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TLR4 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, E |
|---|---|
| Primary Accession | O00206 |
| Other Accession | NP_612564, 19924149 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 95680 Da |
| Application Notes | TLR4 antibody can be used for detection of TLR4 by immunohistochemistry at 5 µg/mL. |
| Gene ID | 7099 |
|---|---|
| Other Names | TLR4 Antibody: TOLL, CD284, TLR-4, ARMD10, Toll-like receptor 4, hToll, toll-like receptor 4 |
| Target/Specificity | TLR4; TLR4 antibody is predicted to not cross-react with other TLR protein family members. |
| Reconstitution & Storage | TLR4 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
| Precautions | TLR4 Antibody 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). |
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Provided below are standard protocols that you may find useful for product applications.
Background
TLR4 Antibody: Toll-like receptors (TLRs) are signaling molecules that recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses. These proteins act through adaptor molecules such as MyD88 and TIRAP to activate various kinases and transcription factors such as Protein Kinase C (PKC) alpha/beta and NF-κB. Studies with TLR4-deficient mice indicate that the main ligand for TLR is lipopolysaccharide. Consequently, these mice also showed increased susceptibility to Gram-negative sepsis.
References
Vogel SN, Fitzgerald KA, and Fenton MJ. TLRs: differential adapter utilization by toll-like receptors mediates TLR-specific patterns of gene expression. Mol. Interv. 2003; 3:466-77
Takeda K, Kaisho T, and Akira S. Toll-like receptors. Annu. Rev. Immunol. 2003; 21:335-76
Janeway CA Jr. and Medzhitov R. Innate immune recognition. Annu. Rev. Immunol. 2002; 20:197-216
O’Neill LAJ, Fitzgerald FA, and Bowie AG. The Toll-IL-1 receptor adaptor family grows to five members. Trends in Imm. 2003; 24:286-9.
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