EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72682_C
p38 MAPK抑制剂
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总览
BIRB-796是一种高效的p38 MAPK抑制剂（Kd = 0.1 nM），可阻断LPS刺激的THP-1细胞中TNFα的释放（IC50 = 18 nM）（Pargellis et al.）。在10 μM浓度时，BIRB-796也能体外抑制JNK2α2，但在较低浓度时，BIRB-796能抑制p38 MAPK，而不影响JNK底物的磷酸化(Bain et al.; Kuma et al.)。
维持和自我更新
·恢复老年小鼠肌肉卫星细胞的自我更新能力（Bernet et al.）。
·增加水凝胶中培养的功能性老年骨骼肌干细胞的再生能力（Cosgrove et al.）。
·阻断GADD45G诱导的长期再生造血干细胞的分化（Thalheimer et al.）。
·在添加SCF、TPO和FLT3L的无血清培养基中，增强脐带血来源的造血干细胞的活性（Baudet et al.）。
·抑制myocilin对人间充质干细胞的成骨分化（Kwon et al.）。
细胞类型
造血干/祖细胞，间充质干/祖细胞，肌源干/祖细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
扩增，培养
研究领域
干细胞生物学
CAS 编号
285983-48-4
化学式
C₃₁H₃₇N₅O₃
纯度
≥98%
通路
p38 MAPK
靶点
p38 MAPK
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
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (3)
文献 (8)
Rejuvenation of the muscle stem cell population restores strength to injured aged muscles. Nature medicine 2014 MAR
Abstract
The elderly often suffer from progressive muscle weakness and regenerative failure. We demonstrate that muscle regeneration is impaired with aging owing in part to a cell-autonomous functional decline in skeletal muscle stem cells (MuSCs). Two-thirds of MuSCs from aged mice are intrinsically defective relative to MuSCs from young mice, with reduced capacity to repair myofibers and repopulate the stem cell reservoir in vivo following transplantation. This deficiency is correlated with a higher incidence of cells that express senescence markers and is due to elevated activity of the p38α and p38β mitogen-activated kinase pathway. We show that these limitations cannot be overcome by transplantation into the microenvironment of young recipient muscles. In contrast, subjecting the MuSC population from aged mice to transient inhibition of p38α and p38β in conjunction with culture on soft hydrogel substrates rapidly expands the residual functional MuSC population from aged mice, rejuvenating its potential for regeneration and serial transplantation as well as strengthening of damaged muscles of aged mice. These findings reveal a synergy between biophysical and biochemical cues that provides a paradigm for a localized autologous muscle stem cell therapy for the elderly.
p38 MAPK signaling underlies a cell-autonomous loss of stem cell self-renewal in skeletal muscle of aged mice. Nature medicine 2014 MAR
Abstract
Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and regenerative capacity, which can lead to sarcopenia and increased mortality. Although the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Therefore, identification of signaling pathways affecting satellite cell function during aging may provide insights into therapeutic targets for combating sarcopenia. Here, we show that a cell-autonomous loss in self-renewal occurs via alterations in fibroblast growth factor receptor-1, p38α and p38β mitogen-activated protein kinase signaling in satellite cells from aged mice. We further demonstrate that pharmacological manipulation of these pathways can ameliorate age-associated self-renewal defects. Thus, our data highlight an age-associated deregulation of a satellite cell homeostatic network and reveal potential therapeutic opportunities for the treatment of progressive muscle wasting.
Cytokine-regulated GADD45G induces differentiation and lineage selection in hematopoietic stem cells. Stem cell reports 2014 JUL
Abstract
The balance of self-renewal and differentiation in long-term repopulating hematopoietic stem cells (LT-HSC) must be strictly controlled to maintain blood homeostasis and to prevent leukemogenesis. Hematopoietic cytokines can induce differentiation in LT-HSCs; however, the molecular mechanism orchestrating this delicate balance requires further elucidation. We identified the tumor suppressor GADD45G as an instructor of LT-HSC differentiation under the control of differentiation-promoting cytokine receptor signaling. GADD45G immediately induces and accelerates differentiation in LT-HSCs and overrides the self-renewal program by specifically activating MAP3K4-mediated MAPK p38. Conversely, the absence of GADD45G enhances the self-renewal potential of LT-HSCs. Videomicroscopy-based tracking of single LT-HSCs revealed that, once GADD45G is expressed, the development of LT-HSCs into lineage-committed progeny occurred within 36 hr and uncovered a selective lineage choice with a severe reduction in megakaryocytic-erythroid cells. Here, we report an unrecognized role of GADD45G as a central molecular linker of extrinsic cytokine differentiation and lineage choice control in hematopoiesis.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 285983-48-4 |
| Chemical Formula | C₃₁H₃₇N₅O₃ |
| 纯度 | ≥ 98% |
| Target | p38 MAPK |
| Pathway | p38 MAPK |
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