目录号 | 产品详情 | 靶点 | |
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TQ0165 | NOD-like Receptor (NLR) Transferase NOD Autophagy | ||
Arglabin ((+)-Arglabin) 是从青蒿中分离出的一种天然产物,是一种 NLRP3 炎性体抑制剂,具有抗动脉粥样硬化和抗癌作用。 | |||
T27841 | NOD | ||
Lobeglitazone Sulfate(CKD-501 Sulfate) 是一种新型噻唑烷二酮,具有抗炎活性,抑制LPS诱导的NLRP3炎症小体活化和肝脏炎症,可用于研究 2 型糖尿病 (T2DM)。 | |||
T3092 | Potassium Channel NOD-like Receptor (NLR) Antibacterial Antibiotic NOD | ||
Nigericin sodium salt 属于抗生素,是一种 NLRP3 激活剂,也是一种阳离子离子载体。Nigericin sodium 可以触发 NALP3 炎性体的激活,可抑制高尔基体功能并抑制革兰氏阳性菌的生长。 | |||
T6S1367 | Reactive Oxygen Species NOD | ||
Procyanidin B2 (Proanthocyanidin B2) 是天然黄酮类物质,具有抗肿瘤,抗氧化等活性。 | |||
T13545 | Others | ||
Aluminum Hydroxide 是一种具有口服活性的铝佐剂的主要形式。它也可作为佐剂补偿亚单位疫苗的低固有免疫原性。基于它辅助的研究包括储存库效应、促吞噬作用和激活促炎症的 NLRP3 通路。 | |||
T5716 | advanced glycation end products | ||
4'-Methoxyresveratrol (4'-O-Methylresveratrol) 是一种多酚类化合物,来源于双翅目植物中,具有抗雄激素、抗真菌和抗炎症作用。它能抑制 RAGE- 介导的 MAPK/NF-κB 信号通路,并激活 NLRP3 炎性体,从而缓解 AGE- 诱导的炎症。 | |||
T11474 | RIP kinase | ||
GSK-843 (GSK'843) 是一种具有选择性和高效性的 RIP3 抑制剂,对 RIP3 激酶结构域的IC50 值为 8.6 nM。GSK-843 具有潜在的镇痛活性,抑制 CFA 小鼠 SDH 中 RIP3 和 NLRP3 的表达,可用于辅助治疗炎症。 | |||
T41245 | Reactive Oxygen Species NOD-like Receptor (NLR) TGF-beta/Smad | ||
Trimethylamine N-oxide (TMAO) 是由胆碱、甜菜碱和肉碱通过肠道微生物代谢产生的一种无色氧化胺,积聚在海洋动物的组织中,可预防尿素对蛋白质的破坏作用。Trimethylamine N-oxide 通过激活 ROS/NLRP3 炎性体诱导炎症,可诱导纤维细胞的分化和心脏纤维化。 | |||
T77675 | PARP Wnt/beta-catenin Antibiotic | ||
TNKS-2-IN-1 是一种 TNKS-2 抑制剂。TNKS-2-IN-1 对 TNKS-1 和 TNKS-2有抑制作用,IC50 分别为 259 nM 和 1100 nM。TNKS-2-IN-1 具有抗菌活性,对大肠杆菌和金黄色葡萄球菌具有抑制作用。TNKS-2-IN-1 抑制 NLRP3 炎症小体 (IC505μM)通过抑制ATP刺激的J1A.774细胞释放IL-1β。 | |||
T6454 | Others NF-κB NOD-like Receptor (NLR) | ||
CORM-3 是一种 CO 释放分子,能够减少 NLRP3炎症小体的激活,可以减弱 NF-κB p65的核异位,减少 ROS 的生成,并提高细胞内谷胱甘肽和超氧化物歧化酶的水平。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-01739 | NLRP3 Protein, Human, Recombinant (His) | Human | E. coli | ||
NLRP3 Protein, Human, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 27.7 kDa and the accession number is Q96P20.
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TMPH-02796 | NLRP3 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
NLRP3 Protein, Mouse, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 34.2 kDa and the accession number is Q8R4B8.
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TMPK-01228 | MARCO Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
Macrophage receptor with collagenous structure (MARCO) is the predominant scavenger receptor for recognition and binding of silica particles by alveolar macrophages (AM). MARCO contributes to normal cholesterol uptake in macrophages; therefore, in the absence of MARCO, macrophages are more susceptible to a greater inflammatory response by particulates known to cause NLRP3 inflammasome activation and the effect is due to increased LMP.
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TMPH-02521 | PYCARD Protein, Mouse, Recombinant (His & Myc) | Mouse | E. coli | ||
Functions as key mediator in apoptosis and inflammation. Promotes caspase-mediated apoptosis involving predominantly caspase-8 and also caspase-9 in a probable cell type-specific manner. Involved in activation of the mitochondrial apoptotic pathway, promotes caspase-8-dependent proteolytic maturation of BID independently of FADD in certain cell types and also mediates mitochondrial translocation of BAX and activates BAX-dependent apoptosis coupled to activation of caspase-9, -2 and -3. Involved in macrophage pyroptosis, a caspase-1-dependent inflammatory form of cell death and is the major constituent of the ASC pyroptosome which forms upon potassium depletion and rapidly recruits and activates caspase-1. In innate immune response believed to act as an integral adapter in the assembly of the inflammasome which activates caspase-1 leading to processing and secretion of proinflammatory cytokines. The function as activating adapter in different types of inflammasomes is mediated by the pyrin and CARD domains and their homotypic interactions. Required for recruitment of caspase-1 to inflammasomes containing certain pattern recognition receptors, such as NLRP2, NLRP3, AIM2 and probably IFI16. In the NLRP1 and NLRC4 inflammasomes seems not be required but facilitates the processing of procaspase-1. In cooperation with NOD2 involved in an inflammasome activated by bacterial muramyl dipeptide leading to caspase-1 activation. May be involved in DDX58-triggered proinflammatory responses and inflammasome activation. In collaboration with AIM2 which detects cytosolic double-stranded DNA may also be involved in a caspase-1-independent cell death that involves caspase-8. In adaptive immunity may be involved in maturation of dendritic cells to stimulate T-cell immunity and in cytoskeletal rearrangements coupled to chemotaxis and antigen uptake may be involved in post-transcriptional regulation of the guanine nucleotide exchange factor DOCK2; the latter function is proposed to involve the nuclear form. Also involved in transcriptional activation of cytokines and chemokines independent of the inflammasome; this function may involve AP-1, NF-kappa-B, MAPK and caspase-8 signaling pathways. For regulation of NF-kappa-B activating and inhibiting functions have been reported. Modulates NF-kappa-B induction at the level of the IKK complex by inhibiting kinase activity of CHUK and IKBK. Proposed to compete with RIPK2 for association with CASP1 thereby down-regulating CASP1-mediated RIPK2-dependent NF-kappa-B activation and activating interleukin-1 beta processing. Modulates host resistance to DNA virus infection, probably by inducing the cleavage of and inactivating CGAS in presence of cytoplasmic double-stranded DNA.
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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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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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