| + |
TRIM25 | down-regulates quantity by destabilization 
polyubiquitination
|
MAVS |
0.763 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272042 |
Lys10 |
FAEDKTYkYICRNFS |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 22626058 |
We report here that RLR activation triggers MAVS ubiquitination on lysine 7 and 10 by the E3 ubiquitin ligase TRIM25 and marks it for proteasomal degradation concomitantly with downstream signaling. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272041 |
Lys7 |
kTYKYICR |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 22626058 |
We report here that RLR activation triggers MAVS ubiquitination on lysine 7 and 10 by the E3 ubiquitin ligase TRIM25 and marks it for proteasomal degradation concomitantly with downstream signaling. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
RNF5 | down-regulates quantity by destabilization
ubiquitination
|
MAVS |
0.471 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271488 |
Lys362 |
RAGMVPSkVPTSMVL |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 20483786 |
In this study, we showed that the E3 ubiquitin ligase RING-finger protein 5 (RNF5) interacted with VISA at mitochondria in a viral infection-dependent manner. Domain mapping experiments indicated that the C-terminal transmembrane domain of VISA was required for its interaction with RNF5. RNF5 targeted VISA at K362 and K461 for K48-linked ubiquitination and degradation after viral infection, whereas knockdown of RNF5 reversed virus-induced downregulation of VISA at the early phase. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271489 |
Lys461 |
GPEENEYkSEGTFGI |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 20483786 |
In this study, we showed that the E3 ubiquitin ligase RING-finger protein 5 (RNF5) interacted with VISA at mitochondria in a viral infection-dependent manner. Domain mapping experiments indicated that the C-terminal transmembrane domain of VISA was required for its interaction with RNF5. RNF5 targeted VISA at K362 and K461 for K48-linked ubiquitination and degradation after viral infection, whereas knockdown of RNF5 reversed virus-induced downregulation of VISA at the early phase. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
ITCH | down-regulates quantity by destabilization
ubiquitination
|
MAVS |
0.627 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260362 |
Lys371 |
PTSMVLTkVSASTVP |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 19881509 |
These data collectively indicate that AIP4 is the E3 ligase for MAVS.|We generated single substitutions (K362A, K371A or K420A) and combined point substitutions of MAVS and tested their degradation. K371A or K420A MAVS showed partial resistance to PCBP2-induced degradation (data not shown), whereas MAVS with the combined substitutions K371A and K420A (KK-AA) completely withstood the degradation |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260363 |
Lys420 |
GLGSELSkPGVLASQ |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 19881509 |
These data collectively indicate that AIP4 is the E3 ligase for MAVS.|We generated single substitutions (K362A, K371A or K420A) and combined point substitutions of MAVS and tested their degradation. K371A or K420A MAVS showed partial resistance to PCBP2-induced degradation (data not shown), whereas MAVS with the combined substitutions K371A and K420A (KK-AA) completely withstood the degradation |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
MAVS | up-regulates activity 
binding
|
IRF3 |
0.794 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260143 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25636800 |
Phosphorylated MAVS and STING then bind to a positively charged surface of interferon regulatory factor 3 (IRF3) and thereby recruit IRF3 for its phosphorylation and activation by TBK1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Innate Immune Response, SARS-CoV INNATE RESPONSE TO dsRNA, SARS-CoV STRESS GRANULES |
| + |
NLRX1 | down-regulates activity
binding
|
MAVS |
0.745 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260357 |
|
|
Homo sapiens |
HeLa Cell, HEK-293T Cell |
| pmid |
sentence |
| 18200010 |
Here we describe human NLRX1, a highly conserved nucleotide-binding domain (NBD)- and leucine-rich-repeat (LRR)-containing family member (known as NLR) that localizes to the mitochondrial outer membrane and interacts with MAVS. Expression of NLRX1 results in the potent inhibition of RLH- and MAVS-mediated interferon-beta promoter activity and in the disruption of virus-induced RLH-MAVS interactions. Co-immunoprecipitation studies demonstrate that HA–NLRX1 interacts with MAVS but not with other known mitochondrial outer membrane proteins (BCL2 and BCL2L1), indicating specificity of the NLRX1–MAVS interaction. Finally, endogenous NLRX1 associates strongly with endogenous MAVS after immunoprecipitation with two different MAVS antibodies |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PCBP2 | down-regulates quantity by destabilization
binding
|
MAVS |
0.63 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260360 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 19881509 |
PCBP2 mediates degradation of the adaptor MAVS via the HECT ubiquitin ligase AIP4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAVS | up-regulates quantity by expression 
transcriptional regulation
|
IFNB1 |
0.512 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260372 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22588174 |
ECSIT enhances IPS-1-mediated IFN-Beta promoter activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ECSIT | up-regulates activity
binding
|
MAVS |
0.442 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260371 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22588174 |
ECSIT interacts with IPS-1|ECSIT enhances IPS-1-mediated IFN-Beta promoter activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFIH1 | up-regulates activity
binding
|
MAVS |
0.809 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260140 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19052324 |
Initially, RIG-I and MDA5 sense dsRNA in the cytoplasm, produced as a by-product of RNA virus replication.Once one or both of these sensors are activated, they interact with a mitochondrial membrane protein called MAVS (mitochondrial antiviral) (also called IPS1, Cardif, and VISA). They signal to the mitochondrial membrane protein MAVS, which in turn activates the kinases TBK1 and IKKɛ. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Innate Immune Response, SARS-CoV INNATE RESPONSE TO dsRNA |
| + |
M | down-regulates activity
binding
|
MAVS |
0.1 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262515 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 33110251 |
Here, we identified SARS-CoV-2 membrane glycoprotein M as a negative regulator of the innate immune response. We found that the M protein interacted with the central adaptor protein MAVS in the innate immune response pathways. This interaction impaired MAVS aggregation and its recruitment of downstream TRAF3, TBK1, and IRF3, leading to attenuation of the innate antiviral response. Our findings reveal a mechanism by which SARS-CoV-2 evades the innate immune response and suggest that the M protein of SARS-CoV-2 is a potential target for the development of SARS-CoV-2 interventions. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV INNATE RESPONSE TO dsRNA, SARS-CoV STRESS GRANULES |
| + |
9b | down-regulates quantity by destabilization 
|
MAVS |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260241 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25135833 |
SARS-coronavirus Open Reading frame-9b Suppresses Innate Immunity by Targeting Mitochondria and the MAVS/TRAF3/TRAF6 Signalosome. Acting on mitochondria, ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and the HECT domain E3 ligase AIP4 to trigger the degradation of MAVS, TRAF3, and TRAF 6. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV INNATE RESPONSE TO dsRNA, SARS-CoV STRESS GRANULES |
| + |
MAVS | up-regulates activity
binding
|
STING1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260152 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24622840 |
MAVS also interacts with STING that locates at the ER (endoplasmic reticulum), and induces the ubiquitination and dimerization of STING. The activated STING recruits TBK1 and IRF3 and contributes to the phosphorylation of IRF3 mediated by TBK1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Innate Immune Response, SARS-CoV INNATE RESPONSE TO dsRNA |
| + |
MAVS | up-regulates
relocalization
|
CASP8 |
0.57 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-143572 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16406812 |
Another protein suggested to play a role in caspase-8 translocation to mitochondria is the mitochondrial membrane protein cardif |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
MAVS | up-regulates activity
binding
|
TBK1 |
0.91 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260145 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25636800 |
After ligand binding, cGAS and RIG-I signal through respective adaptor proteins STING and MAVS to recruit the kinases IKK and TBK1, which then activate the transcription factors NF-κB and interferon regulatory factor 3 (IRF3), respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Innate Immune Response, SARS-CoV INNATE RESPONSE TO dsRNA |
| + |
DDX58 | up-regulates activity
binding
|
MAVS |
0.935 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260139 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19052324 |
Initially, RIG-I and MDA5 sense dsRNA in the cytoplasm, produced as a by-product of RNA virus replication.Once one or both of these sensors are activated, they interact with a mitochondrial membrane protein called MAVS (mitochondrial antiviral) (also called IPS1, Cardif, and VISA). They signal to the mitochondrial membrane protein MAVS, which in turn activates the kinases TBK1 and IKKɛ. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Innate Immune Response, SARS-CoV INNATE RESPONSE TO dsRNA, SARS-CoV STRESS GRANULES |
| + |
MAVS | up-regulates activity
binding
|
IKBKE |
0.823 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260144 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25636800 |
After ligand binding, cGAS and RIG-I signal through respective adaptor proteins STING and MAVS to recruit the kinases IKK and TBK1, which then activate the transcription factors NF-κB and interferon regulatory factor 3 (IRF3), respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Innate Immune Response, SARS-CoV INNATE RESPONSE TO dsRNA |
3.0
MAVS
- 
- 