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  Insights into the assembly and architecture of a Staufen-mediated mRNA decay (SMD)-competent mRNP.

Gowravaram, M., Schwarz, J., Khilji, S. K., Urlaub, H., & Chakrabarti, S. (2019). Insights into the assembly and architecture of a Staufen-mediated mRNA decay (SMD)-competent mRNP. Nature Communications, 10(1): 5054. doi:10.1038/s41467-019-13080-x.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0005-3A86-3 Version Permalink: http://hdl.handle.net/21.11116/0000-0005-3A8A-F
Genre: Journal Article

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Gowravaram, M., Author
Schwarz, J.1, Author              
Khilji, S. K., Author
Urlaub, H.2, Author              
Chakrabarti, S., Author
Affiliations:
1Research Group of Sleep and Waking, MPI for biophysical chemistry, Max Planck Society, ou_578607              
2Research Group of Bioanalytical Mass Spectrometry, MPI for biophysical chemistry, Max Planck Society, ou_578613              

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 Abstract: The mammalian Staufen proteins (Stau1 and Stau2) mediate degradation of mRNA containing complex secondary structures in their 3'-untranslated region (UTR) through a pathway known as Staufen-mediated mRNA decay (SMD). This pathway also involves the RNA helicase UPF1, which is best known for its role in the nonsense-mediated mRNA decay (NMD) pathway. Here we present a biochemical reconstitution of the recruitment and activation of UPF1 in context of the SMD pathway. We demonstrate the involvement of UPF2, a core NMD factor and a known activator of UPF1, in SMD. UPF2 acts as an adaptor between Stau1 and UPF1, stimulates the catalytic activity of UPF1 and plays a central role in the formation of an SMD-competent mRNP. Our study elucidates the molecular mechanisms of SMD and points towards extensive cross-talk between UPF1-mediated mRNA decay pathways in cells.

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Language(s): eng - English
 Dates: 2019-11-07
 Publication Status: Published online
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 Rev. Type: Peer
 Identifiers: DOI: 10.1038/s41467-019-13080-x
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Title: Nature Communications
Source Genre: Journal
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Pages: 14 Volume / Issue: 10 (1) Sequence Number: 5054 Start / End Page: - Identifier: -