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@ARTICLE{Marjault:907657,
author = {Marjault, Henri-Baptiste and Karmi, Ola and Zuo, Ke and
Michaeli, Dorit and Eisenberg-Domovich, Yael and Rossetti,
Giulia and de Chassey, Benoit and Vonderscher, Jacky and
Cabantchik, Ioav and Carloni, Paolo and Mittler, Ron and
Livnah, Oded and Meldrum, Eric and Nechushtai, Rachel},
title = {{A}n anti-diabetic drug targets {NEET} ({CISD}) proteins
through destabilization of their [2{F}e-2{S}] clusters},
journal = {Communications biology},
volume = {5},
number = {1},
issn = {2399-3642},
address = {London},
publisher = {Springer Nature},
reportid = {FZJ-2022-02136},
pages = {437},
year = {2022},
abstract = {Elevated levels of mitochondrial iron and reactive oxygen
species (ROS) accompany the progression of diabetes,
negatively impacting insulin production and secretion from
pancreatic cells. In search for a tool to reduce
mitochondrial iron and ROS levels, we arrived at a molecule
that destabilizes the [2Fe-2S] clusters of NEET proteins
(M1). Treatment of db/db diabetic mice with M1 improved
hyperglycemia, without the weight gain observed with
alternative treatments such as rosiglitazone. The molecular
interactions of M1 with the NEET proteins mNT and NAF-1 were
determined by X-crystallography. The possibility of
controlling diabetes by molecules that destabilize the
[2Fe–2S] clusters of NEET proteins, thereby reducing
iron-mediated oxidative stress, opens a new route for
managing metabolic aberration such as in diabetes.},
cin = {IAS-5 / INM-9 / JSC},
ddc = {570},
cid = {I:(DE-Juel1)IAS-5-20120330 / I:(DE-Juel1)INM-9-20140121 /
I:(DE-Juel1)JSC-20090406},
pnm = {5252 - Brain Dysfunction and Plasticity (POF4-525) / 5111 -
Domain-Specific Simulation $\&$ Data Life Cycle Labs (SDLs)
and Research Groups (POF4-511)},
pid = {G:(DE-HGF)POF4-5252 / G:(DE-HGF)POF4-5111},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35538231},
UT = {WOS:000793196800001},
doi = {10.1038/s42003-022-03393-x},
url = {https://juser.fz-juelich.de/record/907657},
}