目录号 | 产品详情 | 靶点 | |
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TN1788 | Amylase | ||
Isookanin 在多种疾病领域有研究价值,包括肿瘤,皮疹,蛇和昆虫叮咬,糖尿病,腹泻。它可作为抗病毒剂对抗 HSV 和水痘带状疱疹病毒。它也具有抗氧化特性。 | |||
TP1289 | Others | ||
Cardiotoxin Analog (CTX) IV (6-12) TFA(115722-23-1 free base) 是 Cardiotoxin Analog (CTX) IV 的部分肽。从台湾眼镜蛇毒液中分离出的心脏毒素类似物 IV。 CTX IV 是一种独特的蛇毒心脏毒素。 | |||
T80468 | Potassium Channel | ||
δ-Dendrotoxin,作为一种K+通道阻滞剂,来源于黑曼巴蛇的毒液,常用于研究神经系统疾病。 | |||
T26212 | |||
SQ 20858 is a synthetic peptide derived from snake Bothrops jararaca venom; suppresses angiotensin serum converting enzyme. | |||
TN4886 | Others | ||
Quinovic acid 3-O-alpha-L-rhamnopyranoside shows significant inhibitory activity against snake venom phosphodiesterase-I. | |||
T81787 | |||
MitTx-beta为一多肽,源自得克萨斯珊瑚蛇(Micrurus tener tener)之毒液。与MitTx-α配对,组成复合物MitTx,此复合物激活ASIC1通道,存在于辣椒素敏感神经纤维上。 | |||
TN4247 | Phospholipase | ||
Ikshusterol 3-O-glucoside has a potent snake-venom neutralizing capacity and it might be a potential molecule for the therapeutic treatment for snakebites. | |||
T80064 | Potassium Channel | ||
Dendrotoxin-I是一种高效的K+通道阻滞剂,特异性针对KV1.1和KV1.2电压门控钾通道亚基。该化合物为从Dendroaspis蛇毒中提取的神经毒素。 | |||
T75582 | |||
Naja Melanoleuca Venom (Forest Cobra Venom) 是一种蛇毒,可从 Naja Melanoleuca 获得。Naja Melanoleuca Venom 对人类红细胞具有溶血活性。α-神经毒素可以从 Naja Melanoleuca 毒液中分离出来,并抑制 GABAA 受体功能。 | |||
T75408 | |||
Batroxobin (DF-521),一种从Bothrops atrox moojeni获得的蛇毒,能促进血栓溶解,防止血栓复发并具有神经保护作用,显示出在脑静脉血栓性疾病研究中的潜力。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-00586 | CLEC-2 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
CLEC1B, also known as CLEC2, is a C-type lectin-like receptor expressed in myeloid cells and NK cells. Natural killer (NK) cells express multiple calcium-dependent (C-type) lectin-like receptors, such as CD94 and NKG2D, that interact with major histocompatibility complex class I molecules and either inhibit or activate cytotoxicity and cytokine secretion. CLEC2 acts as a receptor for the platelet-aggregating snake venom protein rhodocytin. Rhodocytin binding leads to tyrosine phosphorylation and this promotes the binding of spleen tyrosine kinase (Syk) and initiation of downstream tyrosine phosphorylation events and activation of PLC-gamma-2. CLEC2 contains 1 C-type lectin domain and is expressed preferentially in the liver. It acts as an attachment factor for human immunodeficiency virus type 1 (HIV-1) and facilitates its capture by platelets.
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TMPH-00215 | SVTLE Protein, Bothrops jararaca, Recombinant (His & Myc) | Bothrops jararaca | E. coli | ||
Thrombin-like snake venom serine protease that clots fibrinogen by releasing fibrinopeptide A from the alpha chain of fibrinogen (FGA), induces platelet aggregation through its interaction with GPIb (GP1BA/GP1BB), and activates factor VIII (F8).
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TMPH-00768 | SVTLE Protein, Gloydius ussuriensis, Recombinant (His & Myc) | Gloydius ussuriensis | E. coli | ||
Thrombin-like snake venom serine protease. Has a coagulant activity. Acts on alpha-chains of fibrinogen (FGA) generating fibrinopeptide A.
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TMPH-00038 | Thrombin-like enzyme contortrixobin Protein, Agkistrodon contortrix, Recombinant (His & Myc) | Agkistrodon contortrix | E. coli | ||
Thrombin-like snake venom serine protease that cleaves beta chain of fibrinogen (FGB), releasing fibrinopeptide B. Has a coagulant activity activating blood coagulation factors V (F5) and XIII (F13A1).
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TMPY-03877 | ADAM8/CD156a Protein, Rhesus, Recombinant (His) | Rhesus | HEK293 | ||
ADAM8, also known as CD156, is a member of the ADAM (a disintegrin and metalloprotease domain) family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biological processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. ADAM8 is possiblely involved in extravasation of leukocytes As a metalloprotease, ADAM8 also may be involved in cell adhesion during neurodegeneration, and it is thought to be a target for allergic respiratory diseases, including asthma.
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TMPY-05532 | ADAM8/CD156a Protein, Human, Recombinant (His) | Human | HEK293 | ||
ADAM8, also known as CD156, is a member of the ADAM (a disintegrin and metalloprotease domain) family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biological processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. ADAM8 is possiblely involved in extravasation of leukocytes As a metalloprotease, ADAM8 also may be involved in cell adhesion during neurodegeneration, and it is thought to be a target for allergic respiratory diseases, including asthma.
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TMPY-02162 | Phospholipase A2 IIE/PLA2G2E Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Group IIE secretory phospholipase A2, also known as GIIE sPLA2, sPLA2-IIE, Phosphatidylcholine 2-acylhydrolase 2E and PLA2G2E is a secreted protein that belongs to the phospholipase A2 family. Mammalian secretory phospholipase A2s (sPLA2s) form a family of structurally related enzymes that are involved in a variety of physiological and pathological processes via the release of arachidonic acid from membrane phospholipids or the binding to specific membrane receptors. Phospholipases A2 / PLA2 are enzymes that release fatty acids from the second carbon group of glycerol. This particular phospholipase specifically recognizes the sn-2 acyl bond of phospholipids and catalytically hydrolyzes the bond releasing arachidonic acid and lysophospholipids. Phospholipases A2 / PLA2 are commonly found in mammalian tissues as well as insect and snake venom. Venom from both snakes and insects is largely composed of melittin, which is a stimulant of Phospholipases A2 / PLA2. Due to the increased presence and activity of Phospholipases A2 / PLA2 resulting from a snake or insect bite, arachidonic acid is released from the phospholipid membrane disproportionately. As a result, inflammation and pain occur at the site. PLA2G2E catalyzes the calcium-dependent hydrolysis of the 2-acyl groups in 3-sn-phosphoglycerides. Has a preference for arachidonic-containing phospholipids.
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TMPH-03163 | SVTLE Protein, Protobothrops flavoviridis, Recombinant (His & Myc) | Protobothrops flavoviridis | E. coli | ||
Thrombin-like snake venom serine protease that clots fibrinogen (FGA) by releasing fibrinopeptide A. According to PubMed:8585090, only cleaves rabbit fibrinogen, whereas no specificity is described in PubMed:3910643 (tests done on bovine fibrinogen). Also acts as a C3 convertase that independently cleaves human C3 and kick-starts the complement cascade. Also increases urokinase-type plasminogen activator (PLAU) and plasminogen activator inhibitor (SERPINE1) in cultured bovine pulmonary artery endothelial cells. Dose-dependently inhibits collagen-induced platelet aggregation.
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TMPH-00214 | SVMP Protein, Bothrops atrox, Recombinant (His & Myc) | Bothrops atrox | E. coli | ||
Snake venom zinc metalloproteinase that acts on fibrinogen, fibrin, fibronectin (FN1), type I collagen, type IV collagen, integrin alpha-7/beta-1 (ITGA7/ITGB1) and integrin alpha-1/beta-1 (ITGA1/ITGB1). Binds to fibronectin (FN1), fibrinogen and, weakly, to type I collagen and laminin. Cleaves Xaa-Leu bonds. Inhibits ADP- and collagen-induced platelet aggregation both in the presence (IC(50)=1.4 uM for collagen) and in the absence (IC(50)=2.2 uM for collagen) of cofactors. Has hemorrhagic activity.
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TMPY-02181 | PLA2G12B Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Group XIIB secretory phospholipase A2-like protein, also known as Group XIII secretory phospholipase A2-like protein, GXIII sPLA2-like, sPLA2-GXIIB, GXIIB, PLA2G13 and PLA2G12B, is a secreted protein that belongs to the phospholipase A2 family. PLA2G12B / PLA2G13 is strongly expressed in liver, small intestine and kidney. Mammalian secretory phospholipase A2s ( sPLA2s ) form a family of structurally related enzymes that are involved in a variety of physiological and pathological processes via the release of arachidonic acid from membrane phospholipids or the binding to specific membrane receptors. Phospholipases A2 / PLA2 are enzymes that release fatty acids from the second carbon group of glycerol. This particular phospholipase specifically recognizes the sn-2 acyl bond of phospholipids and catalytically hydrolyzes the bond releasing arachidonic acid and lysophospholipids. Phospholipases A2 / PLA2 are commonly found in mammalian tissues as well as insect and snake venom. Venom from both snakes and insects is largely composed of melittin, which is a stimulant of Phospholipases A2 / PLA2. Due to the increased presence and activity of Phospholipases A2 / PLA2 resulting from a snake or insect bite, arachidonic acid is released from the phospholipid membrane disproportionately. As a result, inflammation and pain occur at the site.
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TMPY-02357 | CLEC-2 Protein, Human, Recombinant (His) | Human | HEK293 | ||
CLEC1B, also known as CLEC2, is a C-type lectin-like receptor expressed in myeloid cells and NK cells. Natural killer (NK) cells express multiple calcium-dependent (C-type) lectin-like receptors, such as CD94 and NKG2D, that interact with major histocompatibility complex class I molecules and either inhibit or activate cytotoxicity and cytokine secretion. CLEC2 acts as a receptor for the platelet-aggregating snake venom protein rhodocytin. Rhodocytin binding leads to tyrosine phosphorylation and this promotes the binding of spleen tyrosine kinase (Syk) and initiation of downstream tyrosine phosphorylation events and activation of PLC-gamma-2. CLEC2 contains 1 C-type lectin domain and is expressed preferentially in the liver. It acts as an attachment factor for human immunodeficiency virus type 1 (HIV-1) and facilitates its capture by platelets.
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TMPH-00324 | SVTLE Protein, Calloselasma rhodostoma, Recombinant (His) | Calloselasma rhodostoma | Yeast | ||
Thrombin-like snake venom serine protease that acts as an anticoagulant. It cleaves fibrinogen (FGA) to split off the A-fibrinopeptides (A, AY and AP), but not the B-fibrinopeptide. The resulting fibrin polymers are imperfectly formed and much smaller in size (1 to 2 um long) than the fibrin polymers produced by the action of thrombin. These ancrod-induced microthrombi are friable, unstable, urea-soluble and have significantly degraded alpha chains. They do not cross-link to form thrombi. They are markedly susceptible to digestion by plasmin and are rapidly removed from circulation by either reticuloendothelial phagocytosis or normal fibrinolysis, or both. Anticoagulation through the removal of fibrinogen from the blood is rapid, occurring within hours following its administration. It does not activate plasminogen and does not degrade preformed, fully cross-linked thrombin fibrin. It also reduces the level of plasminogen activator inhibitor (PAI) and may stimulate the release of tissue plasminogen activator (PLAT) from the endothelium. The profibrinolytic effect of these 2 actions appears to be limited to local microthrombus degradation.
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