Promoter escape

Barthalmus, G. T. and Zielinski, W. J. (1988). Xenopus skin mucus induces oral dyskinesias that promote escape from snakes. Pharmacology,BiochemisttyandBehavior30,957-959. 

Miller TW, Hennessy BT, Gonzalez-Angulo AM et al (2001) Hyperactivation ofphosphati-dylinositol-3 kinase promotes escape from hormone dependence in estrogen receptor-positive human breast cancer. J Clin Invest 120 2406-2413... 

Dvir, A. (2002). Promoter escape by RNA polymerase II. Biochim. Biophys. Acta. 1577(2), 208-223. 

Kugel, J. F., and Goodrich, J. A. (1998). Promoter escape limits the rate of RNA polymerase II transcription and is enhanced by TFIIE, TFIIH, and ATP on negatively supercoiled DNA. Proc. Natl. Acad. Sci. USA 95(16), 9232-9237. 

To study whether these HL vectors were affecting transfection activity through pH-sensitive changes in membrane fusion within the endosome to promote escape, Chaudhuri et al. used a fluorescence resonance energy transfer (FRET) technique. HL-l/Chol liposomes were incubated with Rhodamine Red -containing liposomes and subjected to... 

Davis et al. created a set of insulated bacterial promoters to facilitate promoter transfer from ORF (Open Reading Frame) to ORF without modifying the relative expression level within the promoter set, i.e. promoter one should always be A times stronger than promoter two in different genetic backgrounds. To accomplish this a minimal 51 bp promoter sequence was identified and used as reference. This minimal promoter sequence was insulated up- and downstream with sequences designed to protect against transcription iiutiation and promoter escape (Davis et al. 2011). 

Dehousse et al. added pH-sensitive methacrylic acid (MAA) copolymer to TMC/ siRNA complexes to promote escape of complexes from the endosome to the cytoplasm [74]. MAA/TMC/siRNA complexes were able to transfect L929 cells with greater efficiency of inhibition of RhoA mRNA expression than were TMC/ siRNA complexes owing to the membrane-destabilizing property of MAA in the endosome. 

Generally, isolated olefinic bonds will not escape attack by these reagents. However, in certain cases where the rate of hydroxyl oxidation is relatively fast, as with allylic alcohols, an isolated double bond will survive. Thepresence of other nucleophilic centers in the molecule, such as primary and secondary amines, sulfides, enol ethers and activated aromatic systems, will generate undesirable side reactions, but aldehydes, esters, ethers, ketals and acetals are generally stable under neutral or basic conditions. Halogenation of the product ketone can become but is not always a problem when base is not included in the reaction mixture. The generated acid can promote formation of an enol which in turn may compete favorably with the alcohol for the oxidant. 

Since the endogenous levels of inducible transcription factors like NF-kB and NFAT (Duh et al. 1989 Kinoshita et al. 1997) in these cells have been reported to be very low, HIV-1 promoter activation is inefficient resulting in non-expression of viral gene products (Figs. 5.1 and 5.2). Therefore, these cells can escape immune surveillance and act as passive carriers of HIV-1 for their natural lifespan. 

Fig. 2.2 Simplified scheme of oxidant/antioxidant regulation ofNF-KB activation. Different stimuli, leading to an increase of ROS generation inside the ceU, activate the phosphorylation of IkB inhibitory protein and the subsequent proteolysis. Thioredoxin (Trx) may reduce activated NF-kB proteins facilitating nuclear translocation.Qnce released from IkB, the NF-kB complex translocates into the nucleus and the binding to DNA domain in the promoters and enhancers of genes such as TNF-a, IL-1, proliferation and chemotactic factors, adhesion molecule. Some of these genes, in turn, may further induce NF-kB activation, leading to a vicious circle if the regulatory cellular system escapes from...

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