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Activator of MAPK, Jnk and p38
BML-ST102-0050 50 mg 247.00 USD
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Replaces Prod. #: ALX-380-051

Antibiotic. Activates JNK/SAPKs, p38 and MAP kinases but not ERKs leading to the phosphorylation of S6, histone H3 and HMG-14 and the induction of the immediate-early genes c-fos and c-jun. Induces apoptosis in the human monoblastoid cell line. Used at 300 ng/ml. Inhibits peptidyl transferase at higher concentrations. Used in the eradication of bean mildew. Inhibits other pathogenic fungi in plants. 

Product Details

Alternative Name:2-(p-Methoxybenzyl)-3,4-pyrrolidinediol-3-acetate
Source:Isolated from Streptomyces griseolus.
MI:14: 670
Purity:≥97% (TLC)
Appearance:White solid.
Solubility:Soluble in DMSO (25mg/ml).
Shipping:Ambient Temperature
Long Term Storage:-20°C
Use/Stability:Stable for at least 1 year after receipt when stored, as supplied, at -20°C. Stock solutions are stable for up to 3 months at -20°C.
Regulatory Status:RUO - Research Use Only
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Product Literature References

p38 MAPK regulates the Wnt inhibitor Dickkopf-1 in osteotropic prostate cancer cells: A.J. Browne, et al.; Cell Death Dis. 7, e2119 (2016), Application(s): Cell culture, Abstract;
Anisomycin abrogates repression of protooncogene c-fos transcription in E1A + cHa-ras-transformed cells through activation of MEK/ERK kinase cascade: A. N. Kukushkin, et al.; J. Cell. Biochem. 103, 1005 (2008), Abstract;
A chemical screen identifies anisomycin as an anoikis sensitizer that functions by decreasing FLIP protein synthesis: I.A. Mawji, et al.; Cancer Res. 67, 8307 (2007), Abstract;
Anisomycin and the reconsolidation hypothesis: J.W. Rudy, et al.; Learn. Mem. 13, 1 (2006), Review, Abstract;
Downregulation of Ski and SnoN co-repressors by anisomycin: A. Vazquez-Macias, et al.; FEBS Lett. 579, 3701 (2005), Abstract;
Anisomycin treatment paradigm affects duration of long-term potentiation in slices of the amygdala: P. Okulski, et al.; Neuroscience 114, 1 (2002), Abstract;
Anisomycin selectively desensitizes signalling components involved in stress kinase activation and fos and jun induction: C.A. Hazzalin, et al.; Mol Cell Biol 18, 1844 (1998), Abstract;
Growth-dependent translation of IGF-II mRNA by a rapamycin-sensitive pathway: F.C. Nielsen, et al.; Nature 377, 358 (1995), Abstract;
Neither ERK nor JNK/SAPK MAP kinase subtypes are essential for histone H3/HMG-14 phosphorylation or c-fos and c-jun induction: E. Cano, et al.; J. Cell Sci. 108, 3599 (1995), Abstract;
Protein synthesis inhibitors reveal differential regulation of mitogen-activated protein kinase and stress-activated protein kinase pathways that converge on Elk-1: R. Zinck, et al.; Mol. Cell. Biol. 15, 4930 (1995), Abstract;
Anisomycin and rapamycin define an area upstream of p70/85S6k containing a bifurcation to histone H3-HMG-like protein phosphorylation and c-fos-c-jun induction: E. Kardalinou, et al.; Mol. Cell. Biol. 14, 1066 (1994), Abstract;
Protein synthesis inhibitor phase shifts vasopressin rhythms in long- term suprachiasmatic cultures: K. Shinohara & T. Oka; NeuroReport 5, 2201 (1994), Abstract;
Role of SAPK/ERK kinase-1 in the stress-activated pathway regulating transcription factor c-Jun: I. Sanchez, et al.; Nature 372, 794 (1994), Abstract;
The stress-activated protein kinase subfamily of c-Jun kinases: J.M. Kyriakis, et al.; Nature 369, 156 (1994), Abstract;
DNA fragmentation and cytolysis in U937 cells treated with diphtheria toxin or other inhibitors of protein synthesis: S.K. Kochi & R.J. Collier; Exp. Cell. Res. 208, 296 (1993), Abstract;
Anisomycin, a new anti-protozoan antibiotic: B. A. Sobin & F. W. Tanner; J. Am. Chem. Soc. 76, 4053 (1954),

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