+ |
TLRs | up-regulates
|
Immune_response |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-216304 |
|
|
Homo sapiens |
|
pmid |
sentence |
20404851 |
The negative regulation of TLR-induced responses is important for sup- pressing inflammation and deleterious immune responses. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network, Innate Immune Response, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, Toll like receptors |
+ |
TLRs | up-regulates
|
Interferon_Production |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-216310 |
|
|
Homo sapiens |
|
pmid |
sentence |
20404851 |
TLR signaling pathways can be largely classified as either MyD88-dependent pathways, which drive the induction of inflammatory cytokines, or TRIF-dependent pathways, which are responsible for the induction of type I interferon as well as inflammatory cytokines3. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Toll like receptors |
+ |
TLRs | up-regulates activity
binding
|
TICAM1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252095 |
|
|
Mus musculus |
|
pmid |
sentence |
22664090 |
To initiate the innate immune response, Toll-like receptors (TLRs) associate with cytoplasmic adaptor proteins through TIR (Toll/interleukin-1 receptor) domain interactions. The four principal signaling adaptor proteins include MyD88, MAL, TRIF and TRAM, and the fifth protein SARM, involved in negative regulation of TLR pathways, is usually considered a part of the TIR domain-containing adaptor protein group |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | COVID-19 Causal Network, Innate Immune Response, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, Toll like receptors |
+ |
TLRs | up-regulates activity
binding
|
TIRAP |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-216298 |
|
|
Homo sapiens |
|
pmid |
sentence |
20404851 |
These differences are explained by the discovery of TIR domaincontaining adaptor molecules, including MyD88, TIRAP (Mal), TRIF and TRAM, which are recruited by distinct TLRs and activate distinct signaling pathways |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Innate Immune Response, Toll like receptors |
+ |
TLRs | up-regulates quantity by expression
|
NLRP3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256428 |
|
|
|
|
pmid |
sentence |
28531279 |
The activation of NLRP3 inflammasomes in macrophages requires two stimuli. The first signal, called priming, is provided by an inflammatory stimulus such as TLRs and TNF-α receptor (TNFR) that leads to NF-κB-mediated NLRP3 expression and post-translational modifications of NLRP3 |
|
Publications: |
1 |
+ |
TLRs | up-regulates activity
binding
|
MYD88 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260151 |
|
|
Mus musculus |
|
pmid |
sentence |
22664090 |
To initiate the innate immune response, Toll-like receptors (TLRs) associate with cytoplasmic adaptor proteins through TIR (Toll/interleukin-1 receptor) domain interactions. The four principal signaling adaptor proteins include MyD88, MAL, TRIF and TRAM, and the fifth protein SARM, involved in negative regulation of TLR pathways, is usually considered a part of the TIR domain-containing adaptor protein group |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | COVID-19 Causal Network, Innate Immune Response, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, Toll like receptors |
+ |
DAMPS | up-regulates activity
binding
|
TLRs |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252096 |
|
|
Homo sapiens |
|
pmid |
sentence |
25644504 |
The innate immune system is present in almost all multicellular organisms and its activation occurs in response to pathogens or tissue injury via pattern-recognition receptors (PRRs) that recognize pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Innate Immune Response, Inflammosome Activation, Toll like receptors |
+ |
TLRs | up-regulates activity
binding
|
TICAM2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-216307 |
|
|
Homo sapiens |
|
pmid |
sentence |
20404851 |
These differences are explained by the discovery of TIR domaincontaining adaptor molecules, including MyD88, TIRAP (Mal), TRIF and TRAM, which are recruited by distinct TLRs and activate distinct signaling pathways |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Toll like receptors |
+ |
TLRs | up-regulates activity
binding
|
TLRs |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-216301 |
|
|
Homo sapiens |
|
pmid |
sentence |
24352680 |
Upon activation, tlrs hetero- or homodimerize inducing the recruitment of adaptor proteins via the cytoplasmic tir domain |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network, Innate Immune Response, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, Toll like receptors |
+ |
PAMPs | up-regulates
|
TLRs |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-216295 |
|
|
Homo sapiens |
|
pmid |
sentence |
20404851 |
the discovery of Toll-like receptors (TLRs) in the mid-1990s showed that pathogen recognition by the innate immune system is instead actually specific, relying on germline-encoded pattern-recognition receptors (PRRs) that have evolved to detect components of foreign pathogens referred to as pathogen-associated molecular patterns (PAMPs) |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network, Innate Immune Response, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, Toll like receptors |