SML0629
线粒体融合启动子 M1
≥95% (HPLC), powder
别名:
(E)-4-氯-2-（1-（2-（2,4,6-三氯苯基）肼基）乙基）苯酚, 1-（5-氯-2-羟基苯基）-乙酮 2-（2,4,6-三氯苯基）腙
产品名称
线粒体融合启动子 M1, ≥95% (HPLC)
SMILES string
Clc1c(c(cc(c1)Cl)Cl)NNC(=C)c2c(ccc(c2)Cl)O
InChI key
WMAGOVJOXMBLHY-UHFFFAOYSA-N
assay
≥95% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 10 mg/mL, clear
storage temp.
2-8°C
Quality Level
Application
线粒体融合启动子M1作为融合启动子的应用实例：
- 研究其对乳腺癌细胞中过氧化物酶体增殖物激活受体-γ共激活因子(PGC)-1α的影响
- 研究NME3敲低细胞中核苷二磷酸激酶3(NME3)调节的线粒体波动(mitochondrial fluctuation)和基因组稳定性的关系
- 研究其对神经元细胞的线粒体融合的影响作用
Biochem/physiol Actions
线粒体融合启动子 M1 是一种细胞渗透性腙，可增强线粒体融合。
线粒体融合启动子 M1 是一种细胞渗透性腙，可增强线粒体融合。M1 可保护细胞免受线粒体断裂相关的细胞死亡。线粒体融合启动子 M1 不干扰内质网(ER) 和溶酶体的形态。
wgk
WGK 3
存储类别
11 - Combustible Solids
flash_point_f
Not applicable
flash_point_c
Not applicable
Kehan Ren et al.
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
Minjie Shen et al.
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
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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