目录号 | 产品详情 | 靶点 | |
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T5838 | NO Synthase NOD | ||
L-Canavanine sulfate 是一种诱导型 NO 合酶的选择性抑制剂。 | |||
T10107 | NOS | ||
3-Bromo-7-nitroindazole 是有效的、选择性的神经元型一氧化氮合酶抑制剂,对 eNOS 或诱导型一氧化氮合酶的效果相对较弱。3-Bromo-7-nitroindazole 对全身和大脑中的细胞间信使一氧化氮的合成都有影响。 | |||
T1322 | Dopamine Receptor NO Synthase | ||
Bendazol (Dibazol) 是降压药物,能够提高 NO 合成酶在肾小球和集合小管中的活性。 | |||
T22724 | NOS NO Synthase Histamine Receptor | ||
Dimaprit dihydrochloride 是组胺H2受体的一种选择性激动剂,可刺激胃酸的分泌。它还抑制nNOS,IC50值为 49 μM。 | |||
T5S0285 | Others | ||
Cistanoside A 是一种肉苁蓉中的苯丙素类化合物,能够抑制 NO 的聚集,但不影响诱导型一氧化氮合酶 iNOS 的 mRNA 和蛋白水平及其活性。它具有抗炎作用。 | |||
T73353 | |||
NOS-IN-3 是一个强效的、选择性的由 imidamide 衍生的NOS 抑制剂,对iNOS 的IC50值为20 µM。 NOS-IN-3 不抑制eNOS,几乎没有毒性,可用于研究治疗可诱导亚型涉及的疾病,如感染性休克。 | |||
T61426 | |||
NOS-IN-2 (Compound 4i) 是一个强效的、选择性的由 imidamide 衍生的NOS 抑制剂,对iNOS 的IC50值为20 μM。NOS-IN-2 不抑制 eNOS,几乎没有毒性,可用于研究炎症性疾病。 | |||
T4808 | Endogenous Metabolite NO Synthase Imidazoline Receptor | ||
Agmatine sulfate (Agmatine sulfate salt) 是咪唑啉受体的内源性激动剂和一氧化氮合酶抑制剂。它靶向神经递质系统,离子通道和一氧化氮合成。 | |||
T2791 | Apoptosis Others NO Synthase Prostaglandin Receptor Interleukin | ||
Pectolinarin 抑制 IL-6和 IL-8分泌以及 PGE2和 NO 产生,可通过抑制 PI3K/Akt 途径来抑制细胞增殖和炎症反应并诱导凋亡,具有抗炎活性。 | |||
T7597 | Endogenous Metabolite NO Synthase NOD | ||
6-Biopterin (L-Biopterin) 是一种蝶呤衍生物,是一氧化氮合酶 (NO synthase) 辅因子。 |
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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