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TLR4 Antibody (Internal)
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P |
|---|---|
| Primary Accession | O00206 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 96kDa |
| Dilution | IHC-P (5 µg/ml) |
| Gene ID | 7099 |
|---|---|
| Other Names | Toll-like receptor 4, hToll, CD284, TLR4 |
| Target/Specificity | Human TLR4. BLAST analysis of the peptide immunogen showed no homology with other human proteins. |
| Reconstitution & Storage | Long term: -70°C; Short term: +4°C |
| Precautions | TLR4 Antibody (Internal) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | TLR4 |
|---|---|
| Function | Transmembrane receptor that functions as a pattern recognition receptor recognizing pathogen- and damage-associated molecular patterns (PAMPs and DAMPs) to induce innate immune responses via downstream signaling pathways (PubMed:10835634, PubMed:15809303, PubMed:16622205, PubMed:17292937, PubMed:17478729, PubMed:20037584, PubMed:20711192, PubMed:23880187, PubMed:27022195, PubMed:29038465). At the plasma membrane, cooperates with LY96 to mediate the innate immune response to bacterial lipopolysaccharide (LPS) (PubMed:27022195). Also involved in LPS-independent inflammatory responses triggered by free fatty acids, such as palmitate, and Ni(2+) (PubMed:20711192). Mechanistically, acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response (PubMed:10835634, PubMed:21393102, PubMed:27022195, PubMed:36945827, PubMed:9237759). Alternatively, CD14-mediated TLR4 internalization via endocytosis is associated with the initiation of a MYD88-independent signaling via the TICAM1-TBK1-IRF3 axis leading to type I interferon production (PubMed:14517278). In addition to the secretion of proinflammatory cytokines, initiates the activation of NLRP3 inflammasome and formation of a positive feedback loop between autophagy and NF-kappa-B signaling cascade (PubMed:32894580). In complex with TLR6, promotes inflammation in monocytes/macrophages by associating with TLR6 and the receptor CD86 (PubMed:23880187). Upon ligand binding, such as oxLDL or amyloid-beta 42, the TLR4:TLR6 complex is internalized and triggers inflammatory response, leading to NF- kappa-B-dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway (PubMed:23880187). In myeloid dendritic cells, vesicular stomatitis virus glycoprotein G but not LPS promotes the activation of IRF7, leading to type I IFN production in a CD14-dependent manner (PubMed:15265881, PubMed:23880187). Required for the migration- promoting effects of ZG16B/PAUF on pancreatic cancer cells. |
| Cellular Location | Cell membrane; Single-pass type I membrane protein. Early endosome. Cell projection, ruffle {ECO:0000250|UniProtKB:Q9QUK6}. Note=Upon complex formation with CD36 and TLR6, internalized through dynamin-dependent endocytosis (PubMed:20037584). Colocalizes with RFTN1 at cell membrane and then together with RFTN1 moves to endosomes, upon lipopolysaccharide stimulation. Co-localizes with ZG16B/PAUF at the cell membrane of pancreatic cancer cells (PubMed:36232715) |
| Tissue Location | Highly expressed in placenta, spleen and peripheral blood leukocytes (PubMed:9237759, PubMed:9435236). Detected in monocytes, macrophages, dendritic cells and several types of T-cells (PubMed:27022195, PubMed:9237759). Expressed in pancreatic cancer cells but not in normal pancreatic cells (at protein level) (PubMed:36232715). |
| Volume | 50 µl |
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Provided below are standard protocols that you may find useful for product applications.
Background
Cooperates with LY96 and CD14 to mediate the innate immune response to bacterial lipopolysaccharide (LPS). Acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Also involved in LPS- independent inflammatory responses triggered by free fatty acids, such as palmitate, and Ni(2+). Responses triggered by Ni(2+) require non-conserved histidines and are, therefore, species- specific. In complex with TLR6, promotes sterile inflammation in monocytes/macrophages in response to oxidized low-density lipoprotein (oxLDL) or amyloid-beta 42. In this context, the initial signal is provided by oxLDL- or amyloid-beta 42-binding to CD36. This event induces the formation of a heterodimer of TLR4 and TLR6, which is rapidly internalized and triggers inflammatory response, leading to the NF-kappa-B-dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway, as well as IL1B secretion.
References
Medzhitov R.,et al.Nature 388:394-397(1997).
Rock F.L.,et al.Proc. Natl. Acad. Sci. U.S.A. 95:588-593(1998).
Smirnova I.,et al.Genome Biol. 1:RESEARCH002.1-RESEARCH002.10(2000).
Arbour N.C.,et al.Nat. Genet. 25:187-191(2000).
Nakajima T.,et al.Immunogenetics 60:727-735(2008).
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