EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72432_C
缺氧诱导因子-1α（HIF1α）抑制剂
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总览
CAY10585 以浓度和时间依赖性方式抑制缺氧诱导因子 1 (HIF-1) 的积累，并显著抑制 HIF-1 靶基因的转录活性（Lee et al.）。
分化
·抑制 BMP9 和 HIF-1 诱导的间充质干细胞成骨分化（Hu et al.）。
·挽救 Fgfr1(-/-) 小鼠胚胎干细胞的心肌细胞分化（Crescini et al.）。
细胞类型
心肌细胞，PSC衍生，间充质干/祖细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
分化
研究领域
干细胞生物学
CAS 编号
934593-90-5
化学式
C₂₆H₂₉NO₅
纯度
≥ 97 %
通路
HIF-1
靶点
HIF1α
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 (3)
文献 (5)
Ascorbic acid rescues cardiomyocyte development in Fgfr1(-/-) murine embryonic stem cells. Biochimica et biophysica acta 2013 JAN
Abstract
Fibroblast growth factor receptor 1 (Fgfr1) gene knockout impairs cardiomyocyte differentiation in murine embryonic stem cells (mESC). Here, various chemical compounds able to enhance cardiomyocyte differentiation in mESC [including dimethylsulfoxide, ascorbic acid (vitC), free radicals and reactive oxygen species] were tested for their ability to rescue the cardiomyogenic potential of Fgfr1(-/-) mESC. Among them, only the reduced form of vitC, l-ascorbic acid, was able to recover beating cell differentiation in Fgfr1(-/-) mESC. The appearance of contracting cells was paralleled by the expression of early and late cardiac gene markers, thus suggesting their identity as cardiomyocytes. In the attempt to elucidate the mechanism of action of vitC on Fgfr1(-/-) mESC, we analyzed several parameters related to the intracellular redox state, such as reactive oxygen species content, Nox4 expression, and superoxide dismutase activity. The results did not show any relationship between the antioxidant capacity of vitC and cardiomyocyte differentiation in Fgfr1(-/-) mESC. No correlation was found also for the ability of vitC to modulate the expression of pluripotency genes. Then, we tested the hypothesis that vitC was acting as a prolyl hydroxylase cofactor by maintaining iron in a reduced state. We first analyze hypoxia inducible factor (HIF)-1α mRNA and protein levels that were found to be slightly upregulated in Fgfr1(-/-) cells. We treated mESC with Fe(2+) or the HIF inhibitor CAY10585 during the first phases of the differentiation process and, similar to vitC, the two compounds were able to rescue cardiomyocyte formation in Fgfr1(-/-) mESC, thus implicating HIF-1α modulation in Fgfr1-dependent cardiomyogenesis.
BMP9-regulated angiogenic signaling plays an important role in the osteogenic differentiation of mesenchymal progenitor cells. Journal of cell science 2013 JAN
Abstract
Mesenchymal stromal progenitor cells (MSCs) are multipotent progenitors that can be isolated from numerous tissues. MSCs can undergo osteogenic differentiation under proper stimuli. We have recently demonstrated that bone morphogenetic protein 9 (BMP9) is one of the most osteogenic BMPs. As one of the least studied BMPs, BMP9 has been shown to regulate angiogenesis in endothelial cells. However, it is unclear whether BMP9-regulated angiogenic signaling plays any important role in the BMP9-initiated osteogenic pathway in MSCs. Here, we investigate the functional role of hypoxia-inducible factor 1α (HIF1α)-mediated angiogenic signaling in BMP9-regulated osteogenic differentiation of MSCs. We find that BMP9 induces HIF1α expression in MSCs through Smad1/5/8 signaling. Exogenous expression of HIF1α potentiates BMP9-induced osteogenic differentiation of MSCs both in vitro and in vivo. siRNA-mediated silencing of HIF1α or HIF1α inhibitor CAY10585 profoundly blunts BMP9-induced osteogenic signaling in MSCs. HIF1α expression regulated by cobalt-induced hypoxia also recapitulates the synergistic effect between HIF1α and BMP9 in osteogenic differentiation. Mechanistically, HIF1α is shown to exert its synergistic effect with BMP9 by inducing both angiogenic signaling and osteogenic signaling in MSCs. Thus, our findings should not only expand our understanding of the molecular basis behind BMP9-regulated osteoblastic lineage-specific differentiation, but also provide an opportunity to harness the BMP9-induced synergy between osteogenic and angiogenic signaling pathways in regenerative medicine.
(Aryloxyacetylamino)benzoic acid analogues: A new class of hypoxia-inducible factor-1 inhibitors. Journal of medicinal chemistry 2007 APR
Abstract
Structural modification of a compound discovered during screening using an HRE-dependent reporter assay has revealed a novel class of HIF-1 inhibitors, which potently inhibit the HIF-1alpha protein accumulation and its target gene expression under hypoxic conditions in human hepatocellular carcinoma Hep3B cells.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 934593-90-5 |
| Chemical Formula | C₂₆H₂₉NO₅ |
| 纯度 | ≥ 97% |
| Target | HIF1α |
| Pathway | HIF-1 |
