SML0629
Mitochondrial Fusion Promoter M1
≥95% (HPLC)
Sinônimo(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
Produtos recomendados
Ensaio
≥95% (HPLC)
forma
powder
cor
white to beige
solubilidade
DMSO: 10 mg/mL, clear
temperatura de armazenamento
2-8°C
Aplicação
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
Ações bioquímicas/fisiológicas
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.
Código de classe de armazenamento
11 - Combustible Solids
Classe de risco de água (WGK)
WGK 3
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
Certificados de análise (COA)
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Experimental cell research, 400(1), 112493-112493 (2021-01-25)
Most cancer deaths are due to the colonization of tumor cells in distant organs. More evidence indicates that overexpression of RACGAP1 plays a critical role in cancer metastasis. However, the underlying mechanism still remains poorly understood. Here we found that
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
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
Nature neuroscience, 22(3), 386-400 (2019-02-12)
Fragile X syndrome results from a loss of the RNA-binding protein fragile X mental retardation protein (FMRP). How FMRP regulates neuronal development and function remains unclear. Here we show that FMRP-deficient immature neurons exhibit impaired dendritic maturation, altered expression of
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