% 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{Lai:890496,
author = {Lai, Hien T. T. and Giorgetti, Alejandro and Rossetti,
Giulia and Nguyen, Toan T. and Carloni, Paolo and Kranjc
Pietrucci, Agata},
title = {{T}he {I}nterplay of {C}holesterol and {L}igand {B}inding
in h{TSPO} from {C}lassical {M}olecular {D}ynamics
{S}imulations},
journal = {Molecules},
volume = {26},
number = {5},
issn = {1420-3049},
address = {Basel},
publisher = {MDPI},
reportid = {FZJ-2021-00995},
pages = {1250 -},
year = {2021},
abstract = {The translocator protein (TSPO) is a 18kDa transmembrane
protein, ubiquitously present in human mitochondria. It is
overexpressed in tumor cells and at the sites of
neuroinflammation, thus representing an important biomarker,
as well as a promising drug target. In mammalian TSPO, there
are cholesterol–binding motifs, as well as a binding
cavity able to accommodate different chemical compounds.
Given the lack of structural information for the human
protein, we built a model of human (h) TSPO in the apo state
and in complex with PK11195, a molecule routinely used in
positron emission tomography (PET) for imaging of
neuroinflammatory sites. To better understand the
interactions of PK11195 and cholesterol with this
pharmacologically relevant protein, we ran molecular
dynamics simulations of the apo and holo proteins embedded
in a model membrane. We found that: (i) PK11195 stabilizes
hTSPO structural fold; (ii) PK11195 might enter in the
binding site through transmembrane helices I and II of
hTSPO; (iii) PK11195 reduces the frequency of cholesterol
binding to the lower, N–terminal part of hTSPO in the
inner membrane leaflet, while this impact is less pronounced
for the upper, C–terminal part in the outer membrane
leaflet, where the ligand binding site is located; (iv) very
interestingly, cholesterol most frequently binds
simultaneously to the so-called CRAC and CARC regions in TM
V in the free form (residues L150–X–Y152–X(3)–R156
and R135–X(2)–Y138–X(2)–L141, respectively).
However, when the protein is in complex with PK11195,
cholesterol binds equally frequently to the
CRAC–resembling motif that we observed in TM I (residues
L17–X(2)–F20–X(3)–R24) and to CRAC in TM V. We
expect that the CRAC–like motif in TM I will be of
interest in future experimental investigations. Thus, our MD
simulations provide insight into the structural features of
hTSPO and the previously unknown interplay between PK11195
and cholesterol interactions with this pharmacologically
relevant protein.},
cin = {IAS-5 / INM-9},
ddc = {540},
cid = {I:(DE-Juel1)IAS-5-20120330 / I:(DE-Juel1)INM-9-20140121},
pnm = {5241 - Molecular Information Processing in Cellular Systems
(POF4-524)},
pid = {G:(DE-HGF)POF4-5241},
typ = {PUB:(DE-HGF)16},
pubmed = {33652554},
UT = {WOS:000628444600001},
doi = {10.3390/molecules26051250},
url = {https://juser.fz-juelich.de/record/890496},
}