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7LS2

80S ribosome from mouse bound to eEF2 (Class I)

This is a non-PDB format compatible entry.
Summary for 7LS2
Entry DOI10.2210/pdb7ls2/pdb
EMDB information23501
Descriptor60S ribosomal protein L7, 5S rRNA, 5.8S rRNA, ... (89 entities in total)
Functional Keywordsribosome, regulation, translation
Biological sourceMus musculus (Mouse)
More
Total number of polymer chains85
Total formula weight3922907.10
Authors
Loerch, S.,Smith, P.R.,Kunder, N.,Stanowick, A.D.,Lou, T.-F.,Campbell, Z.T. (deposition date: 2021-02-17, release date: 2021-11-03, Last modification date: 2024-12-25)
Primary citationSmith, P.R.,Loerch, S.,Kunder, N.,Stanowick, A.D.,Lou, T.F.,Campbell, Z.T.
Functionally distinct roles for eEF2K in the control of ribosome availability and p-body abundance.
Nat Commun, 12:6789-6789, 2021
Cited by
PubMed Abstract: Processing bodies (p-bodies) are a prototypical phase-separated RNA-containing granule. Their abundance is highly dynamic and has been linked to translation. Yet, the molecular mechanisms responsible for coordinate control of the two processes are unclear. Here, we uncover key roles for eEF2 kinase (eEF2K) in the control of ribosome availability and p-body abundance. eEF2K acts on a sole known substrate, eEF2, to inhibit translation. We find that the eEF2K agonist nelfinavir abolishes p-bodies in sensory neurons and impairs translation. To probe the latter, we used cryo-electron microscopy. Nelfinavir stabilizes vacant 80S ribosomes. They contain SERBP1 in place of mRNA and eEF2 in the acceptor site. Phosphorylated eEF2 associates with inactive ribosomes that resist splitting in vitro. Collectively, the data suggest that eEF2K defines a population of inactive ribosomes resistant to recycling and protected from degradation. Thus, eEF2K activity is central to both p-body abundance and ribosome availability in sensory neurons.
PubMed: 34815424
DOI: 10.1038/s41467-021-27160-4
PDB entries with the same primary citation
Experimental method
ELECTRON MICROSCOPY (3.1 Å)
Structure validation

237735

数据于2025-06-18公开中

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