Maren Oehlmann, Cathal Mahon, Heinz-Peter Nasheuer (auth.),'s Advances in Molecular Oncology: Edited under the auspices of PDF

By Maren Oehlmann, Cathal Mahon, Heinz-Peter Nasheuer (auth.), Director Fabrizio d'Adda di Fagagna, Director Susanna Chiocca, Director Fraser McBlane, Director Ugo Cavallaro (eds.)

ISBN-10: 0387691146

ISBN-13: 9780387691145

ISBN-10: 0387691162

ISBN-13: 9780387691169

Proceedings of the second Annual IFOM-IEO assembly on melanoma. it is a new assembly, it has approximately 2 hundred attendees from Australia, Austria, Belgium, Brazil, Canada, England, France, Germany, Greece, eire, Italy, Japan, Netherlands, Spain, Sweden, Switzerland, and the USA.

The second IFOM-IEO overseas assembly on melanoma will supply a discussion board during which the world’s prime melanoma researchers and younger scientists will talk about the newest advances in molecular oncology. The effect of modern breakthroughs in uncomplicated study and of rising applied sciences on molecular medication in melanoma might be highlighted.

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Extra resources for Advances in Molecular Oncology: Edited under the auspices of the European Institute of Oncology (IEO) and The FIRC Institute of Molecular Oncology Foundation (IFOM)

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As a control, we used an LATS2 knockdown construct (Figure 5F). These results show that a combined effect of RNA destruction and translation inhibition is used by miR-372&3 to silence LATS2. miR-372/3 was predicted to bind two sites in the 3′-UTR of LATS2 that are highly conserved between human, mouse, and zebrafish (Figure 5D). To further substantiate LATS2 as a direct target of miR372&3, we cloned its 3′-UTR downstream of the firefly luciferase gene (pGL3-LATS2) (Figure 5E). We transfected either pGL3-LATS2 or the controls pGL3-372 and pGL3-373 (containing a miR-complementary sequence in their 3′-UTR) or pGL3 into Tera1 and MCF-7 cells (respectively positive and negative for miR-371–3) (Figures 4D and S6).

As demonstrated by RPA, miR-Vec-372mut and miR-Vec-373mut indeed failed to express miR-372 and miR-373, respectively (Figure 3A). Note that miR-Vec-372mut still expressed miR-371 to a similar extent as the original miR-Vec-371&2. We then tested these constructs in a YFP-competition assay to detect possible growth advantages conferred by the miRNAs on 26 P. Mathijs Voorhoeve et al. BJ cells in the absence or presence of RASV12 (Figure 3B). For this purpose we used a miR-Vec vector that expresses YFP instead of a blasticidin resistance marker and compared the growth rates of YFP-tagged and untagged cells within one population.

2003). , 2004). , 2005). These observations suggest that the suppression of LATS2 explains at least in part the sustained activity of CDK in the presence of high p21cip1 levels in miR-372/3-expressing cells. To investigate the possibility that miR-372 and miR-373 suppress the expression of LATS2, we performed immunoblot analysis of cells expressing wt and mutant miR- 372&3, the cluster and the controls p53kd and empty vector. Both in the absence of RASV12 and in its presence, a significant reduction in LATS2 protein level was observed upon miR-372&3 expression 2.

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Advances in Molecular Oncology: Edited under the auspices of the European Institute of Oncology (IEO) and The FIRC Institute of Molecular Oncology Foundation (IFOM) by Maren Oehlmann, Cathal Mahon, Heinz-Peter Nasheuer (auth.), Director Fabrizio d'Adda di Fagagna, Director Susanna Chiocca, Director Fraser McBlane, Director Ugo Cavallaro (eds.)


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