P
Paul J.D. Winyard
Researcher at UCL Institute of Child Health
Publications - 70
Citations - 3237
Paul J.D. Winyard is an academic researcher from UCL Institute of Child Health. The author has contributed to research in topics: Kidney & Kidney disease. The author has an hindex of 33, co-authored 66 publications receiving 2890 citations. Previous affiliations of Paul J.D. Winyard include University College Hospital & University College London.
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Journal ArticleDOI
HNF1B Mutations Associate with Hypomagnesemia and Renal Magnesium Wasting
Shazia Adalat,Adrian S. Woolf,Karen A. Johnstone,A. Wirsing,Lorna W. Harries,David A. Long,Raoul C.M. Hennekam,Sarah Ledermann,Lesley Rees,William van’t Hoff,Stephen D. Marks,Richard S. Trompeter,Kjell Tullus,Paul J.D. Winyard,Janette Cansick,Imran Mushtaq,Harjeeta K. Dhillon,Coralie Bingham,Emma L. Edghill,Rukshana Shroff,Horia Stanescu,Gerhart U. Ryffel,Sian Ellard,Detlef Bockenhauer +23 more
TL;DR: A role for HNF1B not only in nephrogenesis but also in the maintenance of tubular function is described, thus describing a role for a transcription factor expressed in tissues including renal epithelia and regulating transcription of FXYD2 in the tubular handling of Mg(2+).
Journal ArticleDOI
SIX2 and BMP4 Mutations Associate With Anomalous Kidney Development
Stefanie Weber,Jaclyn C. Taylor,Paul J.D. Winyard,Kari Baker,Jessica Sullivan-Brown,Raphael Schild,Tanja Knüppel,Aleksandra Zurowska,Alberto Caldas-Alfonso,Mieczysław Litwin,Sevinç Emre,Gian Marco Ghiggeri,Aysin Bakkaloglu,Otto Mehls,Corinne Antignac,Franz Schaefer,Rebecca D. Burdine +16 more
TL;DR: These studies implicate conserved roles for Six2 and Bmp4 in the development of the renal system, which could affect kidney development at multiple stages, leading to the congenital anomalies observed in patients with RHD.
Journal ArticleDOI
Deregulation of cell survival in cystic and dysplastic renal development.
Paul J.D. Winyard,Jeroen Nauta,David S. Lirenman,P Hardman,Virginia R. Sams,R. Anthony Risdon,Adrian S. Woolf +6 more
TL;DR: It is speculated that deregulation of cell survival in these kidneys may reflect incomplete tissue maturation, and may contribute to the progressive destruction of functional kidney tissue in polycystic kidneys and the spontaneous involution reported in cystic dysplastic kidneys.
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Evolving Concepts in Human Renal Dysplasia
TL;DR: Here, it is possible to begin to understand the normal nephrogenic function of the wild-type proteins and understand how mutations might cause aberrant organogenesis.
Journal ArticleDOI
OFD1 Is a Centrosomal/Basal Body Protein Expressed during Mesenchymal-Epithelial Transition in Human Nephrogenesis
TL;DR: It is shown that during acquisition of epithelial polarity, OFD1 became localized to the apical zone of nephron precursor cells and then to basal bodies at the origin of primary cilia in fully differentiated epithelia, placing the protein at key sites, where it may play roles not only in microtubule organization (centrosomal function) but also in mechanosensation of urine flow (a primary ciliary function).