目录号 | 产品详情 | 靶点 | |
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T11855 | Others | ||
Lipopolysaccharides (LPS) 属于天然产物,是一种来源于革兰氏阴性菌外膜外叶的内毒素。Lipopolysaccharides 是一种高免疫原性抗原,可以增强免疫反应,可以用于炎症模型构建。 | |||
T41078 | Others | ||
Lipopolysaccharides, Escherichiacoli (11C) (LPS E. coli O55:B5)是革兰阴性菌外膜的大分子成分,由脂质a、寡糖核心和o -特异性多糖(O-antigen) 3个区域组成。 | |||
T3826 | NF-κB TLR Akt PI3K | ||
Polygalasaponin F 是从瓜子金中提取的齐墩果烷型三萜皂苷,可通过调节TLR4-PI3K/AKT-NF-kB 信号通路减少神经炎症细胞因子的分泌,能降低炎性细胞因子肿瘤坏死因子 α 的释放。 | |||
T3949 | Others Endogenous Metabolite | ||
Myristic acid (Crodacid) 是饱和的 14 碳脂肪酸,存在于大多数动物、植物的脂肪中,特别是乳脂,椰子油,棕榈油和肉豆蔻油。 | |||
TQ0073 | HIV Protease NO Synthase Parasite | ||
Andropanolide 是一种来自穿心莲的二帖类化合物,具有抗HIV、抗疟和抗癌活性,对 Lipopolysaccharides (LPS) 刺激的 RAW264.7 巨噬细胞中一氧化氮 (NO) 的过量产生有抑制作用。 | |||
TN5090 | Glucokinase | ||
Tachioside has antiobesity, antioxidant and α-glucosidase inhibitory activities, it decreases lipid content in 3T3-L1 adipocytes by inhibiting lipogenesis, shows antiobesity activities. Tachioside can inhibit nitric oxide production in lipopolysaccharides-stimulated RAW 264.7 cells with IC50 value of 12.14 μM. | |||
T37682 | |||
3-hydroxy Tridecanoic acid is a 13-carbon saturated fatty acid found in bacterial lipopolysaccharides (LPS). It can be used as an internal standard to detect markers of microorganisms in complex samples, including 3-hydroxy fatty acids found in LPS-containing bacteria and muramic acid found in bacterial cell wall peptidoglycan. | |||
T37677 | |||
3-hydroxy Docosanoic acid is a hydroxylated form of the 22-carbon saturated docosanoic acid . It is found in lipopolysaccharides from C. trachomatis and C. psittaci and in S. synnaedendra. 3-hydroxy Docosanoic acid, in the form of an acyl-CoA metabolite, is an intermediate in fatty acid chain elongation from arachidic acid to docosanoic acid (C22:0). | |||
T38041 | |||
Lipopolysaccharides (LPS) are components of the cell walls of Gram-negative bacteria. LPS is composed of polysaccharides and lipid A, where lipid A is a phosphoglycolipid containing acyl chains composed of 10 to 16 carbons. The lipid A component of LPS is detected by Toll-like receptor 4 of mammalian leukocytes and, thus, is a key determinant in immune response. (R)-3-Hydroxymyristic Acid is a form of the 14:0 lipid myristic acid that is found in the lipid A component of some Gram-negative bacteria, including Escherichia, Haemophilus, Actinobacillus, and Campylobacter species. | |||
T76273 | |||
Pep19-2.5为合成抗毒素肽,能阻断内毒素信号级联。通过抑制跨膜及胞质模式识别受体(PRRs)介导的脂肽(LP)与脂多糖(LPS)的信号通路,Pep19-2.5关键调控与炎症及细胞焦亡(pyroptosis)相关的信号级联。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02650 | Alkaline phosphatase Protein, Human, Recombinant (His) | Human | HEK293 | ||
ALPI encodes for intestinal phosphatase alkaline, a brush border metalloenzyme that hydrolyses phosphate from the lipid A moiety of lipopolysaccharides and thereby drastically reduces Toll-like receptor 4 agonist activity. ALPI mutations impaired either stability or catalytic activity of ALPI and rendered it unable to detoxify lipopolysaccharide-dependent signalling. ALPI mutations should be included in screening for monogenic causes of inflammatory bowel diseases and lay the groundwork for ALPI-based treatments in intestinal inflammatory disorders.
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TMPY-02204 | LBP Protein, Human, Recombinant (His) | Human | HEK293 | ||
Lipopolysaccharide binding protein ( LBP ) is a glycoprotein that is synthesized principally by hepatocytes. LBP is a trace plasma protein that binds to the lipid A moiety of bacterial lipopolysaccharides ( LPSs ). LBP binds directly to the outer membrane of Gram-negative bacteria and purified aggregates of extracted endotoxin and catalyzes the delivery of endotoxin to the membrane ( mCD14, GPI-Linked ) and soluble ( sCD14 ) forms of CD14, thereby markedly increasing host cell sensitivity to endotoxin. LBP efficiently catalyzes the transfer of individual molecules of endotoxin to (s)CD14 only when LBP–endotoxin aggregates are formed in the presence of albumin. In the presence of EDTA, LBP binding promotes further disaggregation of endotoxin. LBP binding does not have such drastic effects under more physiological conditions, but may still induce more subtle topological rearrangements of endotoxin.
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TMPY-04815 | C1 inhibitor Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
Plasma protease C1 inhibitor, also known as C1-inhibiting factor, C1-INH, C1 esterase inhibitor, SERPING1 and C1IN, is a serine proteinase inhibitor (serpin) that regulates activation of both the complement and contact systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases. The N-terminal end (nonserpin domain) confers to C1-INH the capacity to bind lipopolysaccharides and E-selectin. Owing to this moiety, C1-INH intervenes in regulation of the inflammatory reaction. The heterozygous deficiency of C1-INH results in hereditary angioedema (HAE). Owing to its ability to modulate the contact and complement systems and the convincing safety profile, plasma-derived C1 inhibitor is an attractive therapeutic protein to treat inflammatory diseases other than HAE. Deficiency of C1 inhibitor results in hereditary angioedema, which is characterized by recurrent episodes of localized angioedema of the skin, gastrointestinal mucosa or upper respiratory mucosa. C1 inhibitor may prove useful in a variety of other diseases including septic shock, reperfusion injury, hyperacute transplant rejection, traumatic and hemorrhagic shock, and the increased vascular permeability associated with thermal injury, interleukin-2 therapy and cardiopulmonary bypass.
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TMPH-01058 | Cathelicidin antimicrobial peptide Protein, Human, Recombinant (His & Myc & SUMO) | Human | E. coli | ||
Binds to bacterial lipopolysaccharides (LPS), has antibacterial activity.
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TMPH-01339 | Ficolin 3/FCN3 Protein, Human, Recombinant (His) | Human | E. coli | ||
May function in innate immunity through activation of the lectin complement pathway. Calcium-dependent and GlcNAc-binding lectin. Has affinity with GalNAc, GlcNAc, D-fucose, as mono/oligosaccharide and lipopolysaccharides from S.typhimurium and S.minnesota.
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TMPY-02908 | BPI Protein, Human, Recombinant (His) | Human | HEK293 | ||
Bactericidal/permeability-increasing protein is a member of the BPI/LBP/Plunc superfamily and BPI/LBP family. It is a cationic protein which can be detected in the azurophilic granule and on the surface of polymorphonuclear leukocytes. Bactericidal/permeability-increasing protein also is a lipopolysaccharide binding protein. It is associated with human neutrophil granules and has bactericidal activity on gram-negative organisms. Bactericidal/permeability-increasing protein contains two domains that adopt the same structural fold, even though they have little sequence similarity. It binds to and neutralises lipopolysaccharides from the outer membrane of Gram-negative bacteria. The cytotoxic action of bactericidal/permeability-increasing protein is limited to many species of Gram-negative bacteria; this specificity may be explained by a strong affinity of the very basic N-terminal half for the negatively charged lipopolysaccharides that are unique to the Gram-negative bacterial outer envelope.
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TMPY-02713 | Alkaline phosphatase Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
ALPI encodes for intestinal phosphatase alkaline, a brush border metalloenzyme that hydrolyses phosphate from the lipid A moiety of lipopolysaccharides and thereby drastically reduces Toll-like receptor 4 agonist activity. ALPI mutations impaired either stability or catalytic activity of ALPI and rendered it unable to detoxify lipopolysaccharide-dependent signalling. ALPI mutations should be included in screening for monogenic causes of inflammatory bowel diseases and lay the groundwork for ALPI-based treatments in intestinal inflammatory disorders.
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TMPJ-01303 | Collectin-11 Protein, Human, Recombinant (His) | Human | Human Cells | ||
Collectin-11 is a secreted protein that belongs to the COLEC10/COLEC11 family. Collectin-11 contains one C-type lectin domain and one collagen-like domain. Collectins play important roles in the innate immune system by binding to carbohydrate antigens on microorganisms, facilitating their recognition and removal. Collectin-11 binds to various sugars including fucose and mannose, but does not bind to glucose, N-acetylglucosamine and N-acetylgalactosamine. It has a higher affinity for fucose compared to mannose. Collectin-11 binds lipopolysaccharides (LPS). It also involved in fundamental development serving as a guidance cue for neural crest cell migration. Defects in Collectin-11 are the cause of 3MC syndrome type 2 (3MC2).
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TMPJ-00527 | SP-D Protein, Human, Recombinant (His) | Human | Human Cells | ||
Surfactant Pulmonary-Associated Protein D (SP-D) is a 43 kDa member of the collectin family of innate immune modulators. Its principal components consist of a collagen-like region and a C-terminal carbohydrate recognition domain (CRD), a structure that places it in a subset of pattern recognition proteins termed defense collagens. SP-D is constitutively secreted by alveolar lining cells and epithelium associated with tubular structures and induced in cardiac smooth muscle and endothelial cells. It binds both secreted and transmembrane proteins that transduce its function. It binds human neutrophil defensins, modulating influenza anti-viral defense. It binds MD-2/LY96, a secreted protein that cooperates with Toll-like receptors (TLRs) in the response of macrophages to bacterial lipopolysaccharides (LPS) or cell wall components. It also binds macrophage CD14 and TLRs directly, blocking binding of LPS and down-regulating TNF-α secretion. SP-D binding of both SIRPα and the calreticulin/CD91 complex on macrophages allows for a graded response to environmental challenge.
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TMPY-01183 | C1 inhibitor Protein, Human, Recombinant (His) | Human | HEK293 | ||
Plasma protease C1 inhibitor, also known as C1-inhibiting factor, C1-INH, C1 esterase inhibitor, SERPING1 and C1IN, is a serine proteinase inhibitor (serpin) that regulates activation of both the complement and contact systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases. The N-terminal end (nonserpin domain) confers to C1-INH the capacity to bind lipopolysaccharides and E-selectin. Owing to this moiety, C1-INH intervenes in regulation of the inflammatory reaction. The heterozygous deficiency of C1-INH results in hereditary angioedema (HAE). Owing to its ability to modulate the contact and complement systems and the convincing safety profile, plasma-derived C1 inhibitor is an attractive therapeutic protein to treat inflammatory diseases other than HAE. Deficiency of C1 inhibitor results in hereditary angioedema, which is characterized by recurrent episodes of localized angioedema of the skin, gastrointestinal mucosa or upper respiratory mucosa. C1 inhibitor may prove useful in a variety of other diseases including septic shock, reperfusion injury, hyperacute transplant rejection, traumatic and hemorrhagic shock, and the increased vascular permeability associated with thermal injury, interleukin-2 therapy and cardiopulmonary bypass.
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TMPH-03236 | Alkaline phosphatase/ALPL Protein, Rat, Recombinant (His & SUMO) | Rat | E. coli | ||
Alkaline phosphatase that metabolizes various phosphate compounds and plays a key role in skeletal mineralization and adaptive thermogenesis. Has broad substrate specificity and can hydrolyze a considerable variety of compounds: however, only a few substrates, such as diphosphate (inorganic pyrophosphate; PPi), pyridoxal 5'-phosphate (PLP) and N-phosphocreatine are natural substrates. Plays an essential role in skeletal and dental mineralization via its ability to hydrolyze extracellular diphosphate, a potent mineralization inhibitor, to phosphate: it thereby promotes hydroxyapatite crystal formation and increases inorganic phosphate concentration. Acts in a non-redundant manner with PHOSPHO1 in skeletal mineralization: while PHOSPHO1 mediates the initiation of hydroxyapatite crystallization in the matrix vesicles (MVs), ALPL/TNAP catalyzes the spread of hydroxyapatite crystallization in the extracellular matrix. Also promotes dephosphorylation of osteopontin (SSP1), an inhibitor of hydroxyapatite crystallization in its phosphorylated state; it is however unclear whether ALPL/TNAP mediates SSP1 dephosphorylation via a direct or indirect manner. Catalyzes dephosphorylation of PLP to pyridoxal (PL), the transportable form of vitamin B6, in order to provide a sufficient amount of PLP in the brain, an essential cofactor for enzymes catalyzing the synthesis of diverse neurotransmitters. Additionally, also able to mediate ATP degradation in a stepwise manner to adenosine, thereby regulating the availability of ligands for purinergic receptors. Also capable of dephosphorylating microbial products, such as lipopolysaccharides (LPS) as well as other phosphorylated small-molecules, such as poly-inosine:cytosine (poly I:C). Acts as a key regulator of adaptive thermogenesis as part of the futile creatine cycle: localizes to the mitochondria of thermogenic fat cells and acts by mediating hydrolysis of N-phosphocreatine to initiate a futile cycle of creatine dephosphorylation and phosphorylation. During the futile creatine cycle, creatine and N-phosphocreatine are in a futile cycle, which dissipates the high energy charge of N-phosphocreatine as heat without performing any mechanical or chemical work.
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