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Synonyms | Flagecidin, Wuningmeisu C | Storage (From the date of receipt) |
3 years -20°C powder 1 years -80°C in solvent |
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化学式 | C14H19NO4 |
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分子量 | 265.3 | CAS No. | 22862-76-6 | |
Solubility (25°C)* | 体外 | DMSO | 53 mg/mL warmed with 50ºC water bath (199.77 mM) | |
Ethanol | 42 mg/mL warmed with 50ºC water bath (158.31 mM) | |||
Water | Insoluble | |||
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. |
製品説明 | Anisomycin (Flagecidin, Wuningmeisu C) is a bacterial antibiotic isolated from Streptomyces griseolus, which inhibits protein synthesis, and also act as a JNK activator. Anisomycin upregulates autophagy and increases apoptosis. |
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in vitro | Anisomycin (3 μM) decreases protein synthesis in MDA16 and MDA-MB-468 cells, and reduces colony formation by MDA-MB-468 cells. Anisomycin causes an increase in the number of apoptotic cells in MDA-MB-468 cultures, but not in MDA16 cultures. Anisomycin actives JNK phosphorylation in MDA-MB-468 cells.[2] In U251 and U87 cells, anisomycin (0.01-8 μM) inhibits the cell growth in time- and concentration-dependent manners with the IC50 (48 h) values of 0.233 and 0.192 μmol/L, respectively. Anisomycin (4 μM) causes 21.5% and 25.3% of apoptosis proportion in U251 and U87 cells, respectively, and activates p38 MAPK and JNK, while inactivated ERK1/2. Anisomycin (4 μM) reduces the level of PP2A/C subunit in a time-dependent manner in U251 and U87 cells.[3] Anisomycin inhibits EAC cell proliferation in concentration-dependent manner.[4] |
in vivo | Peritumoral administration of anisomycin (5 mg/kg) significantly suppresses Ehrlich ascites carcinoma (EAC) growth resulting in the survival of approximately 60% of the mice 90 days after EAC inoculation.[4] |
キナーゼアッセイ | JNK phosphorylation | |
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500,000 cells/well are seeded in 6-well plates and incubated overnight. Cells are then incubated for 1 h with test compounds or DMSO as vehicle control (final concentration 1% v/v). Puromycin is added (final concentration of 18 μM) and cells incubated for a further 10 min to label nascent polypeptide chains. Background labelling is determined by incubating cells without puromycin. Cells are then washed in HBSS, harvested by scraping and centrifuged (300 g, 5 min). Cells are resuspended in 0.5 mL 50 mM DTT containing phosphatase inhibitors and incubated at 95℃ for 10 min. Samples are then snap frozen in liquid nitrogen and stored at -20℃ until blotted. Samples (20–30 μg protein/sample) are blotted onto a PVDF membrane. The membrane is blocked and incubated with anti-phospho-Thr183/Tyr185-JNK antibody overnight at 4℃. Secondary antibodies are used to label the primary antibody and detected using an infrared scanner. The intensity of the fluorescence signal for anti-phospho-JNK antibody is background corrected and normalized for loading. | ||
細胞アッセイ | 細胞株 | Ehrlich ascites carcinoma (EAC) cells |
濃度 | 500 ng/mL | |
反応時間 | 48 h | |
実験の流れ | For the assay, EAC cells are plated in 96-well plates at a density of 10,000 cells/well/200 µL of medium. The cells are treated with the different concentrations of anisomycin for 48 h. Adriamycin (500 ng/mL) is used as a positive control. 0.5 mg/mL of MTT is added to each well. 4 h later, the formazan product of MTT reduction is dissolved in DMSO, and absorbance is measured at 570 nm using a Model 680 microplate reader. | |
動物実験 | 動物モデル | Male BALB/c mice |
投薬量 | 5 mg/kg | |
投与方法 | peritumorally |
, , J Cell Biochem, 2017, 118(12):4905-4913
Data from [Data independently produced by , , Redox Biol, 2018, 14:59-71]
Data from [Data independently produced by , , Redox Biol, 2018, 14:576-587]
The DNA-dependent protein kinase catalytic subunit exacerbates endotoxemia-induced myocardial microvascular injury by disrupting the MOTS-c/JNK pathway and inducing profilin-mediated lamellipodia degradation [ Theranostics, 2024, 14(4):1561-1582] | PubMed: 38389837 |
Cell mechanics regulate the migration and invasion of hepatocellular carcinoma cells via JNK signaling [ Acta Biomater, 2024, S1742-7061(24)00036-9] | PubMed: 38272199 |
Inhibition of the HMGB1/RAGE axis protects against cisplatin-induced ototoxicity via suppression of inflammation and oxidative stress [ Int J Biol Sci, 2024, 20(2):784-800] | PubMed: 38169643 |
Short-term tamoxifen administration improves hepatic steatosis and glucose intolerance through JNK/MAPK in mice [ Signal Transduct Target Ther, 2023, 8(1):94] | PubMed: 36864030 |
USP36 stabilizes nucleolar Snail1 to promote ribosome biogenesis and cancer cell survival upon ribotoxic stress [ Nat Commun, 2023, 14(1):6473] | PubMed: 37833415 |
Stress-induced red nucleus attenuation induces anxiety-like behavior and lymph node CCL5 secretion [ Nat Commun, 2023, 14(1):6923] | PubMed: 37903803 |
Stress-induced red nucleus attenuation induces anxiety-like behavior and lymph node CCL5 secretion [ Nat Commun, 2023, 10.1038/s41467-023-42814-1] | PubMed: 37903803 |
USP36 stabilizes nucleolar Snail1 to promote ribosome biogenesis and cancer cell survival upon ribotoxic stress [ Nat Commun, 2023, 14(1):6473] | PubMed: 37833415 |
Down-regulation of WWP2 aggravates Type 2 diabetes mellitus-induced vascular endothelial injury through modulating ubiquitination and degradation of DDX3X [ Cardiovasc Diabetol, 2023, 22(1):107] | PubMed: 37149668 |
PDK4 rescues high-glucose-induced senescent fibroblasts and promotes diabetic wound healing through enhancing glycolysis and regulating YAP and JNK pathway [ Cell Death Discov, 2023, 9(1):424] | PubMed: 38001078 |
長期の保管のために-20°Cの下で製品を保ってください。
人間や獣医の診断であるか治療的な使用のためにでない。
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