557440
Ru360
≥97%, solid, Ca2+ uptake blocker in mitrochondria, Calbiochem®
Synonym(s):
Ru360, (μ)[(HCO₂)(NH₃)₄Ru]₂OCl₃
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About This Item
Empirical Formula (Hill Notation):
C2H26Cl3N8O5Ru2
Molecular Weight:
550.78
UNSPSC Code:
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).
Quality Level
Assay
≥97%
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
desiccated (hygroscopic)
protect from light
color
green
solubility
deoxygenated water: 0.5 mg/mL
shipped in
ambient
storage temp.
−20°C
General description
A cell-permeable oxygen bridged dinuclear ruthenium amine complex that has been shown to bind to mitochondria with high affinity (Kd = 0.34 nM) and specifically blocks Ca2+ uptake into mitochondria in vitro (IC50 = 184 pM) and in situ in intact myocytes (for complete block after incubation with ~10 µM of Ru360 for 30 min. Does not affect other cellular Ca2+ transport processes involved in cardiac muscle contraction even at micromolar levels.
A cell-permeable oxygen-bridged dinuclear ruthenium amine complex that has been shown to bind to mitochondria with high affinity (Kd = 340 pM). Specifically blocks Ca2+ uptake into mitochondria in vitro (IC50 = 184 pM) and in situ in intact myocytes (complete block after incubation with ~10 µM of Ru360 for 30 min). Does not affect other cellular Ca2+ transport processes involved in cardiac muscle contraction, even at micromolar levels.
Note: 1 set = 10 x 100 µg.
Biochem/physiol Actions
Cell permeable: yes
Primary Target
Ca2+ uptake into mitochondria in vitro
Ca2+ uptake into mitochondria in vitro
Product does not compete with ATP.
Reversible: no
Target IC50: 184 pM blocking Ca2+ uptake into mitochondria in vitro; and in situ in intact myocytes; Kd = 340 pM for binding mitochondria
Packaging
Packaged under inert gas
Warning
Toxicity: Standard Handling (A)
Reconstitution
Unstable in solution; reconstitute just prior to use.
Other Notes
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.
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.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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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
Lianne Pope et al.
Cell chemical biology, 27(5), 511-524 (2020-02-16)
The trinuclear ruthenium amine ruthenium red (RuR) inhibits diverse ion channels, including K2P potassium channels, TRPs, the calcium uniporter, CALHMs, ryanodine receptors, and Piezos. Despite this extraordinary array, there is limited information for how RuR engages targets. Here, using X-ray
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)
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