跳转至内容
Merck
所有图片(1)

文件

557440

Sigma-Aldrich

Ru360

≥97%, solid, Ca2+ uptake blocker in mitrochondria, Calbiochem®

别名:

Ru360

登录查看公司和协议定价


About This Item

经验公式(希尔记法):
C2H26Cl3N8O5Ru2
分子量:
550.78
分類程式碼代碼:
12352200
NACRES:
NA.77

product name

Ru360, Ru360, is a cell-permeable oxygen-bridged dinuclear ruthenium amine complex. Binds to mitochondria with high affinity (Kd = 340 pM) and blocks Ca2+ uptake into mitochondria in vitro (IC₅₀ = 184 pM).

品質等級

化驗

≥97%

形狀

solid

製造商/商標名

Calbiochem®

儲存條件

OK to freeze
desiccated (hygroscopic)
protect from light

顏色

green

溶解度

deoxygenated water: 0.5 mg/mL

運輸包裝

ambient

儲存溫度

−20°C

一般說明

一种可渗透性氧桥联双核钌胺络合物,已显示出与线粒体结合的高亲和力 (Kd = 0.34 nM)并可特异性阻断Ca2+体外(IC50 = 184 pM)线粒体中和在原位完整心肌细胞中的摄取(在~10 µM的Ru360中孵育30分钟后完全阻断。即使在微摩尔水平下也不会影响参与心肌收缩的其他细胞Ca2+转运过程。
一种细胞渗透性氧桥联双核钌胺络合物,已显示出与线粒体结合的高亲和力 (Kd = 340 pM)。特异性阻断Ca2+体外(IC50 = 184 pM)线粒体中和在原位完整心肌细胞中的摄取(在~10 µM的Ru360中孵育30分钟后完全阻断)。即使在微摩尔水平下也不会影响参与心肌收缩的其他细胞Ca2+转运过程。
注意:1组 = 10 x 100 µg.

生化/生理作用

产物不与ATP竞争。
可逆:否
细胞可渗透性:具有
靶标IC50:184 pM 阻断Ca2+在体外摄取至线粒体中;以及在原位完整心肌细胞中;结合线粒体的Kd = 340 pM
首要靶标
Ca2+在体外摄取至线粒体中

包裝

用惰性气体包装

警告

毒性:标准处理(A)

重構

溶液中不稳定;仅在使用前进行重悬。

其他說明

Sanchez, J.A., et al. 2001.J. Physiol. 536, 387.
Bassani, R.A., et al. 1998.Cell Calcium23, 433.
Matlib, M.A., et al. 1998.J. Biol. Chem.273, 10223.
Zhou, Z., et al. 1998.J. Physiol.507 (pt 2), 379.
Emerson, J., et al. 1993.J. Am. Chem. Soc.115, 11799.
Ying, W.-L., et al. 1991.Biochemistry30, 4949.

法律資訊

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


分析证书(COA)

输入产品批号来搜索 分析证书(COA) 。批号可以在产品标签上"批“ (Lot或Batch)字后找到。

已有该产品?

在文件库中查找您最近购买产品的文档。

访问文档库

其他客户在看

Madison X Rodriguez et al.
STAR protocols, 2(4), 100979-100979 (2021-12-09)
The mitochondrial calcium uniporter, which mediates mitochondrial Ca2+ uptake, regulates key cellular functions, including intracellular Ca2+ signaling, cell-fate determination, and mitochondrial bioenergetics. Here, we describe two complementary strategies to quantify the uniporter's transport activity. First, we detail a mitochondrial Ca2+
Rachel L Doser et al.
eLife, 13 (2024-03-14)
Our understanding of mitochondrial signaling in the nervous system has been limited by the technical challenge of analyzing mitochondrial function in vivo. In the transparent genetic model Caenorhabditis elegans, we were able to manipulate and measure mitochondrial reactive oxygen species
Michael J Bround et al.
Scientific reports, 14(1), 6751-6751 (2024-03-22)
Mitochondrial Ca2+ overload can mediate mitochondria-dependent cell death, a major contributor to several human diseases. Indeed, Duchenne muscular dystrophy (MD) is driven by dysfunctional Ca2+ influx across the sarcolemma that causes mitochondrial Ca2+ overload, organelle rupture, and muscle necrosis. The
MCU Upregulation Overactivates Mitophagy by Promoting VDAC1 Dimerization and Ubiquitination in the Hepatotoxicity of Cadmium.
Liu, et al.
Advanced science (Weinheim, Baden-Wurttemberg, Germany), 10, e2203869-e2203869 (2023)
Peu Santra et al.
Disease models & mechanisms, 14(7) (2021-07-24)
The vacuolar-type H+-ATPase (V-ATPase) is a multi-subunit proton pump that regulates cellular pH. V-ATPase activity modulates several cellular processes, but cell-type-specific functions remain poorly understood. Patients with mutations in specific V-ATPase subunits can develop sensorineural deafness, but the underlying mechanisms

我们的科学家团队拥有各种研究领域经验,包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.

联系技术服务部门