Signalling to translation: how signal transduction pathways control the protein synthetic machinery
Proud, C.G. (2007) Signalling to translation: how signal transduction pathways control the protein synthetic machinery. Biochemical Journal, 403, (2), 217-234. (doi:10.1042/BJ20070024).
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Recent advances in our understanding of both the regulation of components of the translational machinery and the upstream signalling pathways that modulate them have provided important new insights into the mechanisms by which hormones, growth factors, nutrients and cellular energy status control protein synthesis in mammalian cells. The importance of proper control of mRNA translation is strikingly illustrated by the fact that defects in this process or its control are implicated in a number of disease states, such as cancer, tissue hypertrophy and neurodegeneration. Signalling pathways such as those involving mTOR (mammalian target of rapamycin) and mitogen-activated protein kinases modulate the phosphorylation of translation factors, the activities of the protein kinases that act upon them and the association of RNA-binding proteins with specific mRNAs. These effects contribute both to the overall control of protein synthesis (which is linked to cell growth) and to the modulation of the translation or stability of specific mRNAs. However, important questions remain about both the contributions of individual regulatory events to the control of general protein synthesis and the mechanisms by which the translation of specific mRNAs is controlled.
|Digital Object Identifier (DOI):||doi:10.1042/BJ20070024|
|Keywords:||mammalian target of rapamycin (mTOR), mRNA, mRNA translation, ribosome, signal transduction, translation factor|
|Subjects:||Q Science > QD Chemistry
Q Science > QH Natural history > QH301 Biology
|Divisions :||University Structure - Pre August 2011 > School of Biological Sciences
|Accepted Date and Publication Date:||
|Date Deposited:||06 Aug 2008|
|Last Modified:||31 Mar 2016 12:36|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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