目录号 | 产品详情 | 靶点 | |
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T0049 | Antibacterial Antibiotic Parasite | ||
Azlocillin sodium salt 是一种半合成青霉素,是内酰胺类广谱抗生素。它具有抗假单胞杆菌的活性,并对抗寄生虫Plasmodium falciparum 有效。 | |||
T9741 | Others | ||
INE963 是快速有效的血液阶段抗疟剂,EC50为 3-6 nM。INE963 有单纯性疟疾的研究潜力。 | |||
TN1905 | Antifection | ||
Magnolioside 是分离自Angelica gigas Nakai(Umbelliferae) 中,对谷氨酸诱导的毒性有显著的神经保护作用。 它显示出对金黄色葡萄球菌 CIP 53.154 的中等抗菌活性。它具有抗疟原虫活性,对氯喹敏感的恶性疟原虫菌株具有强烈的生长抑制作用。 | |||
TCS2070 | Antioxidant Endogenous Metabolite | ||
Homogentisic acid (2,5-dihydroxyphenylacetic acid) 是一种尿液和血清代谢物中的特定代谢物,可用于尿黑酸尿症的诊断。 | |||
T1491 | Others P450 Dehydrogenase Antibiotic Parasite | ||
Atovaquone (Atavaquone) 是具有口服活性的选择性寄生虫线粒体细胞色素bc1复合物的抑制剂。它抑制人类和P. falciparum 细胞色素bc1活性,IC50值分别为 460 nM 和 2.0 nM。它有抗疟作用,有潜力用于疟疾、弓形体病、肺孢子虫肺炎和巴贝斯虫病的相关研究。 | |||
TN1019 | Apoptosis Antibacterial Parasite | ||
Beta-mangostin (β-Mangostin) 是存在 Cratoxylum arborescens 中的一种氧杂蒽酮类天然产物,有抗癌和抗菌活性,对结核分枝杆菌的 MIC 值为 6.25 μg/mL。它在体外有抗疟活性,对恶性疟原虫的 IC50值为 3.00 μg/mL。 | |||
Fr13587 | |||
7-Chloro-4-(piperazin-1-yl)quinolone 结构是药物化学中的重要支架,它单独或与其他活性药效团混合显示出多种药理特性。7-Chloro-4-(piperazin-1-yl)quinolone 是有效的sirtuin 抑制剂,并且抑制 5-羟色胺的摄取,IC50值为 50 μM。7-Chloro-4-(piperazin-1-yl)quinolone 对恶性疟原虫 D10 和 K1 菌株表现出抗疟疾活性,IC50分别为 1.18 μM 和 0.97 μM。 | |||
T11039 | Drug Metabolite | ||
Didesethyl chloroquine (Bisdesethylchloroquine) 是一种有效的心肌抑制剂。Didesethyl chloroquine 是抗疟药氯喹的主要代谢产物。 | |||
T35749 | Antioxidant Reactive Oxygen Species | ||
Thymohydroquinone (Thymoquinol) 是中药材百里香、牛至和其他唇形科植物中含有的单萜酚类化合物。 Thymohydroquinone 抑制癌细胞生长、减少氧化应激和调节炎症反应,在无细胞实验中清除2,2-二苯基-1-picrylhydrazyl 自由基(IC50 = 2.4 μg/ml),在浓度为1.6至6.4 μg/ml 的氧自由基吸收能力(ORAC)实验中,它的Trolox 当量值为2.6胸腺对苯二酚对A2780、OVCAR-8和CIS-A2780卵巢癌细胞(IC50分别为3.1、8.9和9.8 μM)和人卵巢永生化上皮细胞(IC50 = 14 μM)的生长有抑制作用,体外对恶性疟原虫也有抑制作用(IC50 = 15.9 μM)。 | |||
T2S2362 | BCL Others PARP p38 MAPK Caspase Parasite Autophagy | ||
Dehydrocorydaline nitrate 是生物碱。Dehydrocorydaline 调节 Bax,Bcl-2蛋白表达,激活 caspase-7,caspase-8,并使 PARP 失活。它能增强 p38 MAPK 活化,具有抗炎、抗癌、抗疟疾等功效。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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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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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-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-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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TMPY-04181 | pfHPRT Protein, P. falciparum, Recombinant (His) | P. falciparum | E. coli | ||
pfHPRT Protein, P. falciparum, Recombinant (His) is expressed in E. coli with His tag. The predicted molecular weight is 28.6 kDa. Accession number: Q76NM3
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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-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-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-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-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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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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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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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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