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@ARTICLE{Kaiser:912181,
author = {Kaiser, Jesko and Gertzen, Christoph G. W. and Bernauer,
Tamara and Höfner, Georg and Niessen, Karin V. and Seeger,
Thomas and Paintner, Franz F. and Wanner, Klaus T. and
Worek, Franz and Thiermann, Horst and Gohlke, Holger},
title = {{A} novel binding site in the nicotinic acetylcholine
receptor for {MB}327 can explain its allosteric modulation
relevant for organophosphorus-poisoning treatment},
journal = {Toxicology letters},
volume = {373},
issn = {0378-4274},
address = {Amsterdam [u.a.]},
publisher = {Elsevier Science},
reportid = {FZJ-2022-05397},
pages = {160-171},
year = {2023},
abstract = {Organophosphorus compounds (OPCs) are highly toxic
compounds that can block acetylcholine esterase (AChE) and
thereby indirectly lead to an overstimulation of muscarinic
and nicotinic acetylcholine receptors (nAChRs). The current
treatment with atropine and AChE reactivators (oximes) is
insufficient to prevent toxic effects, such as respiratory
paralysis, after poisonings with various OPCs. Thus,
alternative treatment options are required to increase
treatment efficacy. Novel therapeutics, such as the
bispyridinium non-oxime MB327, have been found to
reestablish neuromuscular transmission by interacting
directly with nAChR, probably via allosteric mechanisms. To
rationally design new, more potent drugs addressing nAChR,
knowledge of the binding mode of MB327 is fundamental.
However, the binding pocket of MB327 has remained elusive.
Here, we identify a new potential allosteric binding pocket
(MB327-PAM-1) of MB327 located at the transition of the
extracellular to the transmembrane region using blind
docking experiments and molecular dynamics simulations.
MB327 forms striking interactions with the receptor at this
site. The interacting amino acids are highly conserved among
different subunits and different species. Correspondingly,
MB327 can interact with several nAChR subtypes from
different species. We predict by rigidity analysis that
MB327 exerts an allosteric effect on the orthosteric binding
pocket and the transmembrane domain after binding to
MB327-PAM-1. Furthermore, free ligand diffusion MD
simulations reveal that MB327 also has an affinity to the
orthosteric binding pocket, which agrees with recently
published results that related bispyridinium compounds show
inhibitory effects via the orthosteric binding site. The
newly identified binding site allowed us to predict
structural modifications of MB327, resulting in the more
potent resensitizers PTM0062 and PTM0063.},
cin = {NIC / JSC / IBI-7 / IBG-4},
ddc = {610},
cid = {I:(DE-Juel1)NIC-20090406 / I:(DE-Juel1)JSC-20090406 /
I:(DE-Juel1)IBI-7-20200312 / I:(DE-Juel1)IBG-4-20200403},
pnm = {5111 - Domain-Specific Simulation $\&$ Data Life Cycle Labs
(SDLs) and Research Groups (POF4-511) / Forschergruppe
Gohlke $(hkf7_20200501)$ / 5241 - Molecular Information
Processing in Cellular Systems (POF4-524)},
pid = {G:(DE-HGF)POF4-5111 / $G:(DE-Juel1)hkf7_20200501$ /
G:(DE-HGF)POF4-5241},
typ = {PUB:(DE-HGF)16},
pubmed = {36503818},
UT = {WOS:000928240000002},
doi = {10.1016/j.toxlet.2022.11.018},
url = {https://juser.fz-juelich.de/record/912181},
}