Eva Szunyogova

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Spinal Muscular Atrophy (SMA) is caused by mutation or deletion of the survival motor neuron 1 (SMN1) gene. Decreased levels of, cell-ubiquitous, SMN protein is associated with a range of systemic pathologies reported in severe patients. Despite high levels of SMN protein in normal liver, there is no comprehensive study of liver pathology in SMA. We(More)
These errors have now been corrected in the PDF and HTML versions of the Article. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included(More)
The autosomal recessive neuromuscular disease spinal muscular atrophy (SMA) is caused by loss of survival motor neuron (SMN) protein. Molecular pathways that are disrupted downstream of SMN therefore represent potentially attractive therapeutic targets for SMA. Here, we demonstrate that therapeutic targeting of ubiquitin pathways disrupted as a consequence(More)
Description Histological identification of morphological alterations are key indicators of functional defects. For example, liver disease which compromises perfusion and consequently function, is very often associated with abnormal tissue microvasculature. Traditionally an anti-platelet endothelial cell adhesion molecule-1 (PECAM-1/ CD31) antibody is(More)
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