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Wade T. Nottingham

Researcher at John Radcliffe Hospital

Publications -  7
Citations -  907

Wade T. Nottingham is an academic researcher from John Radcliffe Hospital. The author has contributed to research in topics: GNAS complex locus & Genomic imprinting. The author has an hindex of 6, co-authored 7 publications receiving 861 citations. Previous affiliations of Wade T. Nottingham include Medical Research Council & University of Sussex.

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Runx1-mediated hematopoietic stem-cell emergence is controlled by a Gata/Ets/SCL-regulated enhancer

TL;DR: Transplantation experiments demonstrate that the intronic Runx1 enhancer targets all definitive HSCs in the mouse embryo, suggesting that it functions as a crucial cis-regulatory element that integrates the Gata, Ets, and SCL transcriptional networks to initiate HSC generation.
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Identification of an imprinting control region affecting the expression of all transcripts in the Gnas cluster.

TL;DR: It is established that a paternally derived targeted deletion of the germline differentially methylated region (DMR) associated with the antisense Nespas transcript unexpectedly affects both the expression of all transcripts in the Gnas cluster and methylation of two DMRs.
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A cis-acting control region is required exclusively for the tissue-specific imprinting of Gnas.

TL;DR: It is established that the differentially methylated region at exon 1A contains an imprinting control element that specifically regulates Gnas and comprises a characterized ICR for a gene that is only weakly imprinted in a minority of tissues.
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From hemangioblast to hematopoietic stem cell: an endothelial connection?

TL;DR: An overview of the data obtained from the mouse and avian models on the cellular origins of the hematopoietic system is given.
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Runx genes are direct targets of Scl/Tal1 in the yolk sac and fetal liver

TL;DR: The data provide a key component of the transcriptional network of early hematopoiesis by identifying downstream targets of Scl that can explain key aspects of the early Scl(-/-) phenotype.