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Nicholas D. Allen

Researcher at Cardiff University

Publications -  112
Citations -  6278

Nicholas D. Allen is an academic researcher from Cardiff University. The author has contributed to research in topics: Induced pluripotent stem cell & Embryonic stem cell. The author has an hindex of 41, co-authored 106 publications receiving 5673 citations. Previous affiliations of Nicholas D. Allen include UCL Institute of Ophthalmology & Merck & Co..

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Induced Pluripotent Stem Cells from Patients with Huntington’s Disease : Show CAG Repeat-Expansion-Associated Phenotypes

TL;DR: The generation and characterization of 14 induced pluripotent stem cell (iPSC) lines from HD patients and controls reveal CAG-repeat-expansion-associated gene expression patterns that distinguish patient lines from controls, and early onset versus late onset HD.
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A Highly Efficient Human Pluripotent Stem Cell Microglia Model Displays a Neuronal-Co-culture-Specific Expression Profile and Inflammatory Response

TL;DR: Co-culture microglia downregulate pathogen-response pathways, upregulate homeostatic function pathways, and promote a more anti-inflammatory and pro-remodeling cytokine response than corresponding monocultures, demonstrating that co-cultures are preferable for modeling authentic microglial physiology.
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Transactivation of Igf2 in a mouse model of Beckwith–Wiedemann syndrome

TL;DR: Igf2 overexpression is established as a key determinant of Beckwith–Wiedemann syndrome after being introduced into the mouse genome by using embryonic stem cells, which leads to transactivation of the endogenous Igf2 gene.
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Developmental control of allelic methylation in the imprinted mouse Igf2 and H19 genes

TL;DR: The results suggest that allelic methylation patterns in Igf2 and H19 arise early in embryogenesis and change progressively during development, some of these developmental changes are apparently under tissue-specific control.
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Mice lacking the giant protocadherin mFAT1 exhibit renal slit junction abnormalities and a partially penetrant cyclopia and anophthalmia phenotype.

TL;DR: A necessary role for FAT1 in the modified adhesion junctions of the renal glomerular epithelial cell is confirmed and hitherto unsuspected roles for FAT 1 in CNS development are revealed.