目录号 | 产品详情 | 靶点 | |
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T5684 | Apoptosis Others Reactive Oxygen Species HIF/HIF Prolyl-Hydroxylase NO Synthase Autophagy | ||
Ethyl 3,4-dihydroxybenzoate 是从花生种子的种皮中发现的脯氨酰羟化酶抑制剂,是一种抗氧化剂。它是胶原蛋白合成抑制剂,具有骨骼保护作用。它通过激活 NO 合酶并产生线粒体 ROS 来保护心肌,可诱导 ESCC 细胞自噬和凋亡。 | |||
T3918 | NF-κB COX NO Synthase | ||
Ginsenoside Rb3 (Gypenoside IV) 是从三七中提取的一种天然产物。它在 293T 细胞系中抑制 TNFα 诱导的NF-κB 转录活性,IC50为 8.2 μM。它还抑制COX-2和iNOSmRNA 的诱导。 | |||
T3779 | Caspase COX NO Synthase | ||
Crocin II (Crocetin gentiobiosylglucosyl ester) 是从栀子果实中分离出来的一种天然产物,具有抗氧化、抗癌和抗抑郁活性。它抑制 iNOS 和 COX-2的蛋白质和 m-RNA 的表达,还抑制NO 产生,IC50值为 31.1 μM。 | |||
T3805 | TNF COX JAK NO Synthase | ||
Prim-O-glucosylcimifugin (Cimifugin 7-glucoside) 具有强效的抗炎作用。通过调节 JAK2/STAT3 信号传导可抑制iNOS 和COX-2表达。 | |||
T3811 | P450 cell cycle arrest COX NO Synthase | ||
Ginsenoside C-K (Ginsenoside K) 是 Ginsenoside Rb1 的细菌代谢物,可通过抑制诱生型一氧化氮合酶和COX-2来发挥抗炎作用。它在人肝微粒体中抑制CYP2C9和CYP2A6活性,IC50分别为 32.0±3.6 和 63.6±4.2 μM。 | |||
T1102 | Glucocorticoid Receptor Estrogen/progestogen Receptor Progesterone Receptor NO Synthase Autophagy | ||
Mifepristone (C-1073) 是一种黄体酮受体和糖皮质激素受体拮抗剂,在体外实验中的 IC50值分别为 0.2 nM 和 2.6 nM。 | |||
T3S0401 | Arginase NO Synthase | ||
Piceatannol 3'-O-glucoside (Piceatannol 3-glycoside) 是大黄的一种活性成分,通过抑制精氨酸酶活性激活内皮细胞一氧化氮合酶,抑制Arginase I 和Arginase II,IC50值分别为 11.22 和 11.06 μM。它可增加肺血氧分压,减少肺间质水肿,从而保护肺损伤。 | |||
T2758 | Others TNF COX NO Synthase Interleukin | ||
Madecassic acid (L-fucopyranose) 是分离自积雪草的一种天然产物,抑制iNOS、COX-2、TNF-α、IL-1beta 和IL-6,可通过在 RAW 264.7 巨噬细胞中下调NF-κB 激活而具有抗炎作用。 | |||
T5S0754 | NF-κB Wnt/beta-catenin NO Synthase | ||
Isoquercetin (3-Glucosylquercetin) 是天然存在的多酚,具有抗氧化,抗增殖和抗炎特性。它通过调节核因子-κB 转录调节系统调节一氧化氮合酶 2 的表达。它通过 Nrf2/ARE 抗氧化剂信号传导途径减轻乙醇诱导的肝毒性,氧化应激和炎症反应。它具有高生物利用度和低毒性,是预防糖尿病妊娠出生缺陷的有希望的候选药物。 | |||
T22419 | NOS NO Synthase HSV | ||
S-Methylisothiourea sulfate ((S)-Methylisothiourea sulfate) 是一种选择性 iNOS 抑制剂,在感染性休克的啮齿动物模型中发挥有益作用。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-01733 | DDAH2 Protein, Human, Recombinant (GST & His) | Human | E. coli | ||
Hydrolyzes N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA) which act as inhibitors of NOS. Has therefore a role in the regulation of nitric oxide generation.
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TMPH-01732 | DDAH1 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Hydrolyzes N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA) which act as inhibitors of NOS. Has therefore a role in the regulation of nitric oxide generation.
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TMPY-03172 | Argininosuccinate lyase Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
The recycling of citrulline by argininosuccinate synthase 1 (ASS1) and argininosuccinate lyase (ASL) is crucial to maintain arginine availability and nitric oxide (NO) production. Nitric oxide (NO) plays an established role in numerous physiological and pathological processes, but the specific cellular sources of NO in disease pathogenesis remain unclear, preventing the implementation of NO-related therapy. Argininosuccinate lyase (ASL) is the only enzyme able to produce arginine, the substrate for NO generation by nitric oxide synthase (NOS) isoforms. Induction of endogenous NO production by enterocytes with supplements that upregulate ASL expression and complement its substrates results in improved epithelial integrity and alleviation of colitis and of inflammation-associated colon cancer.
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TMPH-02526 | Arginase-2/ARG2 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
May play a role in the regulation of extra-urea cycle arginine metabolism and also in down-regulation of nitric oxide synthesis. Extrahepatic arginase functions to regulate L-arginine bioavailability to nitric oxid synthase (NOS). Arginine metabolism is a critical regulator of innate and adaptive immune responses. Seems to be involved in negative regulation of the survival capacity of activated CD4(+) and CD8(+) T cells. May suppress inflammation-related signaling in asthmatic airway epithelium. May contribute to the immune evasion of H.pylori by restricting M1 macrophage activation and polyamine metabolism. May play a role in promoting prenatal immune suppression. Regulates RPS6KB1 signaling, which promotes endothelial cell senescence and inflammation and implicates NOS3/eNOS dysfunction. Can inhibit endothelial autophagy independently of its enzymatic activity implicating mTORC2 signaling. Involved in vascular smooth muscle cell senescence and apoptosis independently of its enzymatic activity.
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TMPH-02525 | Arginase-1/ARG1 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
Key element of the urea cycle converting L-arginine to urea and L-ornithine, which is further metabolized into metabolites proline and polyamides that drive collagen synthesis and bioenergetic pathways critical for cell proliferation, respectively; the urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.; Functions in L-arginine homeostasis in nonhepatic tissues characterized by the competition between nitric oxide synthase (NOS) and arginase for the available intracellular substrate arginine. Arginine metabolism is a critical regulator of innate and adaptive immune responses. Involved in an antimicrobial effector pathway in polymorphonuclear granulocytes (PMN). Upon PMN cell death is liberated from the phagolysosome and depletes arginine in the microenvironment leading to suppressed T cell and natural killer (NK) cell proliferation and cytokine secretion. In group 2 innate lymphoid cells (ILC2s) promotes acute type 2 inflammation in the lung and is involved in optimal ILC2 proliferation but not survival. Plays a role in the immune response of alternatively activated or M2 macrophages in processes such as wound healing and tissue regeneration, immune defense against multicellular pathogens and parasites, and immune suppression and allergic inflammation; the regulatory outcome seems to be organ specific. In tumor-infiltrating dendritic cells (DCs) and myeloid-derived suppressor cells (MDSCs) plays a role in suppression of T cell-mediated antitumor immunity.
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TMPH-02524 | Arginase-1/ARG1 Protein, Mouse, Recombinant (His) | Mouse | Yeast | ||
Key element of the urea cycle converting L-arginine to urea and L-ornithine, which is further metabolized into metabolites proline and polyamides that drive collagen synthesis and bioenergetic pathways critical for cell proliferation, respectively; the urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.; Functions in L-arginine homeostasis in nonhepatic tissues characterized by the competition between nitric oxide synthase (NOS) and arginase for the available intracellular substrate arginine. Arginine metabolism is a critical regulator of innate and adaptive immune responses. Involved in an antimicrobial effector pathway in polymorphonuclear granulocytes (PMN). Upon PMN cell death is liberated from the phagolysosome and depletes arginine in the microenvironment leading to suppressed T cell and natural killer (NK) cell proliferation and cytokine secretion. In group 2 innate lymphoid cells (ILC2s) promotes acute type 2 inflammation in the lung and is involved in optimal ILC2 proliferation but not survival. Plays a role in the immune response of alternatively activated or M2 macrophages in processes such as wound healing and tissue regeneration, immune defense against multicellular pathogens and parasites, and immune suppression and allergic inflammation; the regulatory outcome seems to be organ specific. In tumor-infiltrating dendritic cells (DCs) and myeloid-derived suppressor cells (MDSCs) plays a role in suppression of T cell-mediated antitumor immunity.
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