目录号 | 产品详情 | 靶点 | |
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T76111 | |||
Hexokinase(ScHEX1) 是一种糖酵解酶己糖激酶,收到 N-乙酰氨基葡萄糖的抑制。N-乙酰氨基葡萄糖对 Hexokinase(ScHEX1) 的抑制导致其与线粒体外膜分离,而导致 NLRP3炎症小体激活。 | |||
T62182 | |||
NIC-0102 是一种口服具有活力的蛋白酶体 (proteasome) 抑制剂 (pIC50:7.55),对 NLRP3 炎症小体激活表现出特异性抑制作用。NIC-0102 对 DSS 诱导的溃疡性结肠炎模型表现出有效的体内抗炎活性。NIC-0102 对前 IL-1β 的产生具有抑制作用。 | |||
T62139 | |||
NDT-30805 是一种三唑吡啶酮衍生物,对 PBMC 中 IL-1β的释放具有抑制作用 (IC50: 0.013 μM)。NDT-30805 也是一种 NLRP3 inflammasome 的选择性抑制剂。NDT-30805 能够用于研究炎症和免疫。 | |||
T73058 | |||
Cloxacillin 是一种口服有效的抗菌剂和β-lactamase 抑制剂,其IC50值为 0.04 µM。Cloxacillin 可通过抑制MAPKs、NF-кB 和NLRP3相关蛋白的激活从而抑制金黄色葡萄球菌所引起的炎症反应。 | |||
T78061 | Gap Junction Protein | ||
Peptide5 TFA,一种connexin 43模拟肽,能够降低动物脊髓损伤后的肿胀、抑制星形胶质细胞增生和神经元死亡。该化合物还可抑制NLRP3炎症小体,具有抗炎作用。 | |||
T16323 | Others | ||
Nigericin is an antibiotic derived from Streptomyces hygroscopicus that acts as a K+/H+ ionophore, promoting K+/H+ exchange across mitochondrial membranes. Nigericin can be an NLRP3 activator that causes the release of IL-1β as a NALP3-dependent manner. N | |||
T79585 | NF-κB | ||
Anti-inflammatory agent 50 (compound a1)是Fusidic acid的衍生物,有效抑制NO、IL-6及TNF-α等炎症因子,调控炎症介质及抑制MAPK、NF-κB和NLRP3炎症小体信号通路,从而减轻急性肺损伤。 | |||
T78056 | |||
HMGB1-IN-1(化合物6)在RAW264.7细胞中具有显著的NO抑制活性,其IC50为15.9 ± 0.6 μM。该化合物能够抑制HMGB1/NF-κB/NLRP3信号通路,并且在肾损伤模型中展现出优异的抗炎及抗脓毒症效果。 | |||
T60356 | |||
Stavudine (d4T) sodium 是一种口服活性核苷逆转录酶抑制剂 (NRTI), 具有抗HIV-1和HIV-2的活性。Stavudine sodium 还抑制线粒体 DNA (mtDNA) 的复制。Stavudine sodium 降低 NLRP3 炎症小体激活并调节淀粉样 β 自噬。Stavudine sodium 诱导细胞凋亡。 | |||
T81637 | NOD-like Receptor (NLR) | ||
NT-0796为一种选择性穿透中枢神经系统的NLRP3炎性体抑制剂,其PBMC方法中的IC50值为0.32 nM。该化合物为异丙酯类,能够在细胞内转化为NDT-197959(羧酸活性物)。NT-0796在神经炎症疾病研究中显示出潜力。 |
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-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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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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