Muscular Dystrophy Duchenne Modifying Genes and Pathways

Name: Muscular Dystrophy Duchenne Modifying Genes and Pathways
Brand: Sudwestdeutscher Verlag Fur Hochschulschriften AG
SKU: 9783838120805
Price: 72.88 EUR
Availability: InStock

Автор: Stefanie Grunwald

Език:

Корици: С меки корици

Издател: Sudwestdeutscher Verlag Fur Hochschulschriften AG

Наличност: Външен склад

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72.88 € 142.53 лв

DMD is the most common muscular dystrophy in childhood and incurable to date. It is caused by the ab...

Информация за книгата

Автор

Stefanie Grunwald

Език

Английски език

Корици

Книга - С меки корици

Издадена

2010

страници

176

EAN

9783838120805

ISBN

3838120809

Enbook ID

06948698

Издател

Sudwestdeutscher Verlag Fur Hochschulschriften AG

Теглоt

268

Размери

152 x 229 x 10

Пълно описание

DMD is the most common muscular dystrophy in childhood and incurable to date. It is caused by the absence of dystrophin, what influences several signal transduction pathways. The thesis is interested in the investigation and modulation of signal transduction pathways that may compensate the lack of dystrophin as an alternative therapy strategy. To study dystrophin downstream pathways, the mRNA expression of DMD patients and two DMD siblings with an intra-familially different course of DMD were analysed. Genes, found differently expressed in the two DMD siblings, are first part of a signalling pathway linking dystrophin, which is first represented in a Petri net. The central point of this pathway is the transcription factor NFATc. Invariant and theoretical knockout analyses of the net were applied. On human SkMCs, modulation of protein activity and of gene expression using siRNA, vector-DNA, and chemical substances were performed. The cells were studied by proliferation and vitality tests as well as expression analyses at mRNA and protein level. According to the basic idea of this study, a new therapeutic strategy becomes apparent, which considers dystrophin downstream processes.

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Muscular Dystrophy Duchenne Modifying Genes and Pathways

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