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，其它细胞系，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)
Garcinol promotes neurogenesis in rat cortical progenitor cells through the duration of extracellular signal-regulated kinase signaling. Journal of agricultural and food chemistry 2011 MAR
Abstract
Garcinol is a polyisoprenylated benzophenone derivative found in Garcinia indica fruit rind and other species. The potential antioxidative and neuroprotective effects of garcinol in rat cortical astrocyte were demonstrated in our laboratory recently. Here, the effects of garcinol on the neuritogenesis process in cultured cortical progenitor cells were investigated to understand the roles of garcinol in neuronal survival and differentiation. These cells, derived from embryonic day 17 rats, differentiated into EGF-responsive neural precursor cells, would further form neurospheres. Our data exhibited garcinol induced neurite outgrowth in early developing EGF-treated neurospheres and significantly enhanced the expression of neuronal proteins, microtubule-associated protein 2 (MAP-2), and glial fibrillary acidic protein (GFAP). Furthermore, the neuronal marker, high-molecular-weight subunit of neurofilaments (NFH), was highly expressed after 5 μM garcinol treatment in neural precursor cells for 20 days. To identify the extracellular mechanism, rat cortical progenitor cells were treated garcinol and accordingly mediated the sustained activation of extracellular signal-regulated kinase (ERK) for different periods up to 20 h. In this regard, NMDA receptor-mediated calcium influx led to excitotoxic death and activated tyrosine phosphatase which limited the duration of ERK in cultured neurons. MK801, the NMDA receptor antagonist, treatment also induced the sustained phosphorylation of ERK and therefore enhanced neuronal survival. In our observation, garcinol treatment reduced growth factor deprivation-mediated cell death and nuclear import of C/EBPβ levels. Noteworthy, garcinol could promote neurite outgrowth in EGF-responsive neural precursor cells and modulate the ERK pathway in the enhancement of neuronal survival.
Ex vivo expansion of human hematopoietic stem cells by garcinol, a potent inhibitor of histone acetyltransferase. PloS one 2011 JAN
Abstract
BACKGROUND: Human cord blood (hCB) is the main source of hematopoietic stem and progenitor cells (HSCs/PCs) for transplantation. Efforts to overcome relative shortages of HSCs/PCs have led to technologies to expand HSCs/PCs ex vivo. However, methods suitable for clinical practice have yet to be fully established. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we screened biologically active natural products for activity to promote expansion of hCB HSCs/PCs ex vivo, and identified Garcinol, a plant-derived histone acetyltransferase (HAT) inhibitor, as a novel stimulator of hCB HSC/PC expansion. During a 7-day culture of CD34(+)CD38(-) HSCs supplemented with stem cell factor and thrombopoietin, Garcinol increased numbers of CD34(+)CD38(-) HSCs/PCs more than 4.5-fold and Isogarcinol, a derivative of Garcinol, 7.4-fold. Furthermore, during a 7-day culture of CD34(+) HSCs/PCs, Garcinol expanded the number of SCID-repopulating cells (SRCs) 2.5-fold. We also demonstrated that the capacity of Garcinol and its derivatives to expand HSCs/PCs was closely correlated with their inhibitory effect on HAT. The Garcinol derivatives which expanded HSCs/PCs inhibited the HAT activity and acetylation of histones, while inactive derivatives did not. CONCLUSIONS/SIGNIFICANCE: Our findings identify Garcinol as the first natural product acting on HSCs/PCs and suggest the inhibition of HAT to be an alternative approach for manipulating HSCs/PCs.
Cryptococcus neoformans histone acetyltransferase Gcn5 regulates fungal adaptation to the host. Eukaryotic cell 2010 AUG
Abstract
Cryptococcus neoformans is an environmental fungus and an opportunistic human pathogen. Previous studies have demonstrated major alterations in its transcriptional profile as this microorganism enters the hostile environment of the human host. To assess the role of chromatin remodeling in host-induced transcriptional responses, we identified the C. neoformans Gcn5 histone acetyltransferase and demonstrated its function by complementation studies of Saccharomyces cerevisiae. The C. neoformans gcn5Delta mutant strain has defects in high-temperature growth and capsule attachment to the cell surface, in addition to increased sensitivity to FK506 and oxidative stress. Treatment of wild-type cells with the histone acetyltransferase inhibitor garcinol mimics cellular effects of the gcn5Delta mutation. Gcn5 regulates the expression of many genes that are important in responding to the specific environmental conditions encountered by C. neoformans inside the host. Accordingly, the gcn5Delta mutant is avirulent in animal models of cryptococcosis. Our study demonstrates the importance of chromatin remodeling by the conserved histone acetyltransferase Gcn5 in regulating the expression of specific genes that allow C. neoformans to respond appropriately to the human host.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 78824-30-3 |
| Chemical Formula | C₃₈H₅₀O₆ |
| 纯度 | ≥ 95% |
| Target | HAT |
| Pathway | Epigenetic |
