目录号 | 产品详情 | 靶点 | |
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T4938 | AhR Endogenous Metabolite | ||
Potassium 1H-indol-3-yl sulfate (Potassium 3-indoxyl sulfate) 是人芳烃受体(AhR)的激动剂。芳烃受体(AhR)最近被发现是免疫炎症条件的病理生理调节剂,Potassium 1H-indol-3-yl sulfate 已被证明是AhR的配体。Potassium 1H-indol-3-yl sulfate 也是膳食蛋白质中色氨酸的代谢物。色氨酸被肠道细菌代谢为吲哚,吲哚被吸收到血液中,然后在肝脏中进一步代谢为硫酸吲哚,通常通过尿液排出体外。在肾功能受损的慢性肾病患者中,Potassium 1H-indol-3-yl sulfate 可作为尿毒症毒素在血清中积累,诱导氧化应激并加速疾病进展。250 μM Potassium 1H-indol-3-yl sulfate 可诱导NF-Κb活化,促进大鼠近端小管细胞TGF-β1和Smad3的表达,与促纤维化活性相关。 | |||
T76660 | |||
pTH (1-37) (human) 为甲状旁腺激素(PTH)的一段,能诱导cAMP产生并提升碱性磷酸酶活性,进而增强尿毒症动物的生长速度、骨钙含量及骨矿物质密度(BMD),显示出对骨质疏松症研究的应用潜力。 | |||
T70313 | |||
Indoxyl sulfate-d5 is intended for use as an internal standard for the quantification of indoxyl sulfate by GC- or LC-MS. Indoxyl sulfate is a uremic toxin and a metabolite of tryptophan. It is formed via sulfation of indole, an intermediate generated from tryptophan by intestinal bacteria, by the sulfotransferase (SULT) isoform 1A1 variant 2 (SULT1A1*2) in the liver. Indoxyl sulfate activates the aryl hydrocarbon receptor (AhR) in HepG2 40/6 hepatoma cells (EC50 = 12.1 nM in a reporter assay). It also inhibits the organic anion transporter (OAT) isoforms OAT1 and OAT3 (Kis = 34.2 and 74.4 µM, respectively for the rat transporters) in S2 proximal tubule cells. Indoxyl sulfate (0.2 and 1 mM) increases superoxide anion and nitric oxide levels in isolated human mononuclear blood cells. It increases serum creatinine and blood urea nitrogen (BUN) levels in the 5/6 nephrectomized rat model of chronic renal failure when administered at a dose of 50 mg/kg. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-01075 | Von Willebrand Factor/vWF Protein, Human, Recombinant (His) | Human | CHO | ||
Von Willebrand Factor (VWF) is a multimeric glycoprotein involved in hemostasis in blood, binds receptors on the surface of platelets and in connective tissue, thereby mediating the adhesion of platelets to sites of vascular injury. From studies it appears that VWF protein uncoils under these circumstances, decelerating passing platelets. VWF protein is deficient or defective in von Willebrand disease (VWD) and is involved in a large number of other diseases, including thrombosis, thrombotic thrombocytopenic purpura, Stroke, Heyde's syndrome, possibly hemolytic-uremic syndrome and so on.
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TMPJ-01306 | CFHR5 Protein, Human, Recombinant (His) | Human | Human Cells | ||
Complement factor H-related protein 5(FHR-5 for short), is a secreted protein which contains 9 Sushi (CCP/SCR) domains. It is expressed by the liver and secreted in plasma. The pattern of the deposits is similar to other complement components, suggesting that FHR-5 may play a role in complement activation and regulation. Defects in CFHR5 have been found in patients with atypical hemolytic uremic syndrome and may contribute to the disease. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease.
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TMPK-00790 | Complement factor H/CFH Protein, Human, Recombinant (His) | Human | HEK293 | ||
Factor H is the major soluble inhibitor of complement, where its binding to self markers (i.e., particular glycan structures) prevents complement activation and amplification on host surfaces. Not surprisingly, mutations and polymorphisms that affect recognition of self by factor H are associated with diseases of complement dysregulation, such as age-related macular degeneration and atypical haemolytic uremic syndrome. In addition, pathogens (i.e., non-self) and cancer cells (i.e., altered-self) can hijack factor H to evade the immune response.
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TMPY-02023 | CD46 Protein, Human, Recombinant (His) | Human | HEK293 | ||
CD46, also known as Membrane Cofactor Protein (MCP), is a complement regulatory protein. CD46 is a type 1 membrane protein that plays an important inhibitory role in the complement system. CD46 is expressed in white blood cells, platelets, epithelial cells, and fibroblasts. Human CD46 shares 5% amino acid sequence identity with mouse and rat CD46. The importance of CD46 to complement regulation is underscored by the observation that genetic loss of CD46 leads to development of atypical hemolytic-uremic syndrome (aHUS), a disease characterized by uncontrolled complement activation. CD46 is implicated in the development and/or progression of selected cancer types.
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TMPY-05829 | Thrombomodulin Protein, Human, Recombinant (His) | Human | HEK293 | ||
Thrombomodulin, also known as THBD (CD141), is an integral membrane protein that reduces blood coagulation by converting thrombin to an anticoagulant enzyme from a procoagulant enzyme. Thrombomodulin is expressed on the surface of endothelial cells and serves as a cofactor for thrombin. It is also expressed on human mesothelial cell, monocyte and a dendritic cell subset. Thrombomodulin functions as a cofactor in the thrombin-induced activation of protein C in the anticoagulant pathway by forming a 1:1 stoichiometric complex with thrombin. Thrombomodulin also regulates C3b inactivation by factor I. Mutations in the thrombomodulin gene have also been reported to be associated with atypical hemolytic-uremic syndrome.
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TMPY-03271 | Thrombomodulin Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
Thrombomodulin, also known as THBD (CD141), is an integral membrane protein that reduces blood coagulation by converting thrombin to an anticoagulant enzyme from a procoagulant enzyme. Thrombomodulin is expressed on the surface of endothelial cells and serves as a cofactor for thrombin. It is also expressed on human mesothelial cell, monocyte and a dendritic cell subset. Thrombomodulin functions as a cofactor in the thrombin-induced activation of protein C in the anticoagulant pathway by forming a 1:1 stoichiometric complex with thrombin. Thrombomodulin also regulates C3b inactivation by factor I. Mutations in the thrombomodulin gene have also been reported to be associated with atypical hemolytic-uremic syndrome.
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TMPY-04129 | Complement factor H/CFH Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Complement factor H, also known as H factor 1, and CFH, is a sialic acid containing glycoprotein that plays an integral role in the regulation of the complement-mediated immune system that is involved in microbial defense, immune complex processing, and programmed cell death. Factor H protects host cells from injury resulting from unrestrained complement activation. CFH regulates complement activation on self cells by possessing both cofactor activity for the Factor I mediated C3b cleavage, and decay accelerating activity against the alternative pathway C3 convertase, C3bBb. CFH protects self cells from complement activation but not bacteria/viruses. Due to the central role that CFH plays in the regulation of complement, there are many clinical implications arrising from aberrant CFH activity. Mutations in the Factor H gene are associated with severe and diverse diseases including the rare renal disorders hemolytic uremic syndrome (HUS) and membranoproliferative glomerulonephritis (MPGN) also termed dense deposit disease (DDD), membranoproliferative glomuleronephritis type II or dense deposit disease, as well as the more frequent retinal disease age related macular degeneration (AMD). In addition to its complement regulatory activities, factor H has multiple physiological activities and 1) acts as an extracellular matrix component, 2) binds to cellular receptors of the integrin type, and 3) interacts with a wide selection of ligands, such as the C-reactive protein, thrombospondin, bone sialoprotein, osteopontin, and heparin.
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TMPY-04141 | Complement factor H/CFH Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
Complement factor H, also known as H factor 1, and CFH, is a sialic acid containing glycoprotein that plays an integral role in the regulation of the complement-mediated immune system that is involved in microbial defense, immune complex processing, and programmed cell death. Factor H protects host cells from injury resulting from unrestrained complement activation. CFH regulates complement activation on self cells by possessing both cofactor activity for the Factor I mediated C3b cleavage, and decay accelerating activity against the alternative pathway C3 convertase, C3bBb. CFH protects self cells from complement activation but not bacteria/viruses. Due to the central role that CFH plays in the regulation of complement, there are many clinical implications arrising from aberrant CFH activity. Mutations in the Factor H gene are associated with severe and diverse diseases including the rare renal disorders hemolytic uremic syndrome (HUS) and membranoproliferative glomerulonephritis (MPGN) also termed dense deposit disease (DDD), membranoproliferative glomuleronephritis type II or dense deposit disease, as well as the more frequent retinal disease age related macular degeneration (AMD). In addition to its complement regulatory activities, factor H has multiple physiological activities and 1) acts as an extracellular matrix component, 2) binds to cellular receptors of the integrin type, and 3) interacts with a wide selection of ligands, such as the C-reactive protein, thrombospondin, bone sialoprotein, osteopontin, and heparin.
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