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David A. Pearce
Researcher at Northumbria University
Publications - 405
Citations - 20297
David A. Pearce is an academic researcher from Northumbria University. The author has contributed to research in topics: Batten disease & CLN3. The author has an hindex of 72, co-authored 396 publications receiving 18416 citations. Previous affiliations of David A. Pearce include University of Zurich & University of York.
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The yeast model for batten disease: mutations in BTN1, BTN2, and HSP30 alter pH homeostasis.
TL;DR: DNA microarray analysis shows that deletion of either HSP30 or BTN2 in either BTN1(+) or btn1-Delta strains does not alter vacuolar pH but does lead to an increased activity of the plasma membrane H(+)-ATPase, reinforcing the view that altered pH homeostasis is the underlying cause of Batten disease.
Journal Article
A preliminary study of airborne microbial biodiversity over Peninsular Antarctica.
TL;DR: This study used PCR-based molecular biological identification techniques to examine the biodiversity of air sampled over Rothera Point (Antarctic Peninsula), revealing a range of microorganisms, including cyanobacteria, actinomycetes, diatom plastids and other uncultivated bacterial groups.
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Nitric Oxide Signaling Is Disrupted in the Yeast Model for Batten Disease
Nuno S. Osório,Agostinho Carvalho,Agostinho J. Almeida,Sergio Padilla-Lopez,Cecília Leão,João Laranjinha,Paula Ludovico,David A. Pearce,Fernando Rodrigues +8 more
TL;DR: It is proposed that in JNCL, a limited capacity to synthesize .NO directly caused by the absence of Cln3 function may contribute to the pathology of the disease.
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SGK3 regulates Ca(2+) entry and migration of dendritic cells.
Evi Schmid,Madhuri Bhandaru,Meerim K. Nurbaeva,Wenting Yang,Kalina Szteyn,Antonella Russo,Christina Leibrock,Leonid Tyan,David A. Pearce,Ekaterina Shumilina,Florian Lang +10 more
TL;DR: SGK3 contributes to the regulation of store-operated Ca-operated entry into and migration of dendritic cells, effects at least partially mediated through SGK3-dependent upregulation of STIM2 expression.
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The neuronal ceroid lipofuscinoses: mutations in different proteins result in similar disease.
TL;DR: The function of the CLN-proteins is reviewed and the possibility that a disruption in a common biological process leads to an NCL-disease is discussed, suggesting many shared similarities in the pathology of these diseases.