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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Dibutyryl-cAMP sodium salt is a cell-permeable cAMP that activates cAMP-dependent protein kinase (PKA) and is a phosphodiesterase inhibitor. Because it mimics cAMP and induces normal physiological responses when added to cells under experimental conditions, dibutyryl-cAMP is widely used in a variety of research applications[1,2].
References:[1]. Bartsch M, Zorn-Kruppa M, Kühl N, et al. Bioactivatable, membrane-permeant analogs of cyclic nucleotides as biological tools for growth control of C6 glioma cells. Biological Chemistry, 2003, 384(9): 1321-1326.[2]. Rundfeldt C, Steckel H, Sörensen T, et al. The stable cyclic adenosine monophosphate analogue, dibutyryl cyclo-adenosine monophosphate (bucladesine), is active in a model of acute skin inflammation. Archives of Dermatological Research, 2012, 304(4): 313-317.
Cell lines
Hippocampal neurons from 17E Sprague-Dawley rats
Reaction Conditions
0, 0.5, 1, 5, 10 and 50 μM dibutyryl cAMP for 1 h incubation
Applications
Dibutyryl cAMP significantly inhibited neuronal glucose uptake in a dose-dependent manner. Neurons exposed to 50 μM dibutyryl cAMP showed only 13% of glucose uptake by the control neurons.
Animal models
Mice, 20 ~ 25 g
Dosage form
600 nM/mouse
Injected intraperitoneally for 4 days
Treatment with intraperitoneal injection of dibutyryl cAMP (600 nM/mouse) reversed zinc chloride- and lead acetate-induced avoidance memory retention impairments in mice. Thus, dibutyryl cAMP could be used to explore the potential role of protein kinase A pathways in zinc chloride- and lead acetate-induced avoidance memory alterations.
Note
The technical data provided above is for reference only.
References:
1. Prapong T, Uemura E, Hsu WH. G protein and cAMP-dependent protein kinase mediate amyloid beta-peptide inhibition of neuronal glucose uptake. Experimental Neurology, 2001, 167(1): 59-64.
2. Tabrizian K, Yazdani A, Baheri B, et al. Zinc chloride and lead acetate-induced passive avoidance memory retention deficits reversed by nicotine and bucladesine in mice. Biological Trace Element Research, 2016, 169(1): 106-113.
