目录号 | 产品详情 | 靶点 | |
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T6S1653 | Reactive Oxygen Species | ||
Albiflorin (Alibiflorin) 是一种牡丹根中的主要成分,是一种单萜糖苷。它具有神经保护、抗炎、抗氧化和缓解疼痛作用。 | |||
T21919 | Apoptosis | ||
UCF 101 是竞争性的促凋亡蛋白酶Omi/HtrA2选择性抑制剂。它对 MI/R 损伤具有明显的心脏保护作用,还具有一定的神经保护作用。它在 543 nm 处具有天然的红色荧光,可用于监视其进入哺乳动物细胞的能力。 | |||
T8551 | AChR Adenosine Receptor | ||
Nitrobenzylthioinosine (NBMPR) 是一种 ENT1 转运蛋白抑制剂,可与 ENT1 转运蛋白以高亲和力结合。它是一种可穿过血脑屏障的光亲和探针,用于追踪大脑中腺苷的摄取位点。 | |||
T7683 | Adenosine Receptor | ||
Adenosine amine congener (ADAC) 是一种选择性的 A1 腺苷受体激动剂,具有神经保护作用,可以改善噪音和顺铂引起的耳蜗损伤。 | |||
T3866 | Others COX | ||
Macelignan (Anwuligan) 是一种从肉豆蔻中分离得到的木脂素,具有抗炎、抗癌、抗糖尿病和神经保护活性。 | |||
TN1911 | transporter Akt HDAC AMPK | ||
Marein 能通过CaMKK/AMPK/GLUT1促进葡萄糖摄取,IRS/Akt/GSK-3β增加糖原合成,并通过Akt/FoxO1减少糖异生,从而改善 HepG2 细胞中高葡萄糖诱导的胰岛素抵抗。它对甲基乙二醛诱导的 PC12 细胞损伤具有神经保护作用,还有抗氧化、降压、降血脂和抗糖尿病作用。 | |||
T7512 | Potassium Channel | ||
BMS-191011 (BMS-A) 是一种大电导 Ca2+激活的钾通道 (Ca2+-activated potassium (maxi-K) channel) 激活剂,在中风模型中有研究价值。 | |||
T4283 | TGF-beta/Smad | ||
SRI011381 是口服具有活力的 TGF-β信号通路的激活剂,具有神经保护活性。 | |||
TN2423 | Antioxidant | ||
Safranal 是藏红花的主要成分,具有口服活性,是这种香料的独特香气来源。它具有神经保护和抗炎作用,对帕金森氏病具有潜在的研究价值。 | |||
T8516 | Others | ||
Levomenol ((-)-α-BISABOLOL) 是一种单环倍半萜醇,具有有神经保护、抗氧化、抗炎和抗凋亡的作用。它可减轻三叉神经性疼痛啮齿动物模型的伤害性行为和中枢敏感性。它通过减少小鼠永久性局灶性脑缺血诱导的促炎标志物,防止神经元损伤和记忆缺陷。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPK-00810 | tPA Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
Tissue plasminogen activator (tPA) is the predominant plasminogen activator present in the vascular and nervous systems.t tPA is not only neuroprotective for postnatal primary cortical neurons, but also that the
predominant route for enhancing cell survival is via an mTORdependent mechanism.
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TMPH-03391 | TRIM2 Protein, Rat, Recombinant (His) | Rat | E. coli | ||
E3 ubiquitin-protein ligase that mediates the ubiquitination of phosphorylated BCL2L11. Also mediates the UBE2D1-dependent ubiquitination of NEFL. Plays a neuroprotective function. May play a role in neuronal rapid ischemic tolerance. TRIM2 Protein, Rat, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 85.5 kDa and the accession number is D3ZQG6.
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TMPH-01502 | Humanin Protein, Human, Recombinant (GST) | Human | E. coli | ||
Plays a role as a neuroprotective factor. Protects against neuronal cell death induced by multiple different familial Alzheimer disease genes and amyloid-beta proteins in Alzheimer disease. Mediates its neuroprotective effect by interacting with a receptor complex composed of IL6ST/GP130, IL27RA/WSX1 and CNTFR. Also acts as a ligand for G-protein coupled receptors FPR2/FPRL1 and FPR3/FPRL2. Inhibits amyloid-beta protein 40 fibril formation. Also inhibits amyloid-beta protein 42 fibril formation. Suppresses apoptosis by binding to BAX and preventing the translocation of BAX from the cytosol to mitochondria. Also suppresses apoptosis by binding to BID and inhibiting the interaction of BID with BAX and BAK which prevents oligomerization of BAX and BAK and suppresses release of apoptogenic proteins from mitochondria. Forms fibers with BAX and also with BID, inducing BAX and BID conformational changes and sequestering them into the fibers which prevents their activation. Can also suppress apoptosis by interacting with BIM isoform BimEL, inhibiting BimEL-induced activation of BAX, blocking oligomerization of BAX and BAK, and preventing release of apoptogenic proteins from mitochondria. Plays a role in up-regulation of anti-apoptotic protein BIRC6/APOLLON, leading to inhibition of neuronal cell death. Binds to IGFBP3 and specifically blocks IGFBP3-induced cell death. Competes with importin KPNB1 for binding to IGFBP3 which is likely to block IGFBP3 nuclear import. Induces chemotaxis of mononuclear phagocytes via FPR2/FPRL1. Reduces aggregation and fibrillary formation by suppressing the effect of APP on mononuclear phagocytes and acts by competitively inhibiting the access of FPR2 to APP. Protects retinal pigment epithelium (RPE) cells against oxidative stress-induced and endoplasmic reticulum (ER) stress-induced apoptosis. Promotes mitochondrial biogenesis in RPE cells following oxidative stress and promotes STAT3 phosphorylation which leads to inhibition of CASP3 release. Also reduces CASP4 levels in RPE cells, suppresses ER stress-induced mitochondrial superoxide production and plays a role in up-regulation of mitochondrial glutathione. Reduces testicular hormone deprivation-induced apoptosis of germ cells at the nonandrogen-sensitive stages of the seminiferous epithelium cycle. Protects endothelial cells against free fatty acid-induced inflammation by suppressing oxidative stress, reducing expression of TXNIP and inhibiting activation of the NLRP3 inflammasome which inhibits expression of proinflammatory cytokines IL1B and IL18. Protects against high glucose-induced endothelial cell dysfunction by mediating activation of ERK5 which leads to increased expression of transcription factor KLF2 and prevents monocyte adhesion to endothelial cells. Inhibits the inflammatory response in astrocytes. Increases the expression of PPARGC1A/PGC1A in pancreatic beta cells which promotes mitochondrial biogenesis. Increases insulin sensitivity.
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TMPJ-00990 | S100B Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
S100-B, is an acidic protein with a molecular weight of 21 kDa belonging to the S100 family. S100-B contains two EF-hand-type calcium-binding motifs separated by a hinge region with a hydrophobic cleft. S100-B plays an important role in neurodevelopment, differentiation, and brain construction. S100-B has neuroprotective effects, but at high concentrations S100-B is neurotoxic. Extracellular concentration of S100-B increases following brain damage, which easily penetrates into cerebrospinal fluid in brain damage and then into the blood. S100-B is expressed and produced by astrocytes in vertebrate brains and in the CNS, and the astrocytes are the major cells producing S100-B protein in gray matter, as well as oligodendrocytes are the predominant S100-B in protein producing cells in white matter. The major advantage of using S100-B is that elevations in serum or CSF levels provide a sensitive measure for determining CNS injury at the molecular level before gross changes develop, enabling timely delivery of crucial medical intervention before irreversible damage occurs. In addition, S100-B, which is also present in Mouse melanocytes, is a reliable marker for melanoma malignancy both in bioptic tissue and in serum.
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TMPH-01503 | Humanin Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Plays a role as a neuroprotective factor. Protects against neuronal cell death induced by multiple different familial Alzheimer disease genes and amyloid-beta proteins in Alzheimer disease. Mediates its neuroprotective effect by interacting with a receptor complex composed of IL6ST/GP130, IL27RA/WSX1 and CNTFR. Also acts as a ligand for G-protein coupled receptors FPR2/FPRL1 and FPR3/FPRL2. Inhibits amyloid-beta protein 40 fibril formation. Also inhibits amyloid-beta protein 42 fibril formation. Suppresses apoptosis by binding to BAX and preventing the translocation of BAX from the cytosol to mitochondria. Also suppresses apoptosis by binding to BID and inhibiting the interaction of BID with BAX and BAK which prevents oligomerization of BAX and BAK and suppresses release of apoptogenic proteins from mitochondria. Forms fibers with BAX and also with BID, inducing BAX and BID conformational changes and sequestering them into the fibers which prevents their activation. Can also suppress apoptosis by interacting with BIM isoform BimEL, inhibiting BimEL-induced activation of BAX, blocking oligomerization of BAX and BAK, and preventing release of apoptogenic proteins from mitochondria. Plays a role in up-regulation of anti-apoptotic protein BIRC6/APOLLON, leading to inhibition of neuronal cell death. Binds to IGFBP3 and specifically blocks IGFBP3-induced cell death. Competes with importin KPNB1 for binding to IGFBP3 which is likely to block IGFBP3 nuclear import. Induces chemotaxis of mononuclear phagocytes via FPR2/FPRL1. Reduces aggregation and fibrillary formation by suppressing the effect of APP on mononuclear phagocytes and acts by competitively inhibiting the access of FPR2 to APP. Protects retinal pigment epithelium (RPE) cells against oxidative stress-induced and endoplasmic reticulum (ER) stress-induced apoptosis. Promotes mitochondrial biogenesis in RPE cells following oxidative stress and promotes STAT3 phosphorylation which leads to inhibition of CASP3 release. Also reduces CASP4 levels in RPE cells, suppresses ER stress-induced mitochondrial superoxide production and plays a role in up-regulation of mitochondrial glutathione. Reduces testicular hormone deprivation-induced apoptosis of germ cells at the nonandrogen-sensitive stages of the seminiferous epithelium cycle. Protects endothelial cells against free fatty acid-induced inflammation by suppressing oxidative stress, reducing expression of TXNIP and inhibiting activation of the NLRP3 inflammasome which inhibits expression of proinflammatory cytokines IL1B and IL18. Protects against high glucose-induced endothelial cell dysfunction by mediating activation of ERK5 which leads to increased expression of transcription factor KLF2 and prevents monocyte adhesion to endothelial cells. Inhibits the inflammatory response in astrocytes. Increases the expression of PPARGC1A/PGC1A in pancreatic beta cells which promotes mitochondrial biogenesis. Increases insulin sensitivity.
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