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87917

Sigma-Aldrich

Tetramethylrhodamine ethyl ester perchlorate

suitable for fluorescence, ≥90% (HPCE)

Synonyme(s) :

TMRE, TMRE perchlorate

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About This Item

Formule empirique (notation de Hill):
C26H27ClN2O7
Numéro CAS:
115532-52-0
Poids moléculaire :
514.95
Numéro MDL:
MFCD00467973
Code UNSPSC :
12352116
ID de substance PubChem :
329769616
Nomenclature NACRES :
NA.32

Niveau de qualité

100

Pureté

≥90% (HPCE)

Forme

solid

Solubilité

DMSO: soluble
alcohols: soluble

Fluorescence

λex 540 nm; λem 595 nm in DMSO

Adéquation

suitable for fluorescence

Température de stockage

2-8°C

Chaîne SMILES 

[O-]Cl(=O)(=O)=O.CCOC(=O)c1ccccc1-c2c3ccc(cc3[o+]c4cc(ccc24)N(C)C)N(C)C

InChI

1S/C26H27N2O3.ClHO4/c1-6-30-26(29)20-10-8-7-9-19(20)25-21-13-11-17(27(2)3)15-23(21)31-24-16-18(28(4)5)12-14-22(24)25;2-1(3,4)5/h7-16H,6H2,1-5H3;(H,2,3,4,5)/q+1;/p-1

Clé InChI

NBAOBNBFGNQAEJ-UHFFFAOYSA-M

Description générale

Tetramethylrhodamine ethyl ester perchlorate (TMRE), also known as TMRE perchlorate, is a potential mitochondrial dye. TMRE staining process is reversible, and it doesn’t affect cell proliferation and viability.

The sorted cells containing TMRE perchlorate don’t interfere with the subsequent functional assays and hence are a preferred choice for the enrichment of functionally active, unbiased cell populations.

Application

Tetramethylrhodamine ethyl ester perchlorate (TMRE) is used to study the effects of high glucose in inducing mitochondrial morphology and metabolic changes.

TMRE perchlorate is also used to study Fullerene C 60 penetration into Leukemic Cells and the subsequent photoinduced Cytotoxic Effects.

Conditionnement

Bottomless glass bottle. Contents are inside inserted fused cone.

Autres remarques

Potential-sensitive probe for measuring membrane potential changes in mitochondria

Pictogrammes

Exclamation mark
GHS07

Mention d'avertissement

Warning

Mentions de danger

H302 + H332,H315,H319

Classification des risques

Acute Tox. 4 Oral - Eye Irrit. 2 - Skin Irrit. 2

Code de la classe de stockage

13 - Non Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

dust mask type N95 (US), Eyeshields, Gloves

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Natasha S Barteneva et al.
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 62(4), 265-275 (2014-01-08)
High-speed fluorescence-activated cell sorting is relevant for a plethora of applications, such as PCR-based techniques, microarrays, cloning, and propagation of selected cell populations. We suggest a simple cell-sorting technique to eliminate early and late apoptotic and necrotic cells, with good
Yun Shan Chen et al.
Cancer management and research, 11, 7353-7367 (2019-09-10)
The role of endothelin receptor type B (EDNRB) isoform 3 involved in Temozolomide (TMZ)-induced melanoma cell death has not yet been elucidated. The subcellular localization of EDNRB isoform 3 was determined by confocal and immunoblotting assays. Silencing EDNRB isoform 3
Kyle Trudeau et al.
Investigative ophthalmology & visual science, 52(12), 8657-8664 (2011-10-08)
Mitochondrial dysfunction is known to play a role in retinal vascular cell loss, a prominent lesion of diabetic retinopathy. High glucose (HG) has been reported to induce mitochondrial fragmentation and dysfunction in retinal endothelial cells, contributing to apoptosis. In this
Garima Sharma et al.
Journal of biochemical and molecular toxicology, 33(8), e22337-e22337 (2019-04-09)
Elevated levels of saturated fatty acids show a strong cytotoxic effect in liver cells. Sirtuin 3 (SIRT3), a mitochondrially localized member of NAD+ -dependent deacetylase has been shown to protect hepatocytes against the oxidative stress. The role of SIRT3 on
Phong Lu et al.
Molecular pharmaceutics, 16(8), 3386-3398 (2019-06-27)
Clinical trials involving p53 gene therapy for ovarian cancer failed due to the dominant negative inhibition of wild-type p53 and multiple genetic aberrations in ovarian cancer. To overcome this problem, we have designed a more potent chimeric gene fusion, called
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