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@ARTICLE{Lim:143827,
author = {J. Lim and J. H. Park and A. Baude$^*$ and J. Fellenberg
and J. Zustin and F. Haller and I. Krücken and H. G. Kang
and Y. J. Park and C. Plass$^*$ and A. M. Lindroth},
title = {{T}ranscriptome and protein interaction profiling in cancer
cells with mutations in histone {H}3.3.},
journal = {Scientific data},
volume = {5},
issn = {2052-4463},
address = {London},
publisher = {Nature Publ. Group},
reportid = {DKFZ-2019-01389},
pages = {180283},
year = {2018},
abstract = {Mutations of histone variant H3.3 are highly recurrent in
childhood glioblastoma and in young adults with Giant Cell
Tumor of the Bone (GCTB). The heterozygotic representation
of the mutations in the tumors, and with potential histone
H3 and H3.3 redundancy, suggest that the mutations are
gain-of-function by nature. To address common H3.3 point
mutations, we have generated data from GCTB patient samples
with H3.3 G34W substitutions and engineered human GFP-tagged
H3.3-mutated isogenic cell lines for high throughput data
comparisons. First, a total of thirty-six patient samples
and cell lines were used to acquire gene expression
transcriptome data using microarray and RNA-sequencing. The
expression data were validated with the orthogonal nCounter
assay. Second, to uncover the H3.3-GFP interaction proteomes
from the isogenic cell lines, immunoprecipitation of
unmutated wild type, K27M, G34R, and G34W substitutions were
performed. The RNA-sequencing data and the H3.3 interaction
proteome enable potentially important functional insight
into the tumorigenic process and should spur further
detailed analysis.},
keywords = {H3 histone family member 3A, human (NLM Chemicals) /
Histones (NLM Chemicals)},
cin = {C010},
ddc = {500},
cid = {I:(DE-He78)C010-20160331},
pnm = {313 - Cancer risk factors and prevention (POF3-313)},
pid = {G:(DE-HGF)POF3-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30532024},
pmc = {pmc:PMC6289111},
doi = {10.1038/sdata.2018.283},
url = {https://inrepo02.dkfz.de/record/143827},
}