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About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
4B10, monoclonal
form
buffered aqueous solution
mol wt
antigen 34.32 kDa
species reactivity
human
technique(s)
indirect ELISA: suitable
western blot: 1-5 μg/mL
isotype
IgG2bκ
NCBI accession no.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... TLR4(7099)
General description
The protein encoded by this gene is a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize pathogen-associated molecular patterns (PAMPs) that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity. The various TLRs exhibit different patterns of expression. This receptor is most abundantly expressed in placenta, and in myelomonocytic subpopulation of the leukocytes. It has been implicated in signal transduction events induced by lipopolysaccharide (LPS) found in most gram-negative bacteria. Mutations in this gene have been associated with differences in LPS responsiveness. Also, several transcript variants of this gene have been found, but the protein coding potential of most of them is uncertain. (provided by RefSeq)
Toll like receptor 4 (TLR4) is an extracellular pathogen recognition receptor (PRR), encoded by the gene mapped to human chromosome 9q32–33. The encoded protein belongs to the interleukin-1 (IL-1)/toll receptor family and is present on both immune and nonimmune cells.
Immunogen
TLR4 (NP_612564, 214 a.a. ~ 291 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Sequence
PMNFIQPGAFKEIRLHKLTLRNNFDSLNVMKTCIQGLAGLEVHRLVLGEFRNEGNLEKFDKSALEGLCNLTIEEFRLA
Sequence
PMNFIQPGAFKEIRLHKLTLRNNFDSLNVMKTCIQGLAGLEVHRLVLGEFRNEGNLEKFDKSALEGLCNLTIEEFRLA
Biochem/physiol Actions
Toll like receptor 4 (TLR4) is a bacterial lipopolysaccharide (LPS) sensor. It plays a vital role in regulation of innate immunity. Palmitic acid (PA) interacts with TLR4 to stimulate pro-inflammatory cytokine interleukin-1β (IL-1β) secretion in human immune cells. Elevated expression of TLR4 is associated with the lupus nephritis (LN) and chronic cutaneous lupus erythematosus (CLE) pathogenesis. Genetic variations in the gene has been observed in patients with esophageal adenocarcinoma (EAC).
Physical form
Solution in phosphate buffered saline, pH 7.4
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
常规特殊物品
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Find documentation for the products that you have recently purchased in the Document Library.
Toll like receptor 4 and hepatocellular carcinoma; A systematic review.
Sepehri Z
Life Sciences, 179, 80-87 (2017)
The Increased Expression of Toll-Like Receptor 4 in Renal and Skin Lesions in Lupus Erythematosus.
Elloumi N
The Journal of Histochemistry and Cytochemistry, 65(7), 389-398 (2017)
Impact of mutations in Toll-like receptor pathway genes on esophageal carcinogenesis.
Fels Elliott DR
PLoS Genetics, 13(5), 1-21 (2017)
Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product.
Hoshino K
Journal of Immunology, 162(7), 3749-3752 (1999)
Palmitic acid is a toll-like receptor 4 ligand that induces human dendritic cell secretion of IL-1?.
Nicholas DA
PLoS ONE, 12(5), 1-24 (2017)
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