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Ingo Marenholz

Researcher at Charité

Publications -  61
Citations -  6041

Ingo Marenholz is an academic researcher from Charité. The author has contributed to research in topics: Genome-wide association study & Atopic dermatitis. The author has an hindex of 30, co-authored 56 publications receiving 5193 citations. Previous affiliations of Ingo Marenholz include Humboldt University of Berlin & Max Delbrück Center for Molecular Medicine.

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S100 proteins in mouse and man: from evolution to function and pathology (including an update of the nomenclature)

TL;DR: This work analyzed the structural variations, which are the basis of functional diversification, as well as the genomic organization of the S100 family in human and compared it with the S 100 repertoires in mouse and rat, and identified evolutionary related subgroups of S100 proteins within the three species.
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Genes Encoding Structural Proteins of Epidermal Cornification and S100 Calcium-Binding Proteins Form a Gene Complex (“Epidermal Differentiation Complex”) on Human Chromosome 1q21

TL;DR: It is concluded that these loci constitute a gene complex, for which the name epidermal differentiation complex is proposed, since calcium levels tightly control the differentiation of epithelial cells and the expression of genes encoding epidersmal structural proteins.
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Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis

Lavinia Paternoster, +154 more
- 19 Oct 2015 - 
TL;DR: This paper performed a meta-analysis of >15 million genetic variants in 21,399 cases and 95,464 controls from populations of European, African, Japanese and Latino ancestry, followed by replication in 32,059 cases and 228,628 controls from 18 studies.
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Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology

Manuel A. R. Ferreira, +73 more
- 30 Oct 2017 - 
TL;DR: A genome-wide association study of a broad allergic disease phenotype that considers the presence of any one of these three diseases identified 136 independent risk variants, including 73 not previously reported, which implicate 132 nearby genes in allergic disease pathophysiology.