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findings suggest that oxidative stress-induced (show SQSTM1 ELISA Kits) MAVS oligomerization in SLE patients may contribute to the type I IFN signature that is characteristic of this syndrome.
findings reveal a negative feedback loop of RLR (show DHX58 ELISA Kits) signaling generated by Tetherin (show BST2 ELISA Kits)-MARCH8 (show MARCH8 ELISA Kits)-MAVS-NDP52 (show CALCOCO2 ELISA Kits) axis and provide insights into a better understanding of the crosstalk between selective autophagy and optimal deactivation of type I IFN signaling.
Studied association of genetic variants of the MAVS, MITA and MFN2 genes with leprosy in Han Chinese from Southwest China; found no association between the variants and susceptibility to leprosy.
Mechanistic studies showed that HACE1 (show HACE1 ELISA Kits) exerts its inhibitory role on virus-induced signaling by disrupting the MAVS-TRAF3 (show TRAF3 ELISA Kits) complex.
this study shows that keratinocytes are an important source of IFN-beta (show IFNB1 ELISA Kits) and MAVS is critical to this function, and demonstrates how the epidermis triggers unwanted skin inflammation under disease conditions
Herpes simplex virus 1 blocks MAVS-Pex (show PHEX ELISA Kits) mediated early interferon (show IFNA ELISA Kits)-stimulated gene activation through VP16 to dampen the immediate early (show JUN ELISA Kits) antiviral innate immunity signaling from peroxisomes.
This study demonstrates a novel pathway for elevated IFNbeta signaling in SLE that is not dependent on stimulation by immune complexes but rather is cell intrinsic and critically mediated by IFNbeta and MAVS.
TTLL12 as a negative regulator of RNA-virus-induced type I IFN expression by inhibiting the interaction of VISA with other proteins.
Therefore, Seneca Valley virus suppressed antiviral interferon (show IFNA ELISA Kits) production to escape host antiviral innate immune responses by cleaving host adaptor molecules MAVS, TRIF (show TRIM69 ELISA Kits), and TANK by its 3C protease.
GPATCH3 interacts with VISA and disrupts the assembly of virus-induced VISA signalosome therefore acts as a negative regulator of RLR (show DHX58 ELISA Kits)-mediated innate antiviral immune responses.
RIPK3 (show RIPK3 ELISA Kits) regulates type I IFN both transcriptionally, by interacting with MAVS and limiting RIPK1 (show RIPK1 ELISA Kits) interaction with MAVS, and post-transcriptionally.
Data suggest that activation of either RIG-I (show DDX58 ELISA Kits)/MAVS or STING pathways during acute intestinal tissue injury in mice resulted in IFN-I signaling that maintained gut (show GUSB ELISA Kits) epithelial barrier integrity and reduced GVHD severity.
this paper identifies TRIM31 (show TRIM31 ELISA Kits), an E3 ubiquitin ligase of the TRIM (show TRAT1 ELISA Kits) family of proteins, as a regulator of MAVS aggregation
Taken together, these results suggest that MAVS is essential for boosting optimal primary CD4 (show CD4 ELISA Kits)(+) T cell responses upon NS4B-P38G West Nile virus vaccination and yet is dispensable for host protection and recall T cell responses during secondary wild-type West Nile virus infection.
this study demonstrates that the capacity of hepatitis A virus to evade MAVS-mediated type I interferon (show IFNA ELISA Kits) responses defines its host species range.
Hepatitis C virus NS3-4A inhibits the peroxisomal MAVS-dependent antiviral signaling response.
Rotavirus infection in macrophages depend on MAVS but not involve the NLRP3 (show NLRP3 ELISA Kits) inflammasome nor JNK (show MAPK8 ELISA Kits) and p38 (show CRK ELISA Kits) signal pathway.
MARCH5 (show MARCH5 ELISA Kits) binds MAVS only during viral stimulation when MAVS forms aggregates, and these interactions require the RING domain of MARCH5 (show MARCH5 ELISA Kits) and the CARD domain of MAVS.
The authors determined that porcine reproductive and respiratory syndrome virus 3C protease cleaved MAVS at Glu268.
Real-time quantitative PCR analysis indicated that Tibetan porcine IPS-1 (show ISYNA1 ELISA Kits) mRNA was most abundant in the liver and kidney.
Functions of the two zebrafish MAVS variants are opposite in the induction of IFN1 by targeting IRF7 (show IRF7 ELISA Kits)
Data show that mitochondrial antiviral signaling protein (MAVS) splicing variant 1 (MAVS_tv1) cooperated with DEAD (Asp-Glu-Ala-Asp) box polypeptide 58 RIG-I (show DDX58 ELISA Kits) in the accumulation of RIG-I (show DDX58 ELISA Kits) transcript in a positive feedback loop.
This gene encodes an intermediary protein necessary in the virus-triggered beta interferon signaling pathways. It is required for activation of transcription factors which regulate expression of beta interferon and contributes to antiviral immunity. Multiple transcript variants encoding different isoforms have been found for this gene.
CARD adapter inducing interferon beta
, CARD adaptor inducing IFN-beta
, IFN-B promoter stimulator 1
, interferon beta promoter stimulator protein 1
, mitochondrial antiviral-signaling protein
, putative NF-kappa-B-activating protein 031N
, virus-induced signaling adaptor
, virus-induced-signaling adapter
, virus-induced signaling adapter
, IFN-beta promoter stimulator-1
, mitochondrial anti-viral signaling protein
, mitochondrial IFN-beta promoter stimulator 1
, interferon-beta promoter stimulator protein 1