J
John A. McGrath
Researcher at King's College London
Publications - 674
Citations - 26684
John A. McGrath is an academic researcher from King's College London. The author has contributed to research in topics: Epidermolysis bullosa & Mutation. The author has an hindex of 75, co-authored 631 publications receiving 24078 citations. Previous affiliations of John A. McGrath include Ninewells Hospital & Southampton General Hospital.
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Retrospective diagnosis of Kindler syndrome in a 37-year-old man.
TL;DR: Molecular diagnosis of Kindler syndrome in an infant with acral blisters led to the belated diagnosis in a severely affected relative whose condition had remained unidentified for 37 years.
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Wharton's jelly mesenchymal stromal/stem cells derived under chemically defined animal product-free low oxygen conditions are rich in MSCA-1(+) subpopulation.
Liani Devito,Heba Badraiq,Antonio Galleu,Dheraj K. Taheem,Stefano Codognotto,Richard C.M. Siow,Yacoub Khalaf,Annette Briley,Andrew Shennan,Lucilla Poston,John A. McGrath,Eileen Gentleman,Francesco Dazzi,Dusko Ilic +13 more
TL;DR: Easy accessibility, abundance and genetic 'naivety' make WJ MSCs logistically a more attractive source for clinical applications than BM MSCing, and they display antiproliferative activity similar to clinical-grade BM M SCs.
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Familial progressive hyper- and hypopigmentation and malignancy in two families with new mutations in KITLG.
A. Cuell,N. Bansal,T. Cole,M R Kaur,John Y.W. Lee,A. Loffeld,Celia Moss,M. O'Donnell,Takuya Takeichi,C. K. Thind,John A. McGrath +10 more
TL;DR: Familial progressive hyper‐ and hypopigmentation is an autosomal dominant skin condition presenting in childhood with generalized macular dyspigmentation, usually reported in patients of East Asian origin and can be distinguished by mutations in the KIT ligand gene (KITLG).
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Common Mutations in Arg304 of the p63 Gene in Ectrodactyly, Ectodermal Dysplasia, Clefting Syndrome: Lack of Genotype–Phenotype Correlation and Implications for Mutation Detection Strategies
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Common IL-31 gene haplotype associated with non-atopic eczema is not implicated in epidermolysis bullosa pruriginosa.
TL;DR: Recent data have demonstrated that interleukin-31 (IL-31), a cytokine belonging to the IL-6 family, may be relevant to some pruritic disorders, and a particular IL-31 gene haplotype may be associated with altered regulation of IL- 31 gene expression, and that this can have functional consequences and be more common in subjects with non-atopic eczema.