目录号 | 产品详情 | 靶点 | |
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T6671 | Apoptosis Sirtuin Autophagy | ||
Sirtinol 是一种 sirtuin 的抑制剂,对 ySir2,hSIRT2 和 hSIRT2 的IC50值分别为 48 μM,57.7 μM 和 131 μM。 | |||
T1919 | Mdm2 Dehydrogenase Sirtuin p53 Autophagy | ||
Tenovin-1 抑制 SirT1 和 SirT2 的蛋白质去乙酰化活性,并防止 MDM2 介导的 p53 降解,这涉及泛素化。它具有癌症的研究潜力。 | |||
T4108 | Sirtuin | ||
3-TYP (3-(1H-1,2,3-triazol-4-yl) pyridine) 是选择性SIRT3抑制剂,IC50值为 16 nM。它对 SIRT1 和 SIRT2 的选择性强,IC50值分别为 88 和 92 nM。 | |||
T5S1133 | Apoptosis Sirtuin | ||
Ganoderic acid D 是高度氧化的四环三萜,是灵芝的主要活性成分,可诱导 HeLa 人宫颈癌细胞凋亡。它上调 SIRT3的蛋白质表达并通过 SIRT3 诱导脱乙酰化的亲环蛋白 D 。它抑制结肠癌细胞的能量重编程,包括结肠癌细胞中的葡萄糖摄取,乳酸、丙酮酸和乙酰辅酶的产生。 | |||
T6111 | Sirtuin | ||
Selisistat (EX-527) 是一种去乙酰化酶 SIRT1 的抑制剂 (IC50=38 nM),具有有效性和特异性。Selisistat 可以用于神经系统疾病如亨廷顿舞蹈病的研究。 | |||
T4328 | HBV Sirtuin | ||
OSS_128167 (SIRT6-IN-1) 是一种选择性沉默调节蛋白 6 (SIRT6) 抑制剂,对 SIRT6,SIRT1 和 SIRT2 的 IC50分别为 89 μM,1578 μM 和 751 μM。它具有抗 HBV、抗癌、抗炎和抗病毒活性,可抑制 HBV 的转录和复制。 | |||
T6220 | Sirtuin Endogenous Metabolite | ||
Nicotinamide riboside Chloride 是维生素 B3 的来源,可以增强氧化代谢并防止高脂肪饮食诱导的代谢异常。它是具有口服活性的 NAD+的前体,增加 NAD+水平并激活SIRT1和SIRT3,可用于研究阿尔茨海默氏病的认知退化。 | |||
T1558 | Apoptosis Mitophagy IκB/IKK Lipoxygenase Sirtuin COX NADPH DNA/RNA Synthesis Nrf2 Antibacterial Antibiotic Autophagy Antifungal | ||
Resveratrol (SRT 501) 属于多酚类天然产物,是一种植物抗毒素,具有抗氧化和化学预防活性。Resveratrol 的靶点广泛,包括 COX、SIRT、LOC 等。Resveratrol 可以诱导细胞自噬和凋亡。 | |||
T2750 | MMP Sirtuin Endogenous Metabolite AMPK | ||
Ginkgolide C (BN-52022) 是从银杏叶中分离到的一种黄酮类天然产物,可增强体内大鼠的心脏功能,具有减少血小板聚集,改善阿尔兹海默症等作用。 | |||
T6371 | Apoptosis Sirtuin | ||
AGK2 是一种选择性SIRT2抑制剂,其IC50值为 3.5 μM。它抑制 SIRT1 和 SIRT3,IC50值分别为 30 和 91 μM。 |
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 | ||
The sirtuin SIRT5 resides primarily in the mitochondrial matrix and catalyzes the removal of negatively charged lysine acyl modifications; succinyl, malonyl, and glutaryl groups SIRT5 as a significant regulator of cellular homeostasis, in a context- and cell-type specific manner, as has been observed previously for other sirtuin family members. SIRT5 regulates protein substrates involved in glycolysis, the TCA cycle, fatty acid oxidation, electron transport chain, ketone body formation, nitrogenous waste management, and ROS detoxification, among other processes. SIRT5 plays pivotal roles in cardiac physiology and stress responses and is involved in the regulation of numerous aspects of myocardial energy metabolism. SIRT5 is implicated in neoplasia, as both a tumor promoter and suppressor in a context-specific manner, and may serve a protective function in the setting of neurodegenerative disorders. The SIRT5 downregulation is associated with increased succinylation and activity of ACOX1 and oxidative DNA damage response in hepatocellular carcinoma (HCC).
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TMPY-06954 | SIRT5 Protein, Human, Recombinant (His) | Human | E. coli | ||
The sirtuin SIRT5 resides primarily in the mitochondrial matrix and catalyzes the removal of negatively charged lysine acyl modifications; succinyl, malonyl, and glutaryl groups SIRT5 as a significant regulator of cellular homeostasis, in a context- and cell-type specific manner, as has been observed previously for other sirtuin family members. SIRT5 regulates protein substrates involved in glycolysis, the TCA cycle, fatty acid oxidation, electron transport chain, ketone body formation, nitrogenous waste management, and ROS detoxification, among other processes. SIRT5 plays pivotal roles in cardiac physiology and stress responses and is involved in the regulation of numerous aspects of myocardial energy metabolism. SIRT5 is implicated in neoplasia, as both a tumor promoter and suppressor in a context-specific manner, and may serve a protective function in the setting of neurodegenerative disorders. The SIRT5 downregulation is associated with increased succinylation and activity of ACOX1 and oxidative DNA damage response in hepatocellular carcinoma (HCC).
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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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