目录号 | 产品详情 | 靶点 | |
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T10378 | Others | ||
Artelinic acid, a derivative of Artemisinin, is an antimalarial drug for the treatment of multidrug-resistant strains of Plasmodium falciparum. | |||
T67694 | Parasite | ||
ZY-19489是一种具有抗疟作用的化合物, 是一种潜在的单剂量根治性恶性疟原虫和间日疟原虫疟疾的药物,已获得美国 FDA 的孤儿药认定。 | |||
T10356 | Parasite | ||
AQ-13 dihydrochloride 是一种氨基喹啉类抗疟药,对耐药型菌株 Plasmodium falciparum 有抑制作用。 | |||
T40417 | Antibacterial Parasite | ||
Ethylhydrocupreine hydrochloride (Optochin hydrochloride) 是奎宁的一种衍生物,具有抗菌作用,可抑制肺炎链球菌的活性。Ethylhydrocupreine hydrochloride 具有抗疟活性,对 Plasmodium falciparum 的IC50为 25.75 nM。Ethylhydrocupreine hydrochloride 是Gallus gallus2 受体 (ggTas2r1,ggTas2r2和ggTas2r7) 激动剂。 | |||
T14766 | Others Parasite | ||
BPH-715 抑制恶性疟原虫的肝脏阶段生长,对 HepG2 细胞中的恶性疟原虫外红细胞的形成的 IC50 为 10 μM。 | |||
T3682 | Others COX | ||
(-)-Catechin gallate ((-)-Catechin 3-O-gallate) 是绿茶儿茶素中的微量组分,可抑制COX-1和COX-2活性。它抑制人 Beta-secretase,对氯喹敏感的恶性疟原虫 NF54 和耐氯喹的恶性疟原虫 K1 具有抗疟原虫活性。 | |||
T3266 | Others Parasite Autophagy | ||
Lumefantrine (dl-Benflumelol) 是一种抗疟药,用于治疗急性单纯性疟疾。与Artemether 联用,可提高疗效。 | |||
T10903 | Parasite | ||
CWHM-1552 是一种有效的恶性疟原虫抑制剂。 对于 3D7 和 Dd2 菌株,IC50 分别为 51 nM 和 53 nM。 | |||
T27400L | Others | ||
Ganaplacide phosphate 对疟原虫症状性无性血期感染具有多阶段抗疟活性,并且能够在动物模型中预防传播和阻断感染。 | |||
T16125 | Parasite PI4K | ||
MMV390048 是一种抗疟药,是一种新型化学疟原虫 PI4K 抑制剂。它与疟原虫 PI4K 的 ATP 结合位点结合,不与除人类 PIP4K2C 外的其他恶性疟原虫和人类激酶结合。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-03144 | SEY1 Protein, Plasmodium knowlesi, Recombinant (His) | Plasmodium knowlesi | in vitro E. coli expression system | ||
Probable GTP-binding protein that may be involved in cell development.
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TMPH-03143 | PFD0110w Protein, Plasmodium falciparum, Recombinant | Plasmodium falciparum | E. coli | ||
During the asexual blood stage, binds to a sialic acid containing receptor on the surface of the host erythrocyte and thus is involved in merozoite invasion. Binds erythrocytes via a neuraminidase sensitive and trypsin-, chymotrypsin-resistant receptor. After merozoite attachment and reorientation, RH1 binding to its erythrocyte receptor triggers an increase in intracellular Ca(2+) within the parasite resulting in the release of microneme proteins such as EBA175 which in turn leads to the formation of the tight junction between parasite and host cell.
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TMPH-03139 | MDR1 Protein, Plasmodium falciparum, Recombinant (His & SUMO) | Plasmodium falciparum | E. coli | ||
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells.
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TMPH-03138 | GST Protein, Plasmodium falciparum, Recombinant (His) | Plasmodium falciparum | Yeast | ||
Conjugation of reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles. May also function as a storage protein or ligandin for parasitotoxic ferriprotoporphyrin IX (hemin).
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TMPH-03137 | PFS230 Protein, Plasmodium falciparum, Recombinant | Plasmodium falciparum | E. coli | ||
Gametocyte surface protein required for male/female gamete fusion. Also required for male gamete exflagellation and interaction with erythrocytes.
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TMPH-03140 | Plasmepsin-1 Protein, Plasmodium falciparum, Recombinant (His) | Plasmodium falciparum | E. coli | ||
During the asexual blood stage, catalyzes the initial cleavage of native host hemoglobin (Hb) resulting in Hb denaturation; specifically cleaves between Phe-33 and Leu-34 of Hb alpha-chain. Digestion of host Hb is an essential step which provides the parasite with amino acids for protein synthesis, and regulates osmolarity (Probable).
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TMPH-00990 | ACKR1 Protein, Human, Recombinant (His) | Human | in vitro E. coli expression system | ||
ACKR1 Protein, Human, Recombinant (His) is expressed in in vitro E. coli expression system.
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TMPH-03141 | Plasmepsin-2 Protein, Plasmodium falciparum, Recombinant (His & Myc) | Plasmodium falciparum | Baculovirus | ||
During the asexual blood stage, participates in initial cleavage of native host hemoglobin (Hb) resulting in Hb denaturation. May cleave preferentially denatured hemoglobin that has been cleaved by PMI. Digestion of host Hb is an essential step which provides the parasite with amino acids for protein synthesis, and regulates osmolarity (Probable).
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TMPH-03136 | L-lactate dehydrogenase Protein, Plasmodium berghei, Recombinant (His & Myc) | Plasmodium berghei | E. coli | ||
L-lactate dehydrogenase Protein, Plasmodium berghei, Recombinant (His & Myc) is expressed in E. coli.
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TMPH-03142 | Plasmepsin-2 Protein, Plasmodium falciparum, Recombinant (E. coli, His & Myc) | Plasmodium falciparum | E. coli | ||
During the asexual blood stage, participates in initial cleavage of native host hemoglobin (Hb) resulting in Hb denaturation. May cleave preferentially denatured hemoglobin that has been cleaved by PMI. Digestion of host Hb is an essential step which provides the parasite with amino acids for protein synthesis, and regulates osmolarity (Probable).
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TMPY-04180 | PfLDH Protein, P. falciparum, Recombinant (His) | P. falciparum | E. coli | ||
Plasmodium falciparum lactate dehydrogenase (PfLDH) is a key enzyme for energy generation of malarial parasites and is considered to be a potential antimalarial target. The ability of PfLDH- or PfIDEh-based immuno-PCR assays to detect <1 parasite/microL suggests that improvements of bound antibody sensor technology may greatly increase the sensitivity of malaria rapid diagnostic tests. The PfLDH test could be used to detect failures and, therefore, to assess anti-malarial efficacy.
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TMPY-00981 | ICAM-1/CD54 Protein, Human, Recombinant (aa 1-480,DDDDK) | Human | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-01349 | ICAM-1/CD54 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-01142 | ICAM-1/CD54 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-05017 | ICAM-1/CD54 Protein, Rhesus, Recombinant (His) | Rhesus | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-04765 | PKLR Protein, Human, Recombinant (His) | Human | E. coli | ||
Pyruvate kinase (PKLR) is a critical erythrocyte enzyme that is required for glycolysis and production of ATP. Pyruvate kinase deficiency (PKD) is the most frequent red blood cell enzyme abnormality of the glycolytic pathway and the most common cause of hereditary nonspherocytic hemolytic anemia. Over 250 PKLR-gene mutations have been described, including missense/nonsense, splicing and regulatory mutations, small insertions, small and gross deletions, causing PKD and hemolytic anemia of variable severity. PKLR expression was increased in liver metastases as well as in primary colorectal tumors of patients with metastatic disease. PKLR protein variants may affect the frequency, and the intensity of malaria episodes induced by different Plasmodium parasites in humans living in areas of endemic malaria.
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TMPJ-00292 | CD36 Protein, Human, Recombinant (hFc) | Human | Human Cells | ||
Platelet Glycoprotein 4 (CD36) is an integral membrane glycoprotein that has multiple physiological functions. It is broadly expressed on a variety of cell types including microvascular endothelium, adipocytes, skeletal muscle, epithelial cells of the retina, breast, and intestine, smooth muscle cells, erythroid precursors, platelets, megakaryocytes, dendritic cells, monocytes/macrophages, and microglia. As a member of the scavenger receptor family, CD36 is a multiligand pattern recognition receptor that interacts with a large number of structurally dissimilar ligands, including long chain fatty acid (LCFA), advanced glycation end products (AGE), thrombospondin-1,oxidized lowdensity lipoproteins (oxLDLs), high density lipoprotein (HDL), phosphatidylserine, apoptotic cells, β amyloid fibrils (fAβ), collagens I and IV, and Plasmodium falciparuminfected erythrocytes. CD36 is required for the antiangiogenic effects of thrombospondin-1 in the corneal neovascularization assay. It plays a role in lipid metabolism and has been identified as a fatty acid translocase necessary for the binding and transport of LCFA in cells and tissues.
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TMPJ-00294 | CD36 Protein, Mouse, Recombinant (hFc) | Mouse | Human Cells | ||
Platelet Glycoprotein 4(CD36) is belongs to the class B scavenger receptor family. The molecule CD36 is synthesized as a 472 amino acid (aa) protein that contains a 6 aa N-terminal cytoplasmic domain, a 22 aa N-terminal transmembrane segment, a 420 aa extracellular “loop”, a 22 aa C-terminal transmembrane segment, and a 9 aa C-terminal cytoplasmic tail. Both cytoplasmic tails are palmitoylated, with the C-terminal tail involved in oxidized LDL binding. With respect to the extracellular loop, the N-terminal region is believed to bind both thrombospondin-1 and Plasmodium-infected erythrocytes. Other ligands for CD36 include long-chain fatty acids, collagen, phospholipids and apoptotic cells. Cells known to express CD36 include capillary endothelium, adipocytes, skeletal muscle cells, intestinal epithelium, smooth muscle cells and hematopoietic cells such as RBC’s, platelets and monocytes. On the surface of cells, CD36 is suggested to exist as a dimer in response to ligation (7). CD36 is reported to regulate fatty uptake, act as an angiogenic with TSP-1, and participate in the clearance of apoptotic phagocytes.
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TMPY-06753 | ICAM-1/CD54 Protein, Mouse, Recombinant (His & Avi), Biotinylated | Mouse | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-05393 | ICAM-1/CD54 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-06777 | ICAM-1/CD54 Protein, Human, Recombinant (His & Avi), Biotinylated | Human | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-00825 | ICAM-1/CD54 Protein, Human, Recombinant (His & hFc) | Human | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-02017 | ICAM-1/CD54 Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPJ-00293 | CD36 Protein, Mouse, Recombinant (Avi & His), Biotinylated | Mouse | Human Cells | ||
Platelet Glycoprotein 4(CD36) is belongs to the class B scavenger receptor family. The molecule CD36 is synthesized as a 472 amino acid (aa) protein that contains a 6 aa N-terminal cytoplasmic domain, a 22 aa N-terminal transmembrane segment, a 420 aa extracellular “loop”, a 22 aa C-terminal transmembrane segment, and a 9 aa C-terminal cytoplasmic tail. Both cytoplasmic tails are palmitoylated, with the C-terminal tail involved in oxidized LDL binding. With respect to the extracellular loop, the N-terminal region is believed to bind both thrombospondin-1 and Plasmodium-infected erythrocytes. Other ligands for CD36 include long-chain fatty acids, collagen, phospholipids and apoptotic cells. Cells known to express CD36 include capillary endothelium, adipocytes, skeletal muscle cells, intestinal epithelium, smooth muscle cells and hematopoietic cells such as RBC’s, platelets and monocytes. On the surface of cells, CD36 is suggested to exist as a dimer in response to ligation (7). CD36 is reported to regulate fatty uptake, act as an angiogenic with TSP-1, and participate in the clearance of apoptotic phagocytes.
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TMPY-01320 | ICAM-1/CD54 Protein, Mouse, Recombinant (His & hFc) | Mouse | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-06778 | ICAM-1/CD54 Protein, Human, Recombinant (aa 1-480, LEVLFQ) | Human | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPY-00239 | ICAM-1/CD54 Protein, Rat, Recombinant (hFc) | Rat | HEK293 | ||
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for some immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.
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TMPH-01073 | CD81 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Structural component of specialized membrane microdomains known as tetraspanin-enriched microdomains (TERMs), which act as platforms for receptor clustering and signaling. Essential for trafficking and compartmentalization of CD19 receptor on the surface of activated B cells. Upon initial encounter with microbial pathogens, enables the assembly of CD19-CR2/CD21 and B cell receptor (BCR) complexes at signaling TERMs, lowering the threshold dose of antigen required to trigger B cell clonal expansion and antibody production. In T cells, facilitates the localization of CD247/CD3 zeta at antigen-induced synapses with B cells, providing for costimulation and polarization toward T helper type 2 phenotype. Present in MHC class II compartments, may also play a role in antigen presentation. Can act both as positive and negative regulator of homotypic or heterotypic cell-cell fusion processes. Positively regulates sperm-egg fusion and may be involved in acrosome reaction. In myoblasts, associates with CD9 and PTGFRN and inhibits myotube fusion during muscle regeneration. In macrophages, associates with CD9 and beta-1 and beta-2 integrins, and prevents macrophage fusion into multinucleated giant cells specialized in ingesting complement-opsonized large particles. Also prevents the fusion of mononuclear cell progenitors into osteoclasts in charge of bone resorption. May regulate the compartmentalization of enzymatic activities. In T cells, defines the subcellular localization of dNTPase SAMHD1 and permits its degradation by the proteasome, thereby controlling intracellular dNTP levels. Also involved in cell adhesion and motility. Positively regulates integrin-mediated adhesion of macrophages, particularly relevant for the inflammatory response in the lung.; (Microbial infection) Acts as a receptor for hepatitis C virus (HCV) in hepatocytes. Association with CLDN1 and the CLDN1-CD81 receptor complex is essential for HCV entry into host cell.; (Microbial infection) Involved in SAMHD1-dependent restriction of HIV-1 replication. May support early replication of both R5- and X4-tropic HIV-1 viruses in T cells, likely via proteasome-dependent degradation of SAMHD1.; (Microbial infection) Specifically required for Plasmodium falciparum infectivity of hepatocytes, controlling sporozoite entry into hepatocytes via the parasitophorous vacuole and subsequent parasite differentiation to exoerythrocytic forms.
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