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寡霉素
NMR and HPLC COA下载 MSDS下载 - Names：
Oligomycin
- CAS号：
1404-19-9
MDL Number： MFCD00065705 - MF(分子式)： C45H74O11 MW(分子量)： 791.07
- EINECS:209-437-3 Reaxys Number:
- Pubchem ID: Brand:BIOFOUNT
寡霉素(1404-19-9,Oligomycin)是一种大环内酯类，已发现的寡霉素是寡霉素异构体A，B和C的混合物，寡霉素可作为线粒体ATP合酶的特异性抑制剂并阻止氧化磷酸化。癌细胞研究表明，寡霉素不会激活缺氧诱导因子。已显示寡霉素可降低细胞周期蛋白D1蛋白的表达水平。
| 货品编码 | 规格 | 纯度 | 价格 (¥) | 现价(¥) | 特价(¥) | 库存描述 | 数量 | 总计 (¥) |
|---|---|---|---|---|---|---|---|---|
| SS0333-25mg | 25mg | 90% | ¥ 5760.00 | ¥ 5760.00 | 3598 | 3-5days | ¥ 0.00 | |
| SS0333-5mg | 5mg | 90% | ¥ 1360.00 | ¥ 1360.00 | 898 | 3-5days | ¥ 0.00 |
| 中文别名 | 寡霉素(1404-19-9,Oligomycin);寡霉素,来源于链霉素 |
| 英文别名 | Oligomycin(1404-19-9);Oligomycins;OLIGOMYCIN (A shown) |
| CAS号 | 1404-19-9 |
| Inchi | InChI=1S/C45H74O11/c1-12-34-17-15-13-14-16-27(4)42(51)44(11,53)43(52)32(9)40(50)31(8)39(49)30(7)38(48)26(3)18-21-37(47)54-41-29(6)35(20-19-34)55-45(33(41)10)23-22-25(2)36(56-45)24-28(5)46/h13-15,17-18,21,25-36,38,40-42,46,48,50-51,53H,12,16,19-20,22-24H2,1-11H3/b14-13+,17-15+,21-18+/t25-,26-,27+,28+,29+,30-,31-,32-,33-,34-,35-,36-,38+,40+,41+,42-,44+,45-/m1/s1 |
| InchiKey | MNULEGDCPYONBU-WMBHJXFZSA-N |
| 分子式 Molecular Weight | C45H74O11 |
| 分子量 Formula | 791.07 |
| 溶解度Solubility | Soluble in EtOH, acetone (50 mg/ml), DMSO (300 mg/ml), ethanol, and methanol. Insoluble in water |
| 性状 | 白色固体粉末 |
| 储藏条件 Storage conditions | -20°C，在氮气下储存 |
寡霉素，ATP 合酶抑制剂- 功能研究
寡霉素抑制 3T3-L1 细胞中 ATP 依赖性脂肪生成，诱导细胞进行脂肪细胞分化 (A-D) 5 天，然后加入不同浓度的寡霉素（B，1 µg/ml；C，2 µg/ml 和 D，10 µg/ml）。10天后，将细胞用油红O染色并在光学显微镜下观察。
寡霉素(1404-19-9,Oligomycin)毒理属性测试：
| 生物 | 测试类型 | 路线 | 报告剂量（标准化剂量） | 影响 | 参考 |
|---|---|---|---|---|---|
| rat | LDLo | intraperitoneal | 500 ug/kg (0.5 mg/kg) | Agents and Actions, A Swiss Journal of Pharmacology., 15(660), 1984 [PMID:6532186] | |
| mouse | LDLo | intraperitoneal | 2500 ug/kg (2.5 mg/kg) | BEHAVIORAL: MUSCLE WEAKNESS; BEHAVIORAL: CONVULSIONS OR EFFECT ON SEIZURE THRESHOLD; LUNGS, THORAX, OR RESPIRATION: RESPIRATORY DEPRESSION | Antibiotics and Chemotherapy, 4(962), 1954 |
| mouse | LDLo | intravenous | 2500 ug/kg (2.5 mg/kg) | BEHAVIORAL: CONVULSIONS OR EFFECT ON SEIZURE THRESHOLD; BEHAVIORAL: MUSCLE WEAKNESS; LUNGS, THORAX, OR RESPIRATION: DYSPNEA | Antibiotics and Chemotherapy, 4(962), 1954 |
寡霉素(1404-19-9,Oligomycin)实验注意事项：
1.实验前需戴好防护眼镜，穿戴防护服和口罩，佩戴手套，避免与皮肤接触。
2.实验过程中如遇到有毒或者刺激性物质及有害物质产生，必要时实验操作需要手套箱内完成以免对实验人员造成伤害。
3.取样品的移液枪头需及时更换，必要时为避免交叉污染尽可能选择滤芯吸头。
4.称量药品时选用称量纸，并无风处取药和称量以免扬撒，试剂的容器使用前务必确保干净，并消毒。
5.取药品时尽量采用多个药勺分别使用，使用后清洗干净后，烘干消毒存放。
6.实验后产生的废弃物需分类存储，并交于专业生物废气物处理公司处理，以免造成环境污染。
Oligomycin(1404-19-9) Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.
Tag:寡霉素(1404-19-9,Oligomycin),:寡霉素试剂,寡霉素的活性,寡霉素的含量,寡霉素的价格,寡霉素的生产厂家,寡霉素的外观,寡霉素的储存条件,寡霉素的MSDS,寡霉素的质检报告,寡霉素的注意事项,寡霉素的成分
| 产品说明 | 寡霉素(1404-19-9,Oligomycin)是一种ATP合酶抑制剂。可以阻断质子通道（Fo 亚基）。寡霉素是一种大环内酯类抗生素。 |
| Introduction | Oligomycin (1404-19-9,寡霉素) is only used for scientific research and chemical synthesis intermediates. For the activity of 1404-19-9, 1404-19-9 MSDS and other parameters, please see the homepage |
| Application1 | 寡霉素增强了异质生物能组织细胞的生物能适应性。 |
| Application2 | A specific inhibitor of the mitochondrial ATP-synthase. |
| Application3 | 寡霉素可作为线粒体ATP合酶的特异性抑制剂并阻止氧化磷酸化。 |
| 警示图 | |
| 危险性 | warning |
| 危险性警示 | No data available |
| 安全声明 | H301 |
| 安全防护 | P301+P310 |
| 备注 | 实验过程中防止吸入、食入，做好安全防护 |
| 象形图 |  |
|---|---|
| 信号 | Warning |
| GHS危险说明 | H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral] |
| 防范说明代码 |
P264, P270, P301+P312, P330, and P501 (The corresponding statement to each P-code can be found at the GHS Classification page.) |
| Dieldrin-induced neurotoxicity involves impaired mitochondrial bioenergetics and an endoplasmic reticulum stress response in rat dopaminergic cells(Neurotoxicology,2017) |
| Conserved functional consequences of disease-associated mutations in the slide helix of Kir6.1 and Kir6.2 subunits of the ATP-sensitive potassium channel(The Journal of biological chemistry,2017) |
| Sorafenib targets the mitochondrial electron transport chain complexes and ATP synthase to activate the PINK1-Parkin pathway and modulate cellular drug response(The Journal of biological chemistry) |
| Suppressed translation and ULK1 degradation as potential mechanisms of autophagy limitation under prolonged starvation(Autophagy,2016-11-01) |
| Effects of Tributyltin Chloride on Cybrids with or without an ATP Synthase Pathologic Mutation(Environmental health perspectives,2016-09-01) |
1.ANT1-mediated fatty acid-induced uncoupling as a target for improving myocellular insulin sensitivity.
Sparks LM1,2, Gemmink A3, Phielix E1, Bosma M1,4, Schaart G3, Moonen-Kornips E1, Jörgensen JA1, Nascimento EB1, Hesselink MK3, Schrauwen P1, Hoeks J5. Diabetologia. 2016 May;59(5):1030-9. doi: 10.1007/s00125-016-3885-8. Epub 2016 Feb 17.
AIMS/HYPOTHESIS: Dissipating energy via mitochondrial uncoupling has been suggested to contribute to enhanced insulin sensitivity. We hypothesised that skeletal muscle mitochondria of endurance-trained athletes have increased sensitivity for fatty acid (FA)-induced uncoupling, which is driven by the mitochondrial protein adenine nucleotide translocase 1 (ANT1).
2.Leptin contributes to long-term stabilization of HIF-1α in cancer cells subjected to oxygen limiting conditions.
Calgani A1, Delle Monache S1, Cesare P2, Vicentini C2, Bologna M2, Angelucci A3. Cancer Lett. 2016 Mar 17. pii: S0304-3835(16)30177-X. doi: 10.1016/j.canlet.2016.03.027. [Epub ahead of print]
Leptin, a cytokine produced by the adipose tissue in response to food intake, is a key player in the regulation of energy balance and body weight control. Physiological action of leptin in modulating the metabolic adaptation of different peripheral tissues supports the hypothesis that it could also exert a direct effect on cancer cells. In vitro, treatment with leptin up-regulated HIF-1α and stimulated adhesion and invasion of prostate cancer cells cultured in hypoxia. Leptin action was effective in both low and high glycolytic cancer cell lines, and determined the up-regulation of lactate exporter MCT4 and its associated protein CD147. HIF-1α stabilization was oligomycin-independent and was associated with an important modulation of mitochondrial homeostasis. In fact, leptin treatment produced mitochondrial biogenesis, stabilization of mitochondrial membrane potential and increased uncoupled respiration through the up-regulation of UCP2.
3.Underestimation of the Maximal Capacity of the Mitochondrial Electron Transport System in Oligomycin-Treated Cells.
Ruas JS1, Siqueira-Santos ES1, Amigo I2, Rodrigues-Silva E1, Kowaltowski AJ2, Castilho RF1. PLoS One. 2016 Mar 7;11(3):e0150967. doi: 10.1371/journal.pone.0150967. eCollection 2016.
The maximal capacity of the mitochondrial electron transport system (ETS) in intact cells is frequently estimated by promoting protonophore-induced maximal oxygen consumption preceded by inhibition of oxidative phosphorylation by oligomycin. In the present study, human glioma (T98G and U-87MG) and prostate cancer (PC-3) cells were titrated with different concentrations of the protonophore CCCP to induce maximal oxygen consumption rate (OCR) within respirometers in a conventional growth medium. The results demonstrate that the presence of oligomycin or its A-isomer leads to underestimation of maximal ETS capacity. In the presence of oligomycin, the spare respiratory capacity (SRC), i.e., the difference between the maximal and basal cellular OCR, was underestimated by 25 to 45%. The inhibitory effect of oligomycin on SRC was more pronounced in T98G cells and was observed in both suspended and attached cells. Underestimation of SRC also occurred when oxidative phosphorylation was fully inhibited by the ATP synthase inhibitor citreoviridin.
4.Arsenite Regulates Prolongation of Glycan Residues of Membrane Glycoprotein: A Pivotal Study via Wax Physisorption Kinetics and FTIR Imaging.
Lee CH1, Hsu CY2, Huang PY3, Chen CI4, Lee YC5,6, Yu HS7,8. Int J Mol Sci. 2016 Mar 22;17(3). pii: E427. doi: 10.3390/ijms17030427.
Arsenic exposure results in several human cancers, including those of the skin, lung, and bladder. As skin cancers are the most common form, epidermal keratinocytes (KC) are the main target of arsenic exposure. The mechanisms by which arsenic induces carcinogenesis remains unclear, but aberrant cell proliferation and dysregulated energy homeostasis play a significant role. Protein glycosylation is involved in many key physiological processes, including cell proliferation and differentiation. To evaluate whether arsenite exposure affected protein glycosylation, the alteration of chain length of glycan residues in arsenite treated skin cells was estimated. Herein we demonstrated that the protein glycosylation was adenosine triphosphate (ATP)-dependent and regulated by arsenite exposure by using Fourier transform infrared (FTIR) reflectance spectroscopy, synchrotron-radiation-based FTIR (SR-FTIR) microspectroscopy, and wax physisorption kinetics coupled with focal-plane-array-based FTIR (WPK-FPA-FTIR) imaging.
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