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Human MAVS Protein expressed in HEK-293 Cells - ABIN2725562
He, Zhu, Wen, Yuan, Hu, Chen, An, Dong, Lin, Yu, Wu, Yang, Cai, Li, Li: Dengue Virus Subverts Host Innate Immunity by Targeting Adaptor Protein MAVS. in Journal of virology 2016
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 Proteins) mRNA was most abundant in the liver and kidney.
findings reveal a negative feedback loop of RLR (show DHX58 Proteins) signaling generated by Tetherin (show BST2 Proteins)-MARCH8 (show MARCH8 Proteins)-MAVS-NDP52 (show CALCOCO2 Proteins) 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 Proteins) exerts its inhibitory role on virus-induced signaling by disrupting the MAVS-TRAF3 (show TRAF3 Proteins) complex.
this study shows that keratinocytes are an important source of IFN-beta (show IFNB1 Proteins) 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 Proteins) mediated early interferon (show IFNA Proteins)-stimulated gene activation through VP16 to dampen the immediate early (show JUN Proteins) 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 Proteins) production to escape host antiviral innate immune responses by cleaving host adaptor molecules MAVS, TRIF (show TRIM69 Proteins), 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 Proteins)-mediated innate antiviral immune responses.
this study shows that MAVS silencing upregulates IFN-beta (show IFNB1 Proteins) production via upregulation of NF-kappaB (show NFKB1 Proteins) and IRF3 (show IRF3 Proteins) signaling
RIPK3 (show RIPK3 Proteins) regulates type I IFN both transcriptionally, by interacting with MAVS and limiting RIPK1 (show RIPK1 Proteins) interaction with MAVS, and post-transcriptionally.
Data suggest that activation of either RIG-I (show DDX58 Proteins)/MAVS or STING pathways during acute intestinal tissue injury in mice resulted in IFN-I signaling that maintained gut (show GUSB Proteins) epithelial barrier integrity and reduced GVHD severity.
this paper identifies TRIM31 (show TRIM31 Proteins), an E3 ubiquitin ligase (show MUL1 Proteins) of the TRIM (show TRAT1 Proteins) 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 Proteins)(+) 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 Proteins) 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 Proteins) inflammasome nor JNK (show MAPK8 Proteins) and p38 (show CRK Proteins) signal pathway.
MARCH5 (show MARCH5 Proteins) binds MAVS only during viral stimulation when MAVS forms aggregates, and these interactions require the RING domain of MARCH5 (show MARCH5 Proteins) and the CARD domain of MAVS.
An autoinhibitory mechanism modulates MAVS activity in unstimulated cells and, on viral infection, individual regions of MAVS are released following MAVS filament formation to activate antiviral signalling cascades.
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.
virus-induced signaling adapter
, mitochondrial antiviral-signaling protein
, mitochondrial IFN-beta promoter stimulator 1
, IP6 kinase
, VIP1 homolog
, histidine acid phosphatase domain containing 2A
, histidine acid phosphatase domain-containing protein 2A
, inositol hexakisphosphate and diphosphoinositol-pentakisphosphate kinase 1
, inositol pyrophosphate synthase 1
, insP6 and PP-IP5 kinase 1
, CARD adapter inducing interferon beta
, CARD adaptor inducing IFN-beta
, IFN-B promoter stimulator 1
, interferon beta promoter stimulator protein 1
, putative NF-kappa-B-activating protein 031N
, virus-induced signaling adaptor
, virus-induced-signaling adapter
, IFN-beta promoter stimulator-1
, mitochondrial anti-viral signaling protein
, interferon-beta promoter stimulator protein 1