EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72362_C
L型钙通道抑制剂
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总览
(+)-Bay K8644 是一种潜在调控钙通道的调节剂，存在两种作用相反的对映体 (Hess et al.; Nowycky et al.; O'Neill et al.; Ravens et al.; Yamamoto et al.)。(+)-Bay K8644 是一种 L 型通道阻滞剂，具有负性肌力和血管扩张作用 (Artigas et al.; Franckowiak et al.; Ravens et al.)。
重编程
·当与BIX-01294联合使用时，仅用OCT4和KLF4转导后即可实现小鼠胚胎成纤维细胞的重编程（Shi et al.）。
分化
·促进小鼠出生后脑神经干细胞和祖细胞 (NSC) 向神经元的分化（D'Ascenzo et al.）。
别名
(+)-Bay-K 8644；(+)-Bay-R 4407；(R)-(+)-Bay K 8644；NI 105；R 4407
细胞类型
神经干/祖细胞，神经元，多能干细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
分化，重编程
CAS 编号
98791-67-4
化学式
C₁₆H₁₅F₃N₂O₄
分子量
356.3 克/摩尔
纯度
≥ 95 %
通路
L型钙通道
靶点
L型钙通道
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 (3)
文献 (9)
Induction of pluripotent stem cells from mouse embryonic fibroblasts by Oct4 and Klf4 with small-molecule compounds. Cell stem cell 2008 NOV
Abstract
Somatic cells can be induced into pluripotent stem cells (iPSCs) with a combination of four transcription factors, Oct4/Sox2/Klf4/c-Myc or Oct4/Sox2/Nanog/LIN28. This provides an enabling platform to obtain patient-specific cells for various therapeutic and research applications. However, several problems remain for this approach to be therapeutically relevant due to drawbacks associated with efficiency and viral genome integration. Recently, it was shown that neural progenitor cells (NPCs) transduced with Oct4/Klf4 can be reprogrammed into iPSCs. However, NPCs express Sox2 endogenously, possibly facilitating reprogramming in the absence of exogenous Sox2. In this study, we identified a small-molecule combination, BIX-01294 and BayK8644, that enables reprogramming of Oct4/Klf4-transduced mouse embryonic fibroblasts, which do not endogenously express the factors essential for reprogramming. This study demonstrates that small molecules identified through a phenotypic screen can compensate for viral transduction of critical factors, such as Sox2, and improve reprogramming efficiency.
Role of L-type Ca2+ channels in neural stem/progenitor cell differentiation. The European journal of neuroscience 2006 FEB
Abstract
Ca(2+) influx through voltage-gated Ca(2+) channels, especially the L-type (Ca(v)1), activates downstream signaling to the nucleus that affects gene expression and, consequently, cell fate. We hypothesized that these Ca(2+) signals may also influence the neuronal differentiation of neural stem/progenitor cells (NSCs) derived from the brain cortex of postnatal mice. We first studied Ca(2+) transients induced by membrane depolarization in Fluo 4-AM-loaded NSCs using confocal microscopy. Undifferentiated cells (nestin(+)) exhibited no detectable Ca(2+) signals whereas, during 12 days of fetal bovine serum-induced differentiation, neurons (beta-III-tubulin(+)/MAP2(+)) displayed time-dependent increases in intracellular Ca(2+) transients, with DeltaF/F ratios ranging from 0.4 on day 3 to 3.3 on day 12. Patch-clamp experiments revealed similar correlation between NSC differentiation and macroscopic Ba(2+) current density. These currents were markedly reduced (-77%) by Ca(v)1 channel blockade with 5 microm nifedipine. To determine the influence of Ca(v)1-mediated Ca(2+) influx on NSC differentiation, cells were cultured in differentiative medium with either nifedipine (5 microm) or the L-channel activator Bay K 8644 (10 microm). The latter treatment significantly increased the percentage of beta-III-tubulin(+)/MAP2(+) cells whereas nifedipine produced opposite effects. Pretreatment with nifedipine also inhibited the functional maturation of neurons, which responded to membrane depolarization with weak Ca(2+) signals. Conversely, Bay K 8644 pretreatment significantly enhanced the percentage of responsive cells and the amplitudes of Ca(2+) transients. These data suggest that NSC differentiation is strongly correlated with the expression of voltage-gated Ca(2+) channels, especially the Ca(v)1, and that Ca(2+) influx through these channels plays a key role in promoting neuronal differentiation.
Effects of the enantiomers of BayK 8644 on the charge movement of L-type Ca channels in guinea-pig ventricular myocytes. The Journal of membrane biology 2003 JUN
Abstract
The effects of the agonist enantiomer S(-)Bay K 8644 on gating charge of L-type Ca channels were studied in single ventricular myocytes. From a holding potential (Vh) of -40 mV, saturating (250 nm) S(-)Bay K shifted the half-distribution voltage of the activation charge (Q1) vs. V curve -7.5 +/- 0.8 mV, almost identical to the shift produced in the Ba conductance vs. V curve (-7.7 +/- 2 mV). The maximum Q1 was reduced by 1.7 +/- 0.2 nC/microF, whereas Q2 (charge moved in inactivated channels) was increased in a similar amount (1.4 +/- 0.4 nC/microF). The steady-state availability curves for Q1, Q2, and Ba current showed almost identical negative shifts of -14.8 +/- 1.7 mV, -18.6 +/- 5.8 mV, and -15.2 +/- 2.7 mV, respectively. The effects of the antagonist enantiomer R(+)BayK 8644 were also studied, the Q1 vs. V curve was not significantly shifted, but Q1max (Vh = -40 mV) was reduced and the Q1 availability curve shifted by -24.6 +/- 1.2 mV. We concluded that: a) the left shift in the Q1 vs. V activation curve produced by S(-)BayK is a purely agonistic effect; b) S(-)BayK induced a significantly larger negative shift in the availability curve than in the Q1 vs. V relation, consistent with a direct promotion of inactivation; c) as expected for a more potent antagonist, R(+)Bay K induced a significantly larger negative shift in the availability curve than did S(-)Bay K.
更多信息
| Molecular Weight | 356.3 g/mol |
|---|---|
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
| Alternative Names | (+)-Bay-K 8644; (+)-Bay-R 4407; (R)-(+)-Bay K 8644; NI 105; R 4407 |
| Cas Number | 98791-67-4 |
| Chemical Formula | C₁₆H₁₅F₃N₂O₄ |
| 纯度 | ≥ 95% |
| Target | L-type Calcium Channel |
| Pathway | L-type Calcium Channel |
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质量保证:
产品仅供研究使用，不用于针对人或动物的诊断或治疗。
产品仅供研究使用，不用于针对人或动物的诊断或治疗。
