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@ARTICLE{Horos:862554,
author = {Horos, Rastislav and Büscher, Magdalena and Kleinendorst,
Rozemarijn and Alleaume, Anne-Marie and Tarafder, Abul K.
and Schwarzl, Thomas and Dziuba, Dmytro and Tischer,
Christian and Zielonka, Elisabeth M. and Adak, Asli and
Castello, Alfredo and Huber, Wolfgang and Sachse, Carsten
and Hentze, Matthias W.},
title = {{T}he {S}mall {N}on-coding {V}ault {RNA}1-1 {A}cts as a
{R}iboregulator of {A}utophagy},
journal = {Cell},
volume = {176},
number = {5},
issn = {0092-8674},
address = {New York, NY},
publisher = {Elsevier},
reportid = {FZJ-2019-02848},
pages = {1054 - 1067.e12},
year = {2019},
abstract = {Vault RNAs (vtRNA) are small non-coding RNAs transcribed by
RNA polymerase III found in many eukaryotes. Although they
have been linked to drug resistance, apoptosis, and viral
replication, their molecular functions remain unclear. Here,
we show that vault RNAs directly bind the autophagy receptor
sequestosome-1/p62 in human and murine cells. Overexpression
of human vtRNA1-1 inhibits, while its antisense LNA-mediated
knockdown enhances p62-dependent autophagy. Starvation of
cells reduces the steady-state and p62-bound levels of vault
RNA1-1 and induces autophagy. Mechanistically, p62 mutants
that fail to bind vtRNAs display increased p62
homo-oligomerization and augmented interaction with
autophagic effectors. Thus, vtRNA1-1 directly regulates
selective autophagy by binding p62 and interference with
oligomerization, a critical step of p62 function. Our data
uncover a striking example of the potential of RNA to
control protein functions directly, as previously recognized
for protein-protein interactions and post-translational
modifications.},
cin = {ER-C-3},
ddc = {610},
cid = {I:(DE-Juel1)ER-C-3-20170113},
pnm = {551 - Functional Macromolecules and Complexes (POF3-551)},
pid = {G:(DE-HGF)POF3-551},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30773316},
UT = {WOS:000459257500010},
doi = {10.1016/j.cell.2019.01.030},
url = {https://juser.fz-juelich.de/record/862554},
}