Version 5.4
| Homo sapiens Gene: TLR10 | |||||||||||||||||||||
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| Summary | |||||||||||||||||||||
| InnateDB Gene | IDBG-13548.6 | ||||||||||||||||||||
| Last Modified | 2014-10-13 [Report errors or provide feedback] | ||||||||||||||||||||
| Gene Symbol | TLR10 | ||||||||||||||||||||
| Gene Name | toll-like receptor 10 | ||||||||||||||||||||
| Synonyms | |||||||||||||||||||||
| Species | Homo sapiens | ||||||||||||||||||||
| Ensembl Gene | ENSG00000174123 | ||||||||||||||||||||
| Encoded Proteins |
toll-like receptor 10
toll-like receptor 10
toll-like receptor 10
toll-like receptor 10
toll-like receptor 10
toll-like receptor 10
toll-like receptor 10
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| Protein Structure | |||||||||||||||||||||
| Useful resources | Stemformatics EHFPI ImmGen | ||||||||||||||||||||
| InnateDB Annotation | |||||||||||||||||||||
| Summary |
Human TLR10 is an orphan member of the TLR family with no identified specific ligand
NLRP3 has an important role in IL-1 beta and IL-18 secretion through the inflammasome and mediates responses to LPS, peptidoglycan, bacterial RNA and imidazoquinolines.
Able to homodimerize, heterodimerize with TLR1 and TLR2, and directly associate with MYD88
mmu-mir-155 suppresses Socs1 protein expression and has a pro-inflammatory role in microglia.
NLRP3 complexes with PYCARD (ASC), RIPK2, and CASP1 inflammasome to process IL-1 beta.
Hsa-mir-155 is induced by bacterial and viral infections as well as pro-inflammatory cytokines and functions to suppress FADD, RIPK1 and IKKE expression.
NLRP3 is a critical NOD-like receptor family member that transduces a fungal recognition signal to the inflammasome adaptor PYCARD for CASP1 activation and pro-IL-1beta processing.
Mmu-mir-155 has a pro-inflammatory role in astrocytes and its expression is negatively regulated by Irf3. (Demonstrated in human)
NLRP3-dependent CASP1 activation complex (inflammasome) is triggered when dying tumor cells release ATP, acting on P2X7 purinergic receptors from dendritic cells and allowing for the secretion of IL-1beta.
Hsa-mir-155 induction in response to either poly(I : C) or TNF-alpha is blocked by pharmacological inhibition of JNK, suggesting that its inducing signals use the JNK pathway.
NALP3 inflammasome is activated when CyaA, a virulence factor from B. pertussis, promotes IL-1beta production, which then polarizes T cell responses toward the Th17 subtype and promotes clearance of the bacteria from the respiratory tract.
Mir155 antagonizes progesterone to reverse the inhibition of Tlr3/4 signalling.
NLRP3 is directly activated by certain antibiotics and plays an important role in the antibiotic-mediated secretion of IL1B. In the case of polymyxin B, NLRP3 was also required for the neutrophil influx into the peritoneal cavity. (Demonstrated in murine models)
Hsa-mir-155 expression in monocyte and macrophage cell lines is simulated by viral or bacterial infection in vitro.
NLRP3 inflammasome is essential for host defence against influenza and other RNA viruses (i.e. EMCV, VSV).
Mir155 targets Pmaip1 (Noxa) and Socs1 to mediate natural killer cell expansion during MCMV infection.
NLRP3 recruits adaptor protein PYCARD and CASP1 to form an NLRP3 inflammasome complex in response to Varicella-Zoster Virus (VZV) infection.
hsa-mir-155 feedback positively regulates host antiviral innate immune response by promoting type I IFN signaling via targeting suppressor of cytokine signaling 1 (SOCS1).
NLRP3 is a component of the inflammasome and is required for inflammation in acute pancreatitis. (Demonstrated in murine model)
Mycobacterial infection induces expression of Mir155, which promotes the maturation of phagosomes and represses the expression of Rheb by targeting its 3â??UTR.
NLRP3 is necessary to illicit IL1B response specific to viable, but not heat-killed, E. coli infections. (Demonstrated in murine model)
hsa-mir-155 target IL13RA1 and reduces the IL13RA1 protein expression, and inhibits the expression of M2/pro-Th2 profile genes in macrophages.
The NLRP3 inflammasome plays a role in innate immune responses against mucosal Candida infection. NLRP3 limits the severity of infection when present in either the hematopoietic or stromal compartments. (Demonstrated in mouse)
T-cell-intrinsic Mir155 is required for type-2 immunity, in part through regulation of S1pr1, whereas T-cell-intrinsic Mir146 is required to prevent overt Th1/Th17 skewing.
NLRP3/PYCARD inflammasome activation following human respiratory syncytial virus infection is dependent on the activation of TLR2/MYD88/NF-kB and reactive oxygen species/potassium efflux.
MIR155 upregulation is a feature of the mammalian inflammatory response and MIR155 expression may exert both positive and negative regulatory effects on TLR and NFkB signalling. MIR155 expression is suppressed by IL10 as a part of negative-feedback loop in LPS-stimulated cells.
MIR223 and EBV miR-BART15 regulate the NLRP3 inflammasome and IL-1beta production.
hsa-mir-155 overexpression can enhance innate antiviral immunity by promoting the JAK/STAT signalling pathway to facilitate the clearance of hepatitis B virus in human hepatoma cells.
Uromodulin nanoparticles activate the NLRP3 inflammasome in renal interstitial monocytes.
hsa-mir-155 suppresses SOCS1 protein expression and has a pro-inflammatory role in microglia. (Demonstrated in mice)
Protein-bound polysaccharide-K can activate the NLRP3 inflammasome and induce IL1B in a TLR2- and NLRP3-dependent manner .
MIR155 has a pro-inflammatory role in human astrocytes and its expression is negatively regulated by IRF3.
Endoplasmic reticulum (ER) stress-mediated reactive oxygen species accumulation leads to activation of NLRP3 inflammasome through enhanced secretion of IL1B and binding of TXNIP.
MIR155 antagonizes progesterone to reverse the inhibition of TLR3/4 signalling. (Demonstrated in mice)
Macrophages sense multiple types of bacterially derived RNA (mRNA, tRNA and rRNA) via the NLRP3 inflammasome.
MIR155 exerts anti-HIV-1 effects by targeting several HIV-1 dependency factors involved in post-entry, pre-integration events.
NLRP3 mediates NF-kB activation in both sterile and microbially induced inflammation.
MIR155 is targeted by Borna disease virus (BDV) encoded protein to inhibit type I IFN induction.
Circulating MIR155 activates natural killer cells via the TLR1 signalling pathway.
Hepatitis C virus (HCV)-induced, MIR155-regulated HAVCR2 expression regulates natural killer cell function, suggesting a novel mechanism for balancing immune clearance and immune injury during chronic viral infection.
Mir155 is a post-transcriptional repressor of Arntl (Bmal1), linking the molecular clock and innate immune response.
Mir155 is a post-transcriptional repressor of Arntl (Bmal1), linking the molecular clock and innate immune response.
Influenza A virus non-structural protein 1, NS1, physically interacts with endogenous NLRP3 downregulating NLRP3 inflammasome activation as well as NF-κB, leading to a reduction in the levels of inflammatory cytokines.
TLR10 is a functional receptor involved in the innate immune response to H. pylori infection and the TLR2/TLR10 heterodimer functions in H. pylori lipopolysaccharide recognition.
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| Entrez Gene | |||||||||||||||||||||
| Summary |
The protein encoded by this gene is a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize pathogen-associated molecular patterns (PAMPs) that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity. The various TLRs exhibit different patterns of expression. This gene is most highly expressed in lymphoid tissues such as spleen, lymph node, thymus, and tonsil. Multiple alternatively spliced transcript variants which encode different protein isoforms have been found for this gene. [provided by RefSeq, Aug 2010] |
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| Gene Information | |||||||||||||||||||||
| Type | Protein coding | ||||||||||||||||||||
| Genomic Location | Chromosome 4:38772239-38782990 | ||||||||||||||||||||
| Strand | Reverse strand | ||||||||||||||||||||
| Band | p14 | ||||||||||||||||||||
| Transcripts | |||||||||||||||||||||
| Interactions | |||||||||||||||||||||
| Number of Interactions |
This gene and/or its encoded proteins are associated with 13 experimentally validated interaction(s) in this database.
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| Gene Ontology | |||||||||||||||||||||
Molecular Function |
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| Biological Process |
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| Cellular Component |
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| Orthologs | |||||||||||||||||||||
| No orthologs found for this gene | |||||||||||||||||||||
| Pathways | |||||||||||||||||||||
| NETPATH | |||||||||||||||||||||
| REACTOME |
MyD88 cascade initiated on plasma membrane pathway
Toll Like Receptor 10 (TLR10) Cascade pathway
Toll Like Receptor 5 (TLR5) Cascade pathway
Innate Immune System pathway
Toll-Like Receptors Cascades pathway
Immune System pathway
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| KEGG | |||||||||||||||||||||
| INOH | |||||||||||||||||||||
| PID NCI | |||||||||||||||||||||
| Cross-References | |||||||||||||||||||||
| SwissProt | |||||||||||||||||||||
| TrEMBL | |||||||||||||||||||||
| UniProt Splice Variant | |||||||||||||||||||||
| Entrez Gene | |||||||||||||||||||||
| UniGene | Hs.120551 Hs.730896 | ||||||||||||||||||||
| RefSeq | NM_001017388 NM_001195106 NM_001195107 NM_001195108 NM_030956 | ||||||||||||||||||||
| HUGO | |||||||||||||||||||||
| OMIM | |||||||||||||||||||||
| CCDS | CCDS3445 | ||||||||||||||||||||
| HPRD | 05884 | ||||||||||||||||||||
| IMGT | |||||||||||||||||||||
| EMBL | |||||||||||||||||||||
| GenPept | |||||||||||||||||||||
| RNA Seq Atlas | |||||||||||||||||||||