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Douglas C. Wallace

Researcher at Children's Hospital of Philadelphia

Publications -  495
Citations -  77420

Douglas C. Wallace is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: Mitochondrial DNA & Mitochondrion. The author has an hindex of 134, co-authored 475 publications receiving 72035 citations. Previous affiliations of Douglas C. Wallace include University of California & Stanford University.

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Combination of common mtDNA variants results in mitochondrial dysfunction and a connective tissue dysregulation

TL;DR: In this paper , the authors demonstrate that common mtDNA variants can cause mitochondrial disease when arising on an uncommon mtDNA background, and that idiopathic primary mitochondrial disease patients should be checked for novel combinations of otherwise common variants which may contribute to the etiology of the disorder.
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High throughput gene complementation screening permits identification of a mammalian mitochondrial protein synthesis (ρ−) mutant

TL;DR: A complementation system based on retroviral transduction with a full length cDNA expression library and selection for OXHOS function by growth in galactose is used to transduce the Chinese hamster V79-G7 OXPHOS mutant cell line with a defect in mitochondrial protein synthesis.
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Decreased Intestinal Microbiome Diversity in Pediatric Sepsis: A Conceptual Framework for Intestinal Dysbiosis to Influence Immunometabolic Function.

TL;DR: In this article, the authors explored whether intestinal dysbiosis in children with sepsis leads to changes in microbial-derived short-chain fatty acids in plasma and stool that are associated with immunometabolic dysfunction in peripheral blood mononuclear cells.
Journal Article

Deletion of a Class IIb Histone/protein Deacetylase (HDAC), HDAC10, Enhances FoxP3+ T-regulatory (Treg) Cell Suppressive Function, Gene Expression and Metabolism, and Promotes Allograft Survival

TL;DR: It is found that HDAC10 deletion enhanced Treg suppressive function both in vitro (Treg suppression assays) and in vivo (homeostatic proliferation assays), compared to wild-type Tregs.