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Key Documents

SML0629

Sigma-Aldrich

Mitochondrial Fusion Promoter M1

≥95% (HPLC)

Synonyme(s) :

(E)-4-Chloro-2-(1-(2-(2,4,6-trichlorophenyl)hydrazono)ethyl)phenol, 1-(5-Chloro-2-hydroxyphenyl)-ethanone 2-(2,4,6-trichlorophenyl)hydrazone

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About This Item

Formule empirique (notation de Hill):
C14H10Cl4N2O
Numéro CAS:
Poids moléculaire :
364.05
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

Pureté

≥95% (HPLC)

Forme

powder

Couleur

white to beige

Solubilité

DMSO: 10 mg/mL, clear

Température de stockage

2-8°C

Application

Mitochondrial Fusion Promoter M1 has been used as a fusion promoter:
  • to study its effects on peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α expression in breast cancer cells
  • to study the link between nucleoside diphosphate kinase 3 (NME3)-regulated mitochondrial fluctuations and stability of genome in NME3 knockdown cells
  • to study its effects on mitochondrial fusion in neuronal cells

Actions biochimiques/physiologiques

Mitochondrial Fusion Promoter M1 is a cell permeable hydrazone that enhances mitochondrial fusion. M1 protects cells from mitochondrial fragmentation associated cell death. Mitochondrial Fusion Promoter M1 does not interfere with endoplasmic reticula (ER) and lysosomes morphology.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Chih-Wei Chen et al.
International journal of molecular sciences, 21(14) (2020-07-28)
NME3 is a member of the nucleoside diphosphate kinase (NDPK) family that binds to the mitochondrial outer membrane to stimulate mitochondrial fusion. In this study, we showed that NME3 knockdown delayed DNA repair without reducing the cellular levels of nucleotide
Ryohei Iwata et al.
Science (New York, N.Y.), 369(6505), 858-862 (2020-08-15)
The conversion of neural stem cells into neurons is associated with the remodeling of organelles, but whether and how this is causally linked to fate change is poorly understood. We examined and manipulated mitochondrial dynamics during mouse and human cortical

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