Muscular Dystrophy Duchenne Modifying Genes and Pathways

Name: Muscular Dystrophy Duchenne Modifying Genes and Pathways
Brand: Sudwestdeutscher Verlag Fur Hochschulschriften AG
SKU: 9783838120805
Price: 27111 HUF
Availability: InStock

Szerző: Stefanie Grunwald

Nyelv:

Kötés: Puha kötésű

Kiadó: Sudwestdeutscher Verlag Fur Hochschulschriften AG

Elérhetőség: Beszállítói készleten

Küldés 5-8 napon belül

27 111 Ft

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

Információk a könyvről

Szerző

Stefanie Grunwald

Nyelv

Angol

Kötés

Könyv - Puha kötésű

Kiadva

2010

oldal

176

EAN

9783838120805

ISBN

3838120809

Enbook ID

06948698

Kiadó

Sudwestdeutscher Verlag Fur Hochschulschriften AG

Súly

268

Méretek

152 x 229 x 10

Teljes leírás

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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