -20℃ |
| Name | NLRX1 |
|---|---|
| Function | Participates in antiviral signaling. Acts as a negative regulator of MAVS-mediated antiviral responses, through the inhibition of the virus-induced RLH (RIG-like helicase)-MAVS interaction (PubMed:18200010). Instead, promotes autophagy by interacting with TUFM and subsequently recruiting the autophagy-related proteins ATG5 and ATG12 (PubMed:22749352). Regulates also MAVS-dependent NLRP3 inflammasome activation to attenuate apoptosis (PubMed:27393910). Has no inhibitory function on NF-kappa-B signaling pathway, but enhances NF-kappa-B and JUN N-terminal kinase dependent signaling through the production of reactive oxygen species (PubMed:18219313). Regulates viral mediated-inflammation and energy metabolism in a sex-dependent manner (By similarity). In females, prevents uncontrolled inflammation and energy metabolism and thus, may contribute to the sex differences observed in infectious and inflammatory diseases (By similarity). |
| Cellular Location | Mitochondrion outer membrane |
| Tissue Location | Ubiquitously expressed. Strongest expression in mammary gland, heart and muscle. Detected in HeLa, HEK293T, THP-1, HL- 60, Raji and Jurkat cell lines (at protein level) |
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Provided below are standard protocols that you may find useful for product applications.
Background
Participates in antiviral signaling. Acts as a negative regulator of MAVS-mediated antiviral responses, through the inhibition of the virus-induced RLH (RIG-like helicase)-MAVS interaction (PubMed:18200010). Instead, promotes autophagy by interacting with TUFM and subsequently recruiting the autophagy- related proteins ATG5 and ATG12 (PubMed:22749352). Regulates also MAVS-dependent NLRP3 inflammasome activation to attenuate apoptosis (PubMed:27393910). Has no inhibitory function on NF- kappa-B signaling pathway, but enhances NF-kappa-B and JUN N- terminal kinase dependent signaling through the production of reactive oxygen species (PubMed:18219313).
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