目录号 | 产品详情 | 靶点 | |
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T15697 | NOS | ||
L-NMMA acetate (Tilarginine acetate) 是一氧化氮合酶抑制剂, 对其所有亚型均有抑制作用,包括 NOS1,NOS2和 NOS3。与 nNOS (大鼠), eNOS (人), 和 iNOS (小鼠)结合 的 Ki 值分别为0.18,0.4,6 µM。 | |||
T2980 | MMP Others Endogenous Metabolite NO Synthase | ||
Chondroitin sulfate (Chonsurid) 是一种糖胺聚糖,被广泛用于骨关节炎的研究。它能够减少炎症介质和凋亡过程,并能够减少炎性细胞因子,iNOS 和MMPs 产生。 | |||
TN2139 | NOS COX NO Synthase | ||
Regaloside B 是从麝香百合中分离出来的一种苯丙烷,可抑制iNOS 和COX-2的表达,具有抗炎活性。 | |||
T2S2335 | Others NF-κB COX PGE Synthase NO Synthase | ||
Dehydroevodiamine (DHED) 是从吴茱萸中分离出的一种喹唑啉生物碱,可抑制 LPS 诱导的小鼠巨噬细胞中iNOS、COX-2、PGE2和NF-κB 的表达,对豚鼠心室肌细胞具有抗心律失常作用。 | |||
T21507 | P450 NO Synthase | ||
7-Ethoxyresorufin (Resorufin ethyl ether) 是细胞色素 P450 (尤其是CYP1A1) 的荧光底物和竞争性抑制剂,同时对 NO 合酶具有抑制作用。 | |||
T3491 | NOS NO Synthase | ||
1400W dihydrochloride (N-(3-(Aminomethyl)benzyl)acetamidine) 是高效选择性的诱导型一氧化氮合成酶抑制剂(Ki:7 nM)。 | |||
T3S0364 | IL Receptor Endogenous Metabolite NO Synthase | ||
L-Arginine (L-Arg) 是内皮型一氧化氮合酶(eNOS) 的底物。L-Arginine 通过阳离子氨基酸转运体家族转运到血管平滑肌细胞,并被代谢成一氧化氮、多胺或 L-脯氨酸。 | |||
T19853 | Others | ||
Dimethoxycurcumin (Veratrylcurcuminoid) 是 curcumin 衍生物,拥有抗氧化及抗炎作用。 | |||
T1310 | Thyroid hormone receptor(THR) NO Synthase | ||
2-Thiouracil (Deracil) 是神经型一氧化氮合酶 (nNOS) 的选择性抑制剂(Ki:20 μM),是一种抗甲状腺化合物,可用作高度特异性的黑色素瘤探测物。 | |||
T1479 | Others NO Synthase | ||
Isosorbide dinitrate (Isordil) 是 NO 供体,可预防心肌梗死 (MI) 引起的左室重构及心功能退化。 |
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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