目录号 | 产品详情 | 靶点 | |
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T60064 | EGFR Sirtuin | ||
WAY-270360 (N-[4-(1H-benzimidazol-2-yl)phenyl]-2,4-dimethoxybenzamide) 是一种 Sirtuin 调节剂和一种表皮生长因子受体 (EGFR) 抑制剂。 | |||
T77653 | Sirtuin | ||
Z26395438 是 一种 IC50 值为 1.6 μM 的 Sirtuin-1 的抑制剂。 | |||
T12920 | Sirtuin | ||
Sirt2-IN-1 是 sirtuin 2 的抑制剂 (IC50 = 163 nM)。 | |||
T60001 | Sirtuin | ||
Benzamide, 3-methoxy-N-(3-thiazolo[5,4-b]pyridin-2-ylphenyl) (3-methoxy-N-(3-(thiazolo[5,4-b]pyridin-2-yl)phenyl)benzamide) 是一种 sirtuin 调节剂,可用于延长细胞寿命,治疗和/或预防多种 疾病和障碍包括糖尿病、心血管疾病、凝血障碍、炎症、癌症等。 | |||
Fr13587 | |||
7-Chloro-4-(piperazin-1-yl)quinolone 结构是药物化学中的重要支架,它单独或与其他活性药效团混合显示出多种药理特性。7-Chloro-4-(piperazin-1-yl)quinolone 是有效的sirtuin 抑制剂,并且抑制 5-羟色胺的摄取,IC50值为 50 μM。7-Chloro-4-(piperazin-1-yl)quinolone 对恶性疟原虫 D10 和 K1 菌株表现出抗疟疾活性,IC50分别为 1.18 μM 和 0.97 μM。 | |||
T4S0800 | P450 NOS NF-κB HIF AMPK | ||
Demethyleneberberine 是从黄连中提取的一种天然产物,是线粒体靶向抗氧化剂。它也可作为AMPK 激活剂,用于非酒精性脂肪性肝病的研究。它通过抑制NF-κB 通路和调节 Th 细胞的平衡来减轻小鼠结肠炎并抑制炎症反应。 | |||
T15610 | Others | ||
JFD00244 is an inhibitor of sirtuin 2 (SIRT2). It has an anti-tumor effect. | |||
T78857 | Sirtuin | ||
SIRT5 inhibitor9 (compound 14) 作为SIRT5的一种竞争性抑制剂,其IC50为4.07 μM,显示出潜在的抗癌效应。 | |||
T26259 | |||
Tenovin-D3 is a sirtuin SirT2 inhibitor. It acts by increasing p21 (CDKN1A) expression in a p53-independent manner. | |||
T78856 | Sirtuin | ||
SIRT5 inhibitor8 (compound 10) 作为竞争性去乙酰化酶SIRT5抑制剂,显示出IC50值为5.38 μM的抑制活性,并可能具有抗癌潜力。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-05241 | SIRT5 Protein, Human, Recombinant (Flag) | Human | E. coli | ||
SIRT5 Protein, Human, Recombinant (Flag) is expressed in E. coli expression system with Flag tag. The predicted molecular weight is 34.9 kDa and the accession number is A0A024R012.
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TMPY-06954 | SIRT5 Protein, Human, Recombinant (His) | Human | E. coli | ||
SIRT5 Protein, Human, Recombinant (His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 30.78 kDa and the accession number is NP_036373.1.
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TMPY-01869 | SIRT1 Protein, Human, Recombinant (His) | Human | E. coli | ||
SIRT1 belongs to the sirtuin family. Members of the sirtuin family are characterized by a sirtuin core domain and grouped into four classes. SIRT1 is included in class I of the sirtuin family. It is a NAD-dependent protein deacetylase, which regulates processes such as apoptosis and muscle differentiation by deacetylating key proteins. It deacetylates 'Lys-382' of p53/TP53 and impairs its ability to induce proapoptotic program and modulate cell senescence. SIRT1 also deacetylates TAF1B and thereby represses rDNA transcription by the RNA polymerase I. It is involved in HES1- and HEY2-mediated transcriptional repression. SIRT1 inhibits skeletal muscle differentiation by deacetylating PCAF and MYOD1. It may serve as a sensor of the cytosolic ratio of NAD(+)/NADH, which is essential in skeletal muscle cell differentiation. It also deacetylates 'Lys-16' of histone H4 (in vitro). Component of the eNoSC (energy-dependent nucleolar silencing) complex, a complex that mediates silencing of rDNA in response to intracellular energy status and acts by recruiting histone-modifying enzymes. The eNoSC complex is able to sense the energy status of cell: upon glucose starvation, elevation of NAD(+)/NADP(+) ratio activates SIRT1, leading to histone H3 deacetylation followed by dimethylation of H3 at 'Lys-9' (H3K9me2) by SUV39H1 and the formation of silent chromatin in the rDNA locus.
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TMPY-02893 | NT5C3A/NT5C3 Protein, Human, Recombinant | Human | E. coli | ||
NT5C3A (5'-Nucleotidase, Cytosolic IIIA) is a Protein Coding gene. This gene encodes a member of the 5'-nucleotidase family of enzymes that catalyze the dephosphorylation of nucleoside 5'-monophosphates. The encoded protein is the type 1 isozyme of pyrimidine 5' nucleotidase and catalyzes the dephosphorylation of pyrimidine 5' monophosphates. NT5C3A expression required both an intronic IFN-stimulated response element and the IFN-stimulated transcription factor IRF1. Overexpression of NT5C3A, but not of its catalytic mutants, suppressed IL-8 production by HEK293 cells. NT5C3A-stimulated sirtuin activity resulted in deacetylation of histone H3 and the NF-kappaB subunit RelA (also known as p65), both of which were associated with the proximal region of the Il8 promoter, thus repressing the transcription of Il8 Together.
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