D
David S. Latchman
Researcher at University College London
Publications - 461
Citations - 26300
David S. Latchman is an academic researcher from University College London. The author has contributed to research in topics: Transcription factor & Promoter. The author has an hindex of 76, co-authored 460 publications receiving 25181 citations. Previous affiliations of David S. Latchman include Queen Mary University of London & University College Hospital.
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Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Eriza Maria Valente,Patrick M. Abou-Sleiman,Viviana Caputo,Miratul M. K. Muqit,Kirsten Harvey,Suzana Gispert,Zeeshan Ali,Domenico Del Turco,Anna Rita Bentivoglio,Daniel G. Healy,Alberto Albanese,Robert L. Nussbaum,Rafael González-Maldonado,Thomas Deller,S Salvi,Pietro Cortelli,William P. Gilks,David S. Latchman,Roberk J. Harvey,Bruno Dallapiccola,Georg Auburger,Nicholas W. Wood +21 more
TL;DR: The identification of two homozygous mutations affecting the PINK1 kinase domain in three consanguineous PARK6 families provide a direct molecular link between mitochondria and the pathogenesis of PD.
Journal ArticleDOI
Transcription factors: An overview
TL;DR: This introductory article is to provide an overview of transcription factors, their mechanism of action, their regulation and the manner in which alterations in them can result in disease.
Journal Article
Transcription factors: an overview
TL;DR: An overview of transcription factors, their mechanism of action, their regulation and the manner in which alterations in them can result in disease can be found in a special issue of the International Journal of Biochemistry and Cell Biology as discussed by the authors.
Journal ArticleDOI
PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-induced Cell Death
Sonia Gandhi,Alison Wood-Kaczmar,Zhi Yao,Helene Plun-Favreau,Emma Deas,Kristina Klupsch,Julian Downward,David S. Latchman,Sarah J. Tabrizi,Nicholas W. Wood,Michael R. Duchen,Andrey Y. Abramov +11 more
TL;DR: Reduced mitochondrial calcium capacity and increased ROS lower the threshold of opening of the mitochondrial permeability transition pore (mPTP) such that physiological calcium stimuli become sufficient to induce mPTP opening in PINK1-deficient cells, and propose a mechanism by which Pink1 dysfunction renders neurons vulnerable to cell death.