Catalog No.S7409 Synonyms: Flagecidin
Molecular Weight(MW): 265.3
Anisomycin is an antibiotic, which inhibits protein synthesis, and also act as a JNK activator.
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(c) Immunostaining of Cx32, ALB, CPS1, CK18 and ECAD in hESC-Heps induced with SB or anisomycin.
Sci Rep, 2016, 6:37388. Anisomycin purchased from Selleck.
Effect of TMZ (100 μmol/l for U87 cells, 50 μmol/l for U251 cells), anisomycin (4 μmol/l), SB203580 (10 μmol/l), TMZ+SB203580 (10 μmol/l) treatment on thephosphorylation of p38 and AQP4 for 24 h in U87 cells and U251 cells, detected by Western blotting. (A) Protein expression of p-p38, p38 and AQP4 in U87 cells with differenttreatments. (B) The ration of p-p38/p38 in U87 cells. (C) The proportion of AQP4 in GAPDH in U87 cells. (D) Protein expression of p-p38, p38 and AQP4 in U251 cells withdifferent treatments. (E) The ration of p-p38/p38 in U251 cells. (F) The proportion of AQP4 in GAPDH in U251 cells. *P< 0.05 versus the control group
J Cell Biochem, 2017, 118(12):4905-4913. Anisomycin purchased from Selleck.
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|Description||Anisomycin is an antibiotic, which inhibits protein synthesis, and also act as a JNK activator.|
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. 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. Anisomycin inhibits EAC cell proliferation in concentration-dependent manner.
|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.|
JNK phosphorylation: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.
|In vitro||DMSO||41 mg/mL warmed (154.54 mM)|
|Ethanol||17 mg/mL warmed (64.07 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+corn oil
For best results, use promptly after mixing.
* 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.
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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
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