|
|
|
|
|
| Kameshwar R. Ayasolla; Ravi K. R. Kalathur; Matthias E. Futschik. |
| Although the disease causing gene huntingtin has been known for some time, the exact cause of neuronal cell death during _Huntington's disease_ (HD) remains unknown. One potential mechanism contributing to the massive loss of neurons in HD brains might be the _Unfolded Protein Response_ (UPR) which is activated by accumulation of misfolded proteins in the endoplasmic reticulum (ER). As an adaptive response, UPR upregulates transcription of chaperones, temporarily attenuating new translation and activates protein degradation via the proteasome. However, at high levels of ER stress, UPR signalling can contribute to neuronal apoptosis.

Our primary aims include (a) construction of the UPR signalling network, (b)... |
| Tipo: Poster |
Palavras-chave: Neuroscience; Bioinformatics. |
| Ano: 2012 |
URL: http://precedings.nature.com/documents/7078/version/1 |
| |
|
|
| Ravi K. Kalathur; Matthias E. Futschik. |
| The use of high-throughput technologies has provided us with large amounts of data for _Huntington's disease_ (HD), especially at the gene and protein levels. As phenotypic changes in HD may not just be due to the activity of individual genes but interrelated alterations of whole molecular networks, it is important to systematically analyse and represent accumulated data in a network-based approach.

Methods: To analyse and visualise protein interaction networks through a dedicated database to HD, we have established "HDNetDB": http://hdnetdb.sysbiolab.eu. This platform will not only help to understand molecular mechanisms better, but also assist in identifying potential molecular markers... |
| Tipo: Poster |
Palavras-chave: Neuroscience; Bioinformatics. |
| Ano: 2012 |
URL: http://precedings.nature.com/documents/7090/version/1 |
| |
|
|
|
