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@ARTICLE{Njavro:145058,
author = {Njavro, Jasenka and Klotz, Jakob and Dislich, Bastian and
Wanngren, Johanna and Shmueli, Merav and Herber, Julia and
Kuhn, Peer-Hendrik and Kumar, Rohit and Koeglsperger, Thomas
and Conrad, Marcus and Wurst, Wolfgang and Feederle, Regina
and Vlachos, Andreas and Michalakis, Stylianos and Jedlicka,
Peter and Müller, Stephan A and Lichtenthaler, Stefan F},
title = {{M}ouse brain proteomics establishes {MDGA}1 and {CACHD}1
as in vivo substrates of the {A}lzheimer protease {BACE}1.},
journal = {The FASEB journal},
volume = {34},
number = {2},
issn = {0892-6638},
address = {Hoboken, NJ},
publisher = {Wiley},
reportid = {DZNE-2020-00417},
pages = {2465-2482},
year = {2020},
abstract = {The protease beta-site APP cleaving enzyme 1 (BACE1) has
fundamental functions in the nervous system. Its inhibition
is a major therapeutic approach in Alzheimer's disease,
because BACE1 cleaves the amyloid precursor protein (APP),
thereby catalyzing the first step in the generation of the
pathogenic amyloid beta (Aβ) peptide. Yet, BACE1 cleaves
numerous additional membrane proteins besides APP. Most of
these substrates have been identified in vitro, but only few
were further validated or characterized in vivo. To identify
BACE1 substrates with in vivo relevance, we used isotope
label-based quantitative proteomics of wild type and
BACE1-deficient (BACE1 KO) mouse brains. This approach
identified known BACE1 substrates, including Close homolog
of L1 and contactin-2, which were found to be enriched in
the membrane fraction of BACE1 KO brains. VWFA and cache
domain-containing protein 1 (CACHD)1 and MAM
domain-containing glycosylphosphatidylinositol anchor
protein 1 (MDGA1), which have functions in synaptic
transmission, were identified and validated as new BACE1
substrates in vivo by immunoblots using primary neurons and
mouse brains. Inhibition or deletion of BACE1 from primary
neurons resulted in a pronounced inhibition of substrate
cleavage and a concomitant increase in full-length protein
levels of CACHD1 and MDGA1. The BACE1 cleavage site in both
proteins was determined to be located within the
juxtamembrane domain. In summary, this study identifies and
validates CACHD1 and MDGA1 as novel in vivo substrates for
BACE1, suggesting that cleavage of both proteins may
contribute to the numerous functions of BACE1 in the nervous
system.},
keywords = {Alzheimer Disease: genetics / Alzheimer Disease: metabolism
/ Alzheimer Disease: pathology / Amyloid Precursor Protein
Secretases: genetics / Amyloid Precursor Protein Secretases:
metabolism / Animals / Aspartic Acid Endopeptidases:
genetics / Aspartic Acid Endopeptidases: metabolism / Brain:
metabolism / Brain: pathology / Mice / Mice, Knockout /
Neural Cell Adhesion Molecules: genetics / Neural Cell
Adhesion Molecules: metabolism / Proteomics},
cin = {AG Lichtenthaler / Tübingen Pre 2020 / AG Höglinger 1 /
AG Wurst / AG Feederle / AG Haass old},
ddc = {570},
cid = {I:(DE-2719)1110006 / I:(DE-2719)6000018 /
I:(DE-2719)1110002 / I:(DE-2719)1140001 / I:(DE-2719)1140004
/ I:(DE-2719)1110007},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
- Clinical and Health Care Research (POF3-344)},
pid = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31908000},
doi = {10.1096/fj.201902347R},
url = {https://pub.dzne.de/record/145058},
}