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@ARTICLE{Blunk:157139,
author = {I. Blunk and H. Thomsen$^*$ and N. Reinsch and M. Mayer and
A. Försti$^*$ and J. Sundquist and K. Sundquist and K.
Hemminki$^*$},
title = {{G}enomic imprinting analyses identify maternal effects as
a cause of phenotypic variability in type 1 diabetes and
rheumatoid arthritis.},
journal = {Scientific reports},
volume = {10},
number = {1},
issn = {2045-2322},
address = {[London]},
publisher = {Macmillan Publishers Limited, part of Springer Nature},
reportid = {DKFZ-2020-01425},
pages = {11562},
year = {2020},
note = {#LA:C050#},
abstract = {Imprinted genes, giving rise to parent-of-origin effects
(POEs), have been hypothesised to affect type 1 diabetes
(T1D) and rheumatoid arthritis (RA). However, maternal
effects may also play a role. By using a mixed model that is
able to simultaneously consider all kinds of POEs, the
importance of POEs for the development of T1D and RA was
investigated in a variance components analysis. The analysis
was based on Swedish population-scale pedigree data. With
P = 0.18 (T1D) and P = 0.26 (RA) imprinting
variances were not significant. Explaining up to $19.00\%$
$(± 2.00\%)$ and $15.00\%$ $(± 6.00\%)$ of the
phenotypic variance, the maternal environmental variance was
significant for T1D (P = 1.60 × 10-24) and for RA
(P = 0.02). For the first time, the existence of
maternal genetic effects on RA was indicated, contributing
up to $16.00\%$ $(± 3.00\%)$ of the total variance.
Environmental factors such as the social economic index, the
number of offspring, birth year as well as their
interactions with sex showed large effects.},
cin = {C050 / B062 / HD01},
ddc = {600},
cid = {I:(DE-He78)C050-20160331 / I:(DE-He78)B062-20160331 /
I:(DE-He78)HD01-20160331},
pnm = {313 - Cancer risk factors and prevention (POF3-313)},
pid = {G:(DE-HGF)POF3-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:32665606},
doi = {10.1038/s41598-020-68212-x},
url = {https://inrepo02.dkfz.de/record/157139},
}