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231225s2018 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2018.11.011
|2 doi
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|a pubmed24n0970.xml
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|a (DE-627)NLM291027377
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|a (NLM)30471352
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|a (PII)S1521-6616(18)30620-X
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Weeding, Emma
|e verfasserin
|4 aut
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|a Genome-wide DNA methylation analysis in primary antiphospholipid syndrome neutrophils
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|c 2018
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 14.10.2019
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|a Date Revised 01.03.2022
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2018 Elsevier Inc. All rights reserved.
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|a Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thromboembolic events and pregnancy loss. We sought to characterize the DNA methylation profile of primary APS in comparison to healthy controls and individuals with SLE. In primary APS neutrophils compared to controls, 17 hypomethylated and 25 hypermethylated CpG sites were identified. Notable hypomethylated genes included ETS1, a genetic risk locus for SLE, and PTPN2, a genetic risk locus for other autoimmune diseases. Gene ontology analysis of hypomethylated genes revealed enrichment of genes involved in pregnancy. None of the differentially methylated sites in primary APS were differentially methylated in SLE neutrophils, and there was no demethylation of interferon signature genes in primary APS as is seen in SLE. Hypomethylation within a single probe in the IFI44L promoter (cg06872964) was able to distinguish SLE from primary APS with a sensitivity of 93.3% and specificity of 80.0% at a methylation fraction of 0.329
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|a Journal Article
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|a Research Support, N.I.H., Extramural
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|a Research Support, N.I.H., Intramural
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| 650 |
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|a Research Support, Non-U.S. Gov't
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| 650 |
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|a Antiphospholipid syndrome
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| 650 |
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|a Autoimmunity
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| 650 |
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|a Epigenetics
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|a Lupus
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|a Methylation
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|a Neutrophil
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|a ETS1 protein, human
|2 NLM
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| 650 |
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|a IFI44L protein, human
|2 NLM
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| 650 |
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|a Proto-Oncogene Protein c-ets-1
|2 NLM
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| 650 |
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|a Tumor Suppressor Proteins
|2 NLM
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| 650 |
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|a PTPN2 protein, human
|2 NLM
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| 650 |
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7 |
|a EC 3.1.3.48
|2 NLM
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| 650 |
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|a Protein Tyrosine Phosphatase, Non-Receptor Type 2
|2 NLM
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| 650 |
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|a EC 3.1.3.48
|2 NLM
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| 700 |
1 |
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|a Coit, Patrick
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yalavarthi, Srilakshmi
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Kaplan, Mariana J
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Knight, Jason S
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sawalha, Amr H
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 196(2018) vom: 01. Nov., Seite 110-116
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
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|g volume:196
|g year:2018
|g day:01
|g month:11
|g pages:110-116
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|u http://dx.doi.org/10.1016/j.clim.2018.11.011
|3 Volltext
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