Cat. No. 1290
Chemical Name: (2R,3S,4S)-2-[(4-Methoxyphenyl)meth
Biological ActivityProtein synthesis inhibitor (blocks translation). Potent activator of stress-activated protein kinases (JNK/SAPK) and p38 MAP kinase. Acts as a potent signaling agonist to selectively elicit homologous desensitization of immediate early gene induction (c-fos, fosB, c-jun, junB and junD).
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
Certificate of Analysis / Safety Data Sheet
Cano et al (1994) Anisomycin-activated protein kinases p45 and p55 but not mitogen-activated protein kinases ERK-1 and -2 are implicated in the induction of c-fos and c-jun. Mol.Cell.Biol. 14 7352. PMID: 7935449.
Kyriakis et al (1994) The stress-activated protein kinase subfamily of c-Jun kinases. Nature 369 156. PMID: 8177321.
Sanchez et al (1994) Role of SAPK/ERK kinase-1 in the stress-activated pathway regulating transcription factor c-Jun. Nature 372 794. PMID: 7997269.
Hazzalin et al (1998) Anisomycin selectively desensitizes signalling components involved in stress kinase activation and fos and jun induction. Mol.Cell.Biol. 18 1844. PMID: 9528756.
Croons et al (2009) The protein synthesis inhibitor anisomycin induces macrophage apoptosis in rabbit atherosclerotic plaques through p38 mitogen-activated protein kinase. J.Pharmacol.Exp.Ther. 329 856. PMID: 19286921.
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Keywords: Anisomycin, supplier, Protein, synthesis, inhibitors, blocks, blocker, translation, activates, Activator, JNK, stress-activated, SAPK, p38, MAP, protein, kinases, MAPK, Signaling, Signalling, c-Jun, N-Terminal, Kinase, Mitogen-Activated, antibiotics, Tocris Bioscience, JNK/c-Jun Activators
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