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Rabbit Anti-TLR4/FITC Conjugated antibody
background:
The Toll-like receptor 4 by activating natural immunity, specific immune response involved in the start-up, Toll-like receptor 4 as an important signal transduction transmembrane receptor involved in the toxin-induced inflammation in the pathological process, its mechanisms of control On a growing concern. all regions were either double-stranded or sequenced with an alternatechemistry or covered by high quality data(i.e., phred quality >=30); an attempt was made to resolve all sequencing problems, such as compressions and repeats; all regions were covered by at least one subclone; and the assembly was confirmed by restriction digest, except on the rare occasion of the clone being a YAC. The following abbreviations are used to associate primary accession numbers given in the feature table with their source databases: Em:, EMBL; Sw:, SWISSPROT; Tr:, TREMBL; Wp:, WORMPEP; Information on the WORMPEP database can be found at. TLR-4 plays an important role in microvascular leakage and leukocyte adhesion under the inflammatory condition associated with nonseptic thermal injury.
Function:
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 Ni(2+). These responses require non-conserved histidines and are, therefore, species-specific.
Subcellular Location:
Membrane; Single-pass type I membrane protein.
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.
DISEASE:
Genetic variation in TLR4 is associated with age-related macular degeneration type 10 (ARMD10) [MIM:611488]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.
Similarity:
Belongs to the Toll-like receptor family.
Contains 18 LRR (leucine-rich) repeats.
Contains 1 LRRCT domain.
Contains 1 TIR domain
Database links:
Entrez Gene: 7099 Human
Entrez Gene: 21898 Mouse
Entrez Gene: 29260 Rat
SwissProt: O00206 Human
SwissProt: Q9QUK6 Mouse
SwissProt: Q9QX05 Rat
Unigene: 174312 Human
Unigene: 38049 Mouse
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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