% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Krichel:872750,
author = {Krichel, Carsten and Möckel, Christina and Schillinger,
Oliver and Huesgen, Pitter F. and Sticht, Heinrich and
Strodel, Birgit and Weiergräber, Oliver H. and Willbold,
Dieter and Neudecker, Philipp},
title = {{S}olution structure of the autophagy-related protein
{LC}3{C} reveals a polyproline {II} motif on a mobile tether
with phosphorylation site},
journal = {Scientific reports},
volume = {9},
number = {1},
issn = {2045-2322},
address = {[London]},
publisher = {Macmillan Publishers Limited, part of Springer Nature},
reportid = {FZJ-2020-00228},
pages = {14167},
year = {2019},
abstract = {(Macro-)autophagy is a compartmental degradation pathway
conserved from yeast to mammals. The yeast protein Atg8
mediates membrane tethering/hemifusion and cargo recruitment
and is essential for autophagy. The human MAP1LC3/GABARAP
family proteins show high sequence identity with Atg8, but
MAP1LC3C is distinguished by a conspicuous amino-terminal
extension with unknown functional significance. We have
determined the high-resolution three-dimensional structure
and measured the backbone dynamics of MAP1LC3C by NMR
spectroscopy. From Ser18 to Ala120, MAP1LC3C forms an
α-helix followed by the ubiquitin-like tertiary fold with
two hydrophobic binding pockets used by MAP1LC3/GABARAP
proteins to recognize targets presenting LC3-interacting
regions (LIRs). Unlike other MAP1LC3/GABARAP proteins, the
amino-terminal region of MAP1LC3C does not form a stable
helix α1 but a “sticky arm” consisting of a polyproline
II motif on a flexible linker. Ser18 at the interface
between this linker and the structural core can be
phosphorylated in vitro by protein kinase A, which causes
additional conformational heterogeneity as monitored by NMR
spectroscopy and molecular dynamics simulations, including
changes in the LIR-binding interface. Based on these results
we propose that the amino-terminal polyproline II motif
mediates specific interactions with the microtubule
cytoskeleton and that Ser18 phosphorylation modulates the
interplay of MAP1LC3C with its various target proteins.},
cin = {ICS-6 / ZEA-3},
ddc = {600},
cid = {I:(DE-Juel1)ICS-6-20110106 / I:(DE-Juel1)ZEA-3-20090406},
pnm = {552 - Engineering Cell Function (POF3-552)},
pid = {G:(DE-HGF)POF3-552},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31578424},
UT = {WOS:000488481500030},
doi = {10.1038/s41598-019-48155-8},
url = {https://juser.fz-juelich.de/record/872750},
}