推荐产品
质量水平
检测方案
≥95% (HPLC)
形式
crystalline solid
制造商/商品名称
Calbiochem®
储存条件
OK to freeze
protect from light
颜色
yellow
溶解性
DMSO: 10 mg/mL
methanol: 5 mg/mL
运输
ambient
储存温度
2-8°C
InChI
1S/C13H13N3OS/c1-16-12(17)11(15-13(16)18)6-8-7-14-10-5-3-2-4-9(8)10/h2-5,7,11,14H,6H2,1H3,(H,15,18)
InChI key
TXUWMXQFNYDOEZ-UHFFFAOYSA-N
一般描述
坏死性凋亡的细胞可渗透，强效和选择性阻滞剂（在用TNF-α处理的FADD缺陷型Jurkat细胞中EC50=494 nM），是一种由死亡域受体（DRs）介导的非凋亡性坏死性细胞死亡途径，可在缺血性脑损伤小鼠模型中提供神经保护。对DR诱导的凋亡没有影响。还充当RIP1激酶的选择性和ATP竞争性抑制剂，对RIP2激酶活性的影响可忽略不计。Nec-1靶标似乎是执行事件上游和DR下游的关键常见坏死性凋亡步骤。也可以使用非活性对照Nec-1i（目录号480066）。
坏死性凋亡的细胞可渗透，强效和选择性阻滞剂（在用TNF-α处理的FADD缺陷型Jurkat细胞中EC50=494 nM），是一种由死亡域受体（DRs）介导的非凋亡性坏死性细胞死亡途径，可在缺血性脑损伤小鼠模型中提供神经保护。对DR诱导的凋亡没有影响。还充当RIP1激酶的选择性和ATP竞争性抑制剂，对RIP2激酶活性的影响可忽略不计。Nec-1靶标似乎是执行事件上游和DR下游的关键常见坏死性凋亡步骤。也可以使用非活性对照Nec-1i（目录号480066）。也可以25 mM的DMSO溶液（货号505224）提供。
生化/生理作用
主要靶标
坏死性凋亡的阻滞剂
坏死性凋亡的阻滞剂
产物与ATP竞争。
可逆：否
在阻断用TNF-处理的FADD缺陷型Jurkat细胞的坏死中EC50=494 nMα
细胞可渗透性：具有
包装
用惰性气体包装
警告
毒性：标准处理（A）
重悬
复溶后，等分并冷冻保存（-20°C）。贮备液在-20°C下可稳定保存至多3个月。
其他说明
Degterev, A., et al. 2013.Nat. Chem. Biol.9, 192.
Degterev, A., et al. 2012.Cell Death Differ.20, 366.
Christofferson, D.E., et al. 2012.Cell Death Dis.3, e320.
Takahashi, N., et al. 2012.Cell Death Dis.3, e437.
Degterev, A., et al. 2008.Nat. Chem. Biol.4, 313.
Degterev, A., et al. 2005.Nat. Chem. Biol.1, 112.
Muller, A.J., et al. 2005.Nat. Med.11, 312.
Teng, X., et al. 2005.Bioorg.Med. Chem. Lett.15, 5039.
Degterev, A., et al. 2012.Cell Death Differ.20, 366.
Christofferson, D.E., et al. 2012.Cell Death Dis.3, e320.
Takahashi, N., et al. 2012.Cell Death Dis.3, e437.
Degterev, A., et al. 2008.Nat. Chem. Biol.4, 313.
Degterev, A., et al. 2005.Nat. Chem. Biol.1, 112.
Muller, A.J., et al. 2005.Nat. Med.11, 312.
Teng, X., et al. 2005.Bioorg.Med. Chem. Lett.15, 5039.
法律信息
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Roberto Fernández-Acosta et al.
Molecules (Basel, Switzerland), 27(13) (2022-07-10)
The use of nanomaterials rationally engineered to treat cancer is a burgeoning field that has reported great medical achievements. Iron-based polymeric nano-formulations with precisely tuned physicochemical properties are an expanding and versatile therapeutic strategy for tumor treatment. Recently, a peculiar
Bolin Hou et al.
Cell death discovery, 8(1), 319-319 (2022-07-14)
The underlying mechanism by which growth factor receptor-bound protein 2 (Grb2) regulates necroptosis remains unexplored. In the present study, we found that rasfonin, a fungal natural product and an activator of necroptosis, enhanced Grb2 binding to receptor-interacting serine/threonine kinase 1
Sasker Grootjans et al.
Nature protocols, 11(8), 1444-1454 (2016-07-16)
Several cell death assays have been developed based on a single biochemical parameter such as caspase activation or plasma membrane permeabilization. Our fluorescent apoptosis/necrosis (FAN) assay directly measures cell death and distinguishes between caspase-dependent apoptosis and caspase-independent necrosis of cells
Kana Otsubo et al.
FEBS letters, 594(10), 1586-1595 (2020-01-31)
Autophagy is an intracellular process that regulates the degradation of cytosolic proteins and organelles. Dying cells often accumulate autophagosomes. However, the mechanisms by which necroptotic stimulation induces autophagosomes are not defined. Here, we demonstrate that the activation of necroptosis with
Takashi Kojima et al.
Disease models & mechanisms, 14(11) (2021-10-09)
KCNQ4 encodes the homotetrameric voltage-dependent potassium ion channel Kv7.4, and is the causative gene for autosomal dominant nonsyndromic sensorineural hearing loss, DFNA2. Dominant-negative inhibition accounts for the observed dominant inheritance of many DFNA2-associated KCNQ4 variants. In addition, haploinsufficiency has been
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