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Meanwhile, activation of RIPK1 causes the polyubiquitination and activation of TAK1 and NFκB transcription in the same manner as the MyD88-dependent pathway. [ 50 ] TLR signaling ultimately leads to the induction or suppression of genes that orchestrate the inflammatory response.
The first function described for TLR4 was the recognition of exogenous molecules from pathogens (PAMPs), in particular LPS molecules from gram-negative bacteria. [13] As pattern recognition receptor, TLR4 plays a fundamental role in pathogen recognition and activation of innate immunity which is the first line of defense against invading micro-organisms.
The transcription factor NF-kappa B at the end of the pathway transcribes pro-inflammatory cytokines (such as IL-12) and chemokines. Activation of the Toll pathway also results in the expression of co-stimulatory molecules on dendritic cells, which then go on to activate naïve CD4 cells in the lymph nodes. [11] Toxoplasma gondii
54106 81897 Ensembl ENSG00000239732 ENSMUSG00000045322 UniProt Q9NR96 Q9EQU3 RefSeq (mRNA) NM_138688 NM_017442 NM_031178 RefSeq (protein) NP_059138 NP_112455 Location (UCSC) Chr 3: 52.22 – 52.23 Mb Chr 9: 106.1 – 106.1 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Toll-like receptor 9 is a protein that in humans is encoded by the TLR9 gene. TLR9 has also been designated as ...
Toll-like receptor 2 also known as TLR2 is a protein that in humans is encoded by the TLR2 gene. [5] TLR2 has also been designated as CD282 ( cluster of differentiation 282). TLR2 is one of the toll-like receptors and plays a role in the immune system .
Toll-like receptor 3 (TLR3) also known as CD283 (cluster of differentiation 283) is a protein that in humans is encoded by the TLR3 gene. [5] TLR3 is a member of the toll-like receptor family of pattern recognition receptors of the innate immune system .
TICAM1 is primarily active in the spleen and is often regulated when MyD88 is deficient in the liver, indicating organ-specific regulation of signaling pathways. Curiously, there is a lack of redundancy within the TLR4 signaling pathway that leads to microbial evasion of immune response in the host after mutations occur within intermediates of the pathway. [7]
The TLR pathway is a part of the innate immune system that recognizes structurally conserved molecular patterns of microbial pathogens, leading to an inflammatory immune response. Tollip interacts with cellular and subcellular membrane compartments such as endosome and lysosome through its C2 domain binding with phosphoinositides. [ 9 ]
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