TLR4 Blocking Peptide

Cat# NB-22-76426-250

Size : 250ug

Brand : Neo Biotech

Contact local distributor :


Phone : +1 850 650 7790

General Info

Applications: Immunodepletion/Immunocompetition
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: TLR4 Blocking Peptide for STJ503278 is synthetically produced from the 970-1000 sequence and is suitable for use in western blot applications.
Formulation: Liquid form at 2.5mg/ml concentration in PBS. Up to 5% DMSO can be added. Orders with >1mg can be supplied in lyophilized powder form, or in buffer of choice.
Storage Instruction: Store at-20°C for long term storage. Avoid freeze-thaw cycles.

Information

Gene Symbol: TLR4
Gene ID: 7099
Uniprot ID: TLR4_HUMAN
Immunogen Region: 970-1000
Specificity: This blocking peptide is recommended for use in combination with TLR4 antibody, STJ503278
Immunogen: Synthetic peptide taken within amino acid region 970-1000 on human TLR4 protein.

Description

Tissue Specificity Highly expressed in placenta, spleen and peripheral blood leukocytes. Detected in monocytes, macrophages, dendritic cells and several types of T-cells.
Post Translational Modifications N-glycosylated. Glycosylation of Asn-526 and Asn-575 seems to be necessary for the expression of TLR4 on the cell surface and the LPS-response. Likewise, mutants lacking two or more of the other N-glycosylation sites were deficient in interaction with LPS. Phosphorylated on tyrosine residues by LYN after binding lipopolysaccharide.
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. At the plasma membrane, cooperates with LY96 to mediate the innate immune response to bacterial lipopolysaccharide (LPS). Also involved in LPS-independent inflammatory responses triggered by free fatty acids, such as palmitate, and Ni(2+). Mechanistically, acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. 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. 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. In complex with TLR6, promotes inflammation in monocytes/macrophages by associating with TLR6 and the receptor CD86. 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. 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.
Peptide Name Toll-Like Receptor 4
Htoll
Cd Antigen Cd284
Database Links Reactome: R-HSA-1236974
Reactome: R-HSA-140534
Reactome: R-HSA-166016
Reactome: R-HSA-166058
Reactome: R-HSA-166166
Reactome: R-HSA-2562578
Reactome: R-HSA-5602498
Reactome: R-HSA-5603041
Reactome: R-HSA-5686938
Reactome: R-HSA-936964
Reactome: R-HSA-937041
Reactome: R-HSA-937072
Reactome: R-HSA-9707616
Reactome: R-HSA-975163
Cellular Localisation Cell Membrane
Single-Pass Type I Membrane Protein
Early Endosome
Cell Projection
Ruffle
Upon Complex Formation With Cd36 And Tlr6
Internalized Through Dynamin-Dependent Endocytosis
Colocalizes With Rftn1 At Cell Membrane And Then Together With Rftn1 Moves To Endosomes
Upon Lipopolysaccharide Stimulation
Alternative Peptide Names Toll-Like Receptor 4 protein
Htoll protein
Cd Antigen Cd284 protein
TLR4 protein

Information sourced from Uniprot.org

12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance