EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72462_C
PKC抑制剂
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总览
Gö6983 可抑制多种蛋白激酶 C 亚型 (PKC；PKCα、PKCβ、PKCγ、PKCδ、PKCζ 和 PKCμ 的 IC₅₀ 分别为 7、7、6、10、60 和 20,000 nM) （Gschwendt et al.）。
重编程
·增强小鼠胚胎成纤维细胞向诱导多能干细胞的重编程（Dutta et al.）。
·结合CHIR99021、RepSox、Forskolin、SP600125、丙戊酸和Y-27632，将成纤维细胞直接谱系重编程为成熟神经元（Hu et al.）。
维持和自我更新
·抑制小鼠胚胎干细胞分化并维持其多能性（Dutta et al.）。
·增强人基态多能干细胞的活力和生长（Gafni et al.）。
·抑制人原代胎儿骨细胞的增殖（Krattinger et al.）。
·抑制成年小鼠骨髓巨核细胞形成原血小板（Williams et al.）。
细胞类型
巨核细胞，成骨细胞，多能干细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
培养，重编程
研究领域
干细胞生物学
CAS 编号
133053-19-7
化学式
C₂₆H₂₆N₄O₃
纯度
≥98%
通路
PKC
靶点
PKC
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
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相关材料与文献
技术资料 (4)
文献 (4)
Direct Conversion of Normal and Alzheimer's Disease Human Fibroblasts into Neuronal Cells by Small Molecules. Cell stem cell 2015 AUG
Abstract
Neuronal conversion from human fibroblasts can be induced by lineage-specific transcription factors; however, the introduction of ectopic genes limits the therapeutic applications of such induced neurons (iNs). Here, we report that human fibroblasts can be directly converted into neuronal cells by a chemical cocktail of seven small molecules, bypassing a neural progenitor stage. These human chemical-induced neuronal cells (hciNs) resembled hiPSC-derived neurons and human iNs (hiNs) with respect to morphology, gene expression profiles, and electrophysiological properties. This approach was further applied to generate hciNs from familial Alzheimer's disease patients. Taken together, our transgene-free and chemical-only approach for direct reprogramming of human fibroblasts into neurons provides an alternative strategy for modeling neurological diseases and for regenerative medicine.
PKCα negatively regulates in vitro proplatelet formation and in vivo platelet production in mice. Platelets 2014 JAN
Abstract
Proplatelet formation is a part of the intricate process by which platelets are generated by their precursor cell, the megakaryocyte. The processes that drive megakaryocyte maturation and platelet production are however still not well understood. The protein kinase C (PKC) family of serine/threonine kinases has been demonstrated as an important regulator of megakaryocyte maturation and proplatelet formation, but little investigation has been made on the individual isoforms. We have previously shown, in mouse models, that PKCα plays a vital role in regulating platelet function, so in this study we aimed to investigate the role of PKCα in megakaryocyte function using the same Prkca(-)(/)(-) mice. We assessed the role of global PKC and specifically PKCα in proplatelet formation in vitro, analyzed polyploidy in Prkca(-)(/)(-)-derived megakaryocytes and followed platelet recovery in platelet-depleted Prkca(-)(/)(-) mice. We show reduced proplatelet formation in the presence of global PKC blockade. However, in the presence of a selective classical PKC isoform inhibitor, Go6976, proplatelet formation was conversely enhanced. PKCα null megakaryocytes also showed enhanced proplatelet formation, as well as a shift to greater polyploidy. In vivo, platelet production was enhanced in response to experimentally induced immune thrombocytopenia. In conclusion, our data indicate that classical PKC isoforms, and more specifically PKCα, are negative regulators of proplatelet formation. PKCα appears to negatively regulate endomitosis, with the enhanced polyploidy observed in Prkca(-)(/)(-)-derived megakaryocytes. In vivo, these observations may culminate in the observed ability of Prkca(-)(/)(-) mice to recover more rapidly from a thrombocytopenic insult.
Derivation of novel human ground state naive pluripotent stem cells. Nature 2013 DEC
Abstract
Mouse embryonic stem (ES) cells are isolated from the inner cell mass of blastocysts, and can be preserved in vitro in a naive inner-cell-mass-like configuration by providing exogenous stimulation with leukaemia inhibitory factor (LIF) and small molecule inhibition of ERK1/ERK2 and GSK3β signalling (termed 2i/LIF conditions). Hallmarks of naive pluripotency include driving Oct4 (also known as Pou5f1) transcription by its distal enhancer, retaining a pre-inactivation X chromosome state, and global reduction in DNA methylation and in H3K27me3 repressive chromatin mark deposition on developmental regulatory gene promoters. Upon withdrawal of 2i/LIF, naive mouse ES cells can drift towards a primed pluripotent state resembling that of the post-implantation epiblast. Although human ES cells share several molecular features with naive mouse ES cells, they also share a variety of epigenetic properties with primed murine epiblast stem cells (EpiSCs). These include predominant use of the proximal enhancer element to maintain OCT4 expression, pronounced tendency for X chromosome inactivation in most female human ES cells, increase in DNA methylation and prominent deposition of H3K27me3 and bivalent domain acquisition on lineage regulatory genes. The feasibility of establishing human ground state naive pluripotency in vitro with equivalent molecular and functional features to those characterized in mouse ES cells remains to be defined. Here we establish defined conditions that facilitate the derivation of genetically unmodified human naive pluripotent stem cells from already established primed human ES cells, from somatic cells through induced pluripotent stem (iPS) cell reprogramming or directly from blastocysts. The novel naive pluripotent cells validated herein retain molecular characteristics and functional properties that are highly similar to mouse naive ES cells, and distinct from conventional primed human pluripotent cells. This includes competence in the generation of cross-species chimaeric mouse embryos that underwent organogenesis following microinjection of human naive iPS cells into mouse morulas. Collectively, our findings establish new avenues for regenerative medicine, patient-specific iPS cell disease modelling and the study of early human development in vitro and in vivo.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 133053-19-7 |
| Chemical Formula | C₂₆H₂₆N₄O₃ |
| 纯度 | ≥ 98% |
| Target | PKC |
| Pathway | PKC |
