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@ARTICLE{Holzer:143670,
author = {K. Holzer and A. Ori and A. Cooke and D. Dauch$^*$ and E.
Drucker and P. Riemenschneider and A. Andres-Pons and A. L.
DiGuilio and M.-T. Mackmull and J. Baßler and S. Roessler
and K. Breuhahn and L. Zender$^*$ and J. S. Glavy and F.
Dombrowski and E. Hurt and P. Schirmacher and M. Beck and S.
Singer},
title = {{N}ucleoporin {N}up155 is part of the p53 network in liver
cancer.},
journal = {Nature Communications},
volume = {10},
number = {1},
issn = {2041-1723},
address = {[London]},
publisher = {Nature Publishing Group UK},
reportid = {DKFZ-2019-01244},
pages = {2147},
year = {2019},
abstract = {Cancer-relevant signalling pathways rely on bidirectional
nucleocytoplasmic transport events through the nuclear pore
complex (NPC). However, mechanisms by which individual NPC
components (Nups) participate in the regulation of these
pathways remain poorly understood. We discover by
integrating large scale proteomics, polysome fractionation
and a focused RNAi approach that Nup155 controls mRNA
translation of p21 (CDKN1A), a key mediator of the p53
response. The underlying mechanism involves transcriptional
regulation of the putative tRNA and rRNA methyltransferase
FTSJ1 by Nup155. Furthermore, we observe that Nup155 and
FTSJ1 are p53 repression targets and accordingly find a
correlation between the p53 status, Nup155 and FTSJ1
expression in murine and human hepatocellular carcinoma. Our
data suggest an unanticipated regulatory network linking
translational control by and repression of a structural NPC
component modulating the p53 pathway through its effectors.},
cin = {V076 / L801},
ddc = {500},
cid = {I:(DE-He78)V076-20160331 / I:(DE-He78)L801-20160331},
pnm = {319H - Addenda (POF3-319H)},
pid = {G:(DE-HGF)POF3-319H},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31089132},
pmc = {pmc:PMC6517424},
doi = {10.1038/s41467-019-10133-z},
url = {https://inrepo02.dkfz.de/record/143670},
}