|Application ||IHC-P, E|
|Other Accession||NP_612564, 19924149|
|Calculated MW||95680 Da|
|Application Notes||TLR4 antibody can be used for detection of TLR4 by immunohistochemistry at 5 µg/mL.|
|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.|
|Function||Cooperates with LY96 and CD14 to mediate the innate immune response to bacterial lipopolysaccharide (LPS) (PubMed:27022195). Acts via MYD88, TIRAP and TRAF6, leading to NF- kappa-B activation, cytokine secretion and the inflammatory response (PubMed:9237759, PubMed:10835634, PubMed:27022195). 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 (PubMed:20711192). Both M.tuberculosis HSP70 (dnaK) and HSP65 (groEL-2) act via this protein to stimulate NF-kappa-B expression (PubMed:15809303). 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. Binds electronegative LDL (LDL(-)) and mediates the cytokine release induced by LDL(-) (PubMed:23880187). Stimulation of monocytes in vitro with M.tuberculosis PstS1 induces p38 MAPK and ERK1/2 activation primarily via TLR2, but also partially via this receptor (PubMed:16622205).|
|Cellular Location||Cell membrane; Single-pass type I membrane protein. Early endosome. 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.|
|Tissue Location||Highly expressed in placenta, spleen and peripheral blood leukocytes (PubMed:9435236, PubMed:9237759) Detected in monocytes, macrophages, dendritic cells and several types of T-cells (PubMed:9237759, PubMed:27022195)|
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Provided below are standard protocols that you may find useful for product applications.
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.
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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