EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72452_C
表观遗传修饰剂；抑制组蛋白乙酰转移酶 (HAT) p300 和 pCAF
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总览
Garcinol 是组蛋白乙酰转移酶 (HAT) p300 和 pCAF 的抑制剂（IC₅₀ 分别为 7 μM 和 5 μM）（Balasubramanyam et al.）。它还能抑制新型隐球菌中的 HAT GCN5，从而诱导温度敏感性并抑制其生长（O’Meara et al.）。
维持和自我更新
·促进人造血干细胞的体外扩增（Nishino et al.）。
分化
·促进大鼠皮质祖细胞的神经发生（Weng et al.）。
癌症
·诱导多种癌细胞凋亡，并具有抗炎作用 (Koeberle et al.; Prasad et al.)。
细胞类型
癌细胞及细胞系，造血干/祖细胞，神经干/祖细胞，神经元
种属
人，小鼠，非人灵长类，其他物种，大鼠
应用
分化，扩增
研究领域
癌症，神经科学，干细胞生物学
CAS 编号
78824-30-3
化学式
C₃₈H₅₀O₆
纯度
≥ 95 %
通路
表观遗传学
靶点
HAT
产品说明书及文档
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应用领域
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相关材料与文献
技术资料 (2)
文献 (6)
Polyisoprenylated benzophenone, garcinol, a natural histone acetyltransferase inhibitor, represses chromatin transcription and alters global gene expression.
The Journal of biological chemistry 2004 AUG
Abstract
Histone acetylation is a diagnostic feature of transcriptionally active genes. The proper recruitment and function of histone acetyltransferases (HATs) and deacetylases (HDACs) are key regulatory steps for gene expression and cell cycle. Functional defects of either of these enzymes may lead to several diseases,including cancer. HATs and HDACs thus are potential therapeutic targets. Here we report that garcinol,a polyisoprenylated benzophenone derivative from Garcinia indica fruit rind,is a potent inhibitor of histone acetyltransferases p300 (IC50 approximately 7 microm) and PCAF (IC50 approximately 5 microm) both in vitro and in vivo. The kinetic analysis shows that it is a mixed type of inhibitor with an increased affinity for PCAF compared with p300. HAT activity-dependent chromatin transcription was strongly inhibited by garcinol,whereas transcription from DNA template was not affected. Furthermore,it was found to be a potent inducer of apoptosis,and it alters (predominantly down-regulates) the global gene expression in HeLa cells.
Identification of 5-lipoxygenase and microsomal prostaglandin E2 synthase-1 as functional targets of the anti-inflammatory and anti-carcinogenic garcinol.
Biochemical pharmacology 2009 MAY
Abstract
Garcinol (camboginol) from the fruit rind of Guttiferae species shows anti-carcinogenic and anti-inflammatory properties,but the underlying molecular mechanisms are unclear. Here we show that garcinol potently interferes with 5-lipoxygenase (EC 7.13.11.34) and microsomal prostaglandin (PG)E2 synthase (mPGES)-1 (EC 5.3.99.3),enzymes that play pivotal roles in inflammation and tumorigenesis. In cell-free assays,garcinol inhibited the activity of purified 5-lipoxygenase and blocked the mPGES-1-mediated conversion of PGH2 to PGE2 with IC50 values of 0.1 and 0.3 microM,respectively. Garcinol suppressed 5-lipoxygenase product formation also in intact human neutrophils and reduced PGE2 formation in interleukin-1beta-stimulated A549 human lung carcinoma cells as well as in human whole blood stimulated by lipopolysaccharide. Moreover,garcinol interfered with isolated cyclooxygenase (COX)-1 (EC 1.14.99.1,IC50 = 12 microM) and with the formation of COX-1-derived 12(S)-hydroxy-5-cis-8,10-trans-heptadecatrienoic acid and thromboxane B2 in human platelets. In contrast,neither Ca2+-ionophore (A23187)-induced arachidonic acid release in neutrophils nor COX-2 activity in A549 cells or whole blood,measured as formation of 6-keto PGF1alpha,or isolated human recombinant COX-2 were significantly affected by garcinol (textless or = 30 microM). Together,the high potency of garcinol to selectively suppress PGE2 synthesis and 5-lipoxygenase product formation provides a molecular basis for the anti-inflammatory and anti-carcinogenic effects of garcinol and rationalizes its therapeutic use.
Garcinol potentiates TRAIL-induced apoptosis through modulation of death receptors and antiapoptotic proteins.
Molecular cancer therapeutics 2010 APR
Abstract
Whether garcinol,the active component of Garcinia indica,can modulate the sensitivity of cancer cells to TRAIL,a cytokine currently in phase II clinical trial,was investigated. We found that garcinol potentiated TRAIL-induced apoptosis of cancer cells as indicated by intracellular esterase activity,DNA strand breaks,accumulation of the membrane phospholipid phosphatidylserine,mitochondrial activity,and activation of caspase-8,-9,and -3. We found that garcinol,independent of the cell type,induced both of the TRAIL receptors,death receptor 4 (DR4) and DR5. Garcinol neither induced the receptors on normal cells nor sensitized them to TRAIL. Deletion of DR5 or DR4 by small interfering RNA significantly reduced the apoptosis induced by TRAIL and garcinol. In addition,garcinol downregulated various cell survival proteins including survivin,bcl-2,XIAP,and cFLIP,and induced bid cleavage,bax,and cytochrome c release. Induction of death receptors by garcinol was found to be independent of modulation of CCAAT/enhancer-binding protein-homologous protein,p53,bax,extracellular signal-regulated kinase,or c-Jun-NH(2)-kinase. The effect of garcinol was mediated through the generation of reactive oxygen species,in as much as induction of both death receptors,modulation of antiapoptotic and proapoptotic proteins,and potentiation of TRAIL-induced apoptosis were abolished by N-acetyl cysteine and glutathione. Interestingly,garcinol also converted TRAIL-resistant cells into TRAIL-sensitive cells. Overall,our results indicate that garcinol can potentiate TRAIL-induced apoptosis through upregulation of death receptors and downregulation of antiapoptotic proteins. Mol Cancer Ther; 9(4); 856-68. (c)2010 AACR.
更多信息
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
|---|---|
| Cas Number | 78824-30-3 |
| Chemical Formula | C₃₈H₅₀O₆ |
| 纯度 | ≥ 95 % |
| Target | HAT |
| Pathway | Epigenetic |
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