方案
99%
mp
113-114 °C (lit.)
SMILES字符串
c1ccc-2c(c1)-c3ccccc-23
InChI
1S/C12H8/c1-2-6-10-9(5-1)11-7-3-4-8-12(10)11/h1-8H
InChI key
IFVTZJHWGZSXFD-UHFFFAOYSA-N
包装
Bottomless glass bottle. Contents are inside inserted fused cone.
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
法规信息
新产品
此项目有
Chao-Tao Tang et al.
Cellular signalling, 46, 52-63 (2018-03-03)
NADPH Oxidase 4 (NOX4), a member of the NOX family, has emerged as a significant source of reactive oxygen species, playing an important role in tumor cell proliferation, apoptosis, and other physiological processes. However, the potential function of NOX4 in
Harmanpreet Kaur et al.
Ultrasound in medicine & biology, 43(11), 2699-2712 (2017-08-16)
We evaluated the activation of mitogen-activated protein kinase (MAPK) activation through reactive oxygen species (ROS) by application of low-intensity ultrasound (LIPUS) to MC-3 T3 E1 pre-osteoblasts. The cells were subjected to one LIPUS application for either 10 or 20 min, and
Xiaoliang Wang et al.
Journal of immunology (Baltimore, Md. : 1950), 197(10), 4090-4100 (2016-11-07)
Apoptosis is the most common form of neutrophil death under both physiological and inflammatory conditions. However, forms of nonapoptotic neutrophil death have also been observed. In the current study, we report that human neutrophils undergo necroptosis after exposure to GM-CSF
Yukio Nisimoto et al.
Journal of biochemistry, 163(6), 489-501 (2018-01-25)
Nox4, a member of the NADPH- and oxygen-dependent oxidoreductases that generate reactive oxygen species (ROS), is widely expressed and constitutively active. To understand better its function and regulation, specific mutations in the Nox4 dehydrogenase (DH) domain were examined for effects
Lingdi Wang et al.
Nature communications, 8(1), 523-523 (2017-09-14)
The mitochondrial enriched GCN5-like 1 (GCN5L1) protein has been shown to modulate mitochondrial protein acetylation, mitochondrial content and mitochondrial retrograde signaling. Here we show that hepatic GCN5L1 ablation reduces fasting glucose levels and blunts hepatic gluconeogenesis without affecting systemic glucose
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