Autor: |
János Bencze, Gábor Miklós Mórotz, Woosung Seo, Viktor Bencs, János Kálmán, Christopher Charles John Miller, Tibor Hortobágyi |
Jazyk: |
angličtina |
Rok vydání: |
2018 |
Předmět: |
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Zdroj: |
Molecular Brain, Vol 11, Iss 1, Pp 1-9 (2018) |
Druh dokumentu: |
article |
ISSN: |
1756-6606 |
DOI: |
10.1186/s13041-018-0363-x |
Popis: |
Abstract Neurodegenerative disorders are frequent, incurable diseases characterised by abnormal protein accumulation and progressive neuronal loss. Despite their growing prevalence, the underlying pathomechanism remains unclear. Lemur tyrosine kinase 2 (LMTK2) is a member of a transmembrane serine/threonine-protein kinase family. Although it was described more than a decade ago, our knowledge on LMTK2’s biological functions is still insufficient. Recent evidence has suggested that LMTK2 is implicated in neurodegeneration. After reviewing the literature, we identified three LMTK2-mediated mechanisms which may contribute to neurodegenerative processes: disrupted axonal transport, tau hyperphosphorylation and enhanced apoptosis. Moreover, LMTK2 gene expression is decreased in an Alzheimer’s disease mouse model. According to these features, LMTK2 might be a promising therapeutic target in near future. However, further investigations are required to clarify the exact biological functions of this unique protein. |
Databáze: |
Directory of Open Access Journals |
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