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Simon A. Rudge
Researcher at Babraham Institute
Publications - 33
Citations - 3265
Simon A. Rudge is an academic researcher from Babraham Institute. The author has contributed to research in topics: Phospholipase D & Saccharomyces cerevisiae. The author has an hindex of 24, co-authored 33 publications receiving 3066 citations. Previous affiliations of Simon A. Rudge include University of California, San Diego & University of Oxford.
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Journal ArticleDOI
Human ADP-ribosylation Factor-activated Phosphatidylcholine-specific Phospholipase D Defines a New and Highly Conserved Gene Family
Scott M. Hammond,Yelena M. Altshuller,Tsung Chang Sung,Simon A. Rudge,Kristine Rose,JoAnne Engebrecht,Andrew J. Morris,Michael A. Frohman +7 more
TL;DR: The identification of the first human PLD cDNA is reported, which defines a new and highly conserved gene family and likely encodes the gene product responsible for the most widely studied endogenous PLD activity.
Journal ArticleDOI
Mutagenesis of phospholipase D defines a superfamily including a trans-Golgi viral protein required for poxvirus pathogenicity.
Tsung Chang Sung,Rachel L. Roper,Yue Zhang,Simon A. Rudge,Ryan E. Temel,Scott M. Hammond,Andrew J. Morris,Bernard Moss,JoAnne Engebrecht,Michael A. Frohman +9 more
TL;DR: The results suggest that vaccinia virus and hPLD1 may act through analogous mechanisms to effect viral cellular egress and vesicular trafficking, respectively.
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The pleckstrin homology domain of phospholipase c-delta 1 binds with high affinity to phosphatidylinositol 4,5-bisphosphate in bilayer membranes
Pilar Garcia,Rakesh Gupta,Shefali Shah,Andrew J. Morris,Simon A. Rudge,Suzanne Scarlata,Victoria Petrova,Stuart McLaughlin,Mario J. Rebecchi +8 more
TL;DR: The hypothesis that the intact PH domain, serving as a specific tether, directs PLC-delta 1 to membranes enriched in PI(4,5)P2 and permits the active site, located elsewhere in the protein, to hydrolyze multiple substrate molecules before this enzyme dissociates from the membrane surface is supported.
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Mosaic overgrowth with fibroadipose hyperplasia is caused by somatic activating mutations in PIK3CA
Marjorie J. Lindhurst,Victoria E. R. Parker,Felicity Payne,Julie C. Sapp,Simon A. Rudge,Julie Harris,Alison M. Witkowski,Qifeng Zhang,Matthijs P. Groeneveld,Carol Scott,Allan Daly,Susan M. Huson,Laura L. Tosi,Michael L. Cunningham,Thomas N. Darling,Joseph Geer,Zoran Gucev,V. Reid Sutton,Christos Tziotzios,Adrian K. Dixon,Timothy R. Helliwell,Stephen O'Rahilly,Stephen O'Rahilly,David B. Savage,David B. Savage,Michael J.O. Wakelam,Inês Barroso,Inês Barroso,Leslie G. Biesecker,Robert K. Semple,Robert K. Semple +30 more
TL;DR: The findings characterize a distinct overgrowth syndrome, biochemically demonstrate activation of PI3K signaling and thereby identify a rational therapeutic target.
Journal ArticleDOI
PTEN Mutations as a Cause of Constitutive Insulin Sensitivity and Obesity
Aparna Pal,Thomas M. Barber,Martijn van de Bunt,Simon A. Rudge,Qifeng Zhang,Katherine Lachlan,Nicola S. Cooper,Helen Linden,Jonathan C. Levy,Michael J.O. Wakelam,Lisa Walker,Fredrik Karpe,Anna L. Gloyn +12 more
TL;DR: An apparently divergent effect of PTEN mutations is demonstrated: increased risks of obesity and cancer but a decreased risk of type 2 diabetes owing to enhanced insulin sensitivity.