推荐产品
product name
Q-VD-OPh，非-O-甲基化, InSolution, ≥90%, irreversible broad-spectrum inhibitor of caspases
品質等級
化驗
≥90% (HPLC)
形狀
liquid
製造商／商標名
Calbiochem®
儲存條件
OK to freeze
desiccated (hygroscopic)
protect from light
運輸包裝
wet ice
儲存溫度
−20°C
一般說明
一种细胞渗透性、不可逆、广谱的半胱天冬酶抑制剂（对于半胱天冬酶-1、-8、-9和-3的IC50分别为50、100、430和<25 nM），对所有主要的半胱天冬酶介导的细胞凋亡途径具有有效的抗凋亡特性。即使在极高浓度下也不会表现出细胞毒性作用。显示可减少缺血性脑损伤和中风诱导的胸腺和脾脏中程序性细胞死亡。
生化／生理作用
主要靶标
半胱天冬酶-1
半胱天冬酶-1
产物不与ATP竞争。
可逆：否
细胞可渗透性：是
靶标IC50：对于半胱天冬酶-1、-8、-9和-3分别为50、100、430和<25 nM
包裝
用惰性气体包装
警告
毒性：刺激性（B）
序列
Q-Val-Asp-CH₂-OPh
外觀
以10mM（1mg/195µL）的DMSO溶液的形式提供。
重構
初次融化后，等分并冷冻（-20°C）。
其他說明
Braun, J.S., et al. 2007.Exp.Neurol.206, 183.
Caserta, T.M., et al. 2003.Apoptosis8, 345.
Rebbaa, A., et al. 2003.Oncogene22, 2805.
Caserta, T.M., et al. 2003.Apoptosis8, 345.
Rebbaa, A., et al. 2003.Oncogene22, 2805.
法律資訊
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
儲存類別代碼
10 - Combustible liquids
水污染物質分類（WGK）
WGK 1
閃點（°F）
188.6 °F - closed cup - (Dimethylsulfoxide)
閃點（°C）
87 °C - closed cup - (Dimethylsulfoxide)
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Mitochondria have emerged as key drivers of mammalian innate immune responses, functioning as signaling hubs to trigger inflammation and orchestrating metabolic switches required for phagocyte activation. Mitochondria also contain damage-associated molecular patterns (DAMPs), molecules that share similarity with pathogen-associated molecular
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Science signaling, 14(714), eaba2611-eaba2611 (2021-12-22)
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Javier Chicote et al.
Frontiers in pharmacology, 11, 580343-580343 (2020-11-13)
Macroautophagy (hereafter autophagy) is a multistep intracellular catabolic process with pleiotropic implications in cell fate. Attending to its activation, autophagy can be classified into inducible or constitutive. Constitutive, or basal autophagy, unfolds under nutrient-replete conditions to maintain the cellular homeostasis.
Yuanjiu Lei et al.
Cell, 186(14), 3013-3032 (2023-06-24)
Mitochondrial DNA (mtDNA) is a potent agonist of the innate immune system; however, the exact immunostimulatory features of mtDNA and the kinetics of detection by cytosolic nucleic acid sensors remain poorly defined. Here, we show that mitochondrial genome instability promotes
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