Tetramethylrhodamine methyl ester perchlorate - CAS 115532-50-8
Molecular Formula:
C25H25N2O3·ClO4
Molecular Weight:
500.9
COA:
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Application\Fluorophore:
Cell and Organelle Stains
Description:
Tetramethylrhodamine methyl ester (TMRM) perchlorate is a cell-permeant red fluorescent probe commonly used to monitor membrane potential of mitochondria using live cell fluorescence microscopy and flow cytometry. TMRM is a lipophilic cation accumulated by mitochondria and exhibits a red shift in the emission of 575 nm. However, when the membrane is depolarized, as in apoptosis, TMRM is not accumulated in the mitochondria. Thus, the strength of the fluorescence signal in mitochondria is used to assess cell viability.
Purity:
≥98%
Appearance:
Solid Powder
Synonyms:
TMRM Perchlorate; TMR methyl ester perchlorate; 3,6-bis(dimethylamino)-9-[2-(methoxycarbonyl)phenyl]-xanthylium perchlorate
Storage:
Store at -20°C
MSDS:
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Excitation:
515, 555 nm
Emission:
575 nm
InChIKey:
PFYWPQMAWCYNGW-UHFFFAOYSA-M
InChI:
InChI=1S/C25H25N2O3.ClHO4/c1-26(2)16-10-12-20-22(14-16)30-23-15-17(27(3)4)11-13-21(23)24(20)18-8-6-7-9-19(18)25(28)29-5;2-1(3,4)5/h6-15H,1-5H3;(H,2,3,4,5)/q+1;/p-1
Canonical SMILES:
CN(C)C1=CC2=C(C=C1)C(=C3C=CC(=[N+](C)C)C=C3O2)C4=CC=CC=C4C(=O)OC.[O-]Cl(=O)(=O)=O
1.Involvement of Cyclophilin D and Calcium in Isoflurane-induced Preconditioning.
Teixeira G1, Chiari P, Fauconnier J, Abrial M, Couture-Lepetit E, Harisseh R, Pillot B, Lacampagne A, Tourneur Y, Gharib A, Ovize M. Anesthesiology. 2015 Dec;123(6):1374-84. doi: 10.1097/ALN.0000000000000876.
BACKGROUND: The mitochondrial permeability transition pore (PTP) has been established as an important mediator of ischemia-reperfusion-induced cell death. The matrix protein cyclophilin D (CypD) is the best known regulator of PTP opening. Therefore, the authors hypothesized that isoflurane, by inhibiting the respiratory chain complex I, another regulator of PTP, might reinforce the myocardial protection afforded by CypD inhibition.
2.Dehydroepiandrosterone inhibits the Src/STAT3 constitutive activation in pulmonary arterial hypertension.
Paulin R1, Meloche J, Jacob MH, Bisserier M, Courboulin A, Bonnet S. Am J Physiol Heart Circ Physiol. 2011 Nov;301(5):H1798-809. doi: 10.1152/ajpheart.00654.2011. Epub 2011 Sep 2.
Pulmonary arterial hypertension (PAH) is an obstructive vasculopathy characterized by enhanced pulmonary artery smooth muscle cell (PASMC) proliferation and suppressed apoptosis. This phenotype is sustained by the activation of the Src/signal transducer and activator of transcription 3 (STAT3) axis, maintained by a positive feedback loop involving miR-204 and followed by an aberrant expression/activation of its downstream targets such as Pim1 and nuclear factor of activated T-cells (NFATc2). Dehydroepiandrosterone (DHEA) is a steroid hormone shown to reverse vascular remodeling in systemic vessels. Since STAT3 has been described as modulated by DHEA, we hypothesized that DHEA reverses human pulmonary hypertension by inhibiting Src/STAT3 constitutive activation. Using PASMCs isolated from patients with PAH (n = 3), we demonstrated that DHEA decreases both Src and STAT3 activation (Western blot and nuclear translocation assay), resulting in a significant reduction of Pim1, NFATc2 expression/activation (quantitative RT-PCR and Western blot), as well as Survivin and upregulation of bone morphogenetic protein receptor 2 (BMPR2) and miR-204.
3.Real-Time Live Confocal Fluorescence Microscopy as a New Tool for Assessing Platelet Vitality.
Hermann M1, Nussbaumer O, Knöfler R, Hengster P, Nussbaumer W, Streif W. Transfus Med Hemother. 2010;37(5):299-305. Epub 2010 Sep 15.
BACKGROUND: Assessment of platelet vitality is important for patients presenting with inherited or acquired disorders of platelet function and for quality assessment of platelet concentrates.
4.Mitochondrial activation at the onset of contractions in isolated myofibres during successive contractile periods.
Gandra PG1, Nogueira L, Hogan MC. J Physiol. 2012 Aug 1;590(15):3597-609. doi: 10.1113/jphysiol.2012.232405. Epub 2012 Jun 18.
At the onset of skeletal muscle repetitive contractions, there is a significant delay in the time to achieve oxidative phosphorylation steady state. The purpose of the present study was to examine the factors that limit oxidative phosphorylation at the onset of contractions. NAD(P)H was measured in real time during two contractile periods (2 min each) separated by 5 min of rest in intact single muscle fibres (n = 7) isolated from Xenopus laevis. The fibres were then loaded with the dye tetramethylrhodamine methyl ester perchlorate (TMRM) to evaluate the kinetics of the mitochondrial membrane potential (Δψ (m)) during two further successive contractile periods. At the onset of contractions in the first period, NAD(P)H exhibited a time delay (14.1 ± 1.3 s) before decreasing toward a steady state. In contrast, Δψ(m) decreased immediately after the first contraction and started to be reestablished after 10.7 ± 0.9 s, with restoration to the pre-stimulation values after approximately 32 s.
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CAS 115532-50-8 Tetramethylrhodamine methyl ester perchlorate

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