推荐产品
质量水平
储存温度
2-8°C
一般描述
The Advanced Protein Assay Reagent combines the best properties of low protein-to-protein variance and a wide protein concentration, a sensitive detection limit and a unique red-to-blue color change.
警示用语：
Warning
危险声明
危险分类
Acute Tox. 4 Oral - Met. Corr. 1 - STOT SE 2
靶器官
Eyes,Central nervous system
WGK
WGK 2
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Faceshields, Gloves, Goggles, type ABEK (EN14387) respirator filter
法规信息
新产品
Romain Long et al.
Biochimica et biophysica acta, 1837(1), 201-209 (2013-10-29)
Carbon monoxide is continuously produced in small quantities in tissues and is an important signaling mediator in mammalian cells. We previously demonstrated that CO delivered to isolated rat heart mitochondria using a water-soluble CO-releasing molecule (CORM-3) is able to uncouple
Mathieu Panel et al.
The Journal of pharmacology and experimental therapeutics, 376(3), 348-357 (2020-12-12)
Mitochondrial permeability transition pore (mPTP) opening is a key event in cell death during myocardial ischemia reperfusion. Inhibition of its modulator cyclophilin D (CypD) by cyclosporine A (CsA) reduces ischemia-reperfusion injury. The use of cyclosporine A in this indication is
Stéphanie Paradis et al.
Cardiovascular research, 98(3), 420-427 (2013-04-05)
The translocator protein (TSPO) is located on the outer mitochondrial membrane where it is responsible for the uptake of cholesterol into mitochondria of steroidogenic organs. TSPO is also present in the heart where its role remains uncertain. We recently showed
Mathieu Panel et al.
Scientific reports, 7(1), 4283-4283 (2017-06-29)
Opening of the mitochondrial permeability transition pore (mPTP) plays a major role in cell death during cardiac ischaemia-reperfusion. Adult isolated rodent cardiomyocytes are valuable cells to study the effect of drugs targeting mPTP. This study investigated whether the use of
Matthias Kohlhauer et al.
Shock (Augusta, Ga.), 56(5), 857-864 (2021-05-13)
Mitochondria is often considered as the common nexus of cardiac and cerebral dysfunction after cardiac arrest. Here, our goal was to determine whether the time course of cardiac and cerebral mitochondrial dysfunction is similar after shockable versus non-shockable cardiac arrest
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