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Thomas H. Gillingwater

Thomas H. Gillingwater

D-Index & Metrics

Biology and Biochemistry

D-Index
69
Citations
14817
World Ranking
7513
National Ranking
582

Research.com Recognitions

  • 2020 - Fellow of the Royal Society of Edinburgh

Overview

Thomas H. Gillingwater is affiliated with the University of Edinburgh in the United Kingdom. Their research spans several interdisciplinary domains primarily within medicine and biochemistry, genetics, and molecular biology.

The main fields of study for this scientist include:

  • Medicine
  • Biochemistry, Genetics and Molecular Biology

More specifically, Gillingwater's work focuses on subfields such as:

  • Molecular Biology
  • Genetics
  • Surgery
  • Neurology
  • Cellular and Molecular Neuroscience

The key research topics covered in their publications are:

  • Neurogenetic and Muscular Disorders Research
  • RNA modifications and cancer
  • RNA Research and Splicing
  • Amyotrophic Lateral Sclerosis Research
  • Muscle Physiology and Disorders
  • Congenital Anomalies and Fetal Surgery
  • Neuroscience and Neuropharmacology Research

Frequent publication venues for Gillingwater include:

  • Journal of Anatomy
  • bioRxiv (Cold Spring Harbor Laboratory)
  • Human Molecular Genetics
  • Cell Reports Medicine
  • Brain Communications

Collaborations have involved several co-authors, notably:

  • Helena Chaytow
  • Kiterie M. E. Faller
  • Ross A. Jones
  • Thomas M. Wishart
  • Ewout J. N. Groen

Among recent scientific papers authored by or involving Gillingwater are:

  • Spinal muscular atrophy: From approved therapies to future therapeutic targets for personalized medicine (2021, Cell Reports Medicine)
  • COVID-19 and anatomy: Stimulus and initial response (2020, Journal of Anatomy)
  • SMN-primed ribosomes modulate the translation of transcripts related to spinal muscular atrophy (2020, Nature Cell Biology)
  • Comparative anatomy of the mammalian neuromuscular junction (2020, Journal of Anatomy)
  • Altered network properties in C9ORF72 repeat expansion cortical neurons are due to synaptic dysfunction (2021, Molecular Neurodegeneration)

In 2020, Thomas H. Gillingwater was named a Fellow of the Royal Society of Edinburgh, recognizing their contributions to the scientific community.

Best Publications

  • A mutation in the vesicle-trafficking protein VAPB causes late-onset spinal muscular atrophy and amyotrophic lateral sclerosis.

    Agnes L. Nishimura;Miguel Mitne-Neto;Helga C.A. Silva;Helga C.A. Silva;Antônio Richieri-Costa

  • Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene.

    T G Mack;M Reiner;B Beirowski;W Mi

  • Selective vulnerability of motor neurons and dissociation of pre- and post-synaptic pathology at the neuromuscular junction in mouse models of spinal muscular atrophy

    Lyndsay M. Murray;Laura H. Comley;Derek Thomson;Nick Parkinson

  • Total protein analysis as a reliable loading control for quantitative fluorescent Western blotting.

    Samantha L. Eaton;Sarah L. Roche;Maica Llavero Hurtado;Karla J. Oldknow

  • Spinal muscular atrophy: going beyond the motor neuron

    Gillian Hamilton;Thomas H. Gillingwater

  • Alternative Splicing Events Are a Late Feature of Pathology in a Mouse Model of Spinal Muscular Atrophy

    Dirk Bäumer;Sheena Lee;George Nicholson;Joanna L. Davies

  • Emerging therapies and challenges in Spinal Muscular Atrophy

    Michelle A. Farrar;Susanna B. Park;Steve Vucic;Kate A. Carey

  • Synaptic vulnerability in neurodegenerative disease

    Thomas M Wishart;Simon H Parson;Thomas H Gillingwater

  • Advances in therapy for spinal muscular atrophy: promises and challenges.

    Ewout J N Groen;Kevin Talbot;Thomas H Gillingwater

  • Cellular and Molecular Anatomy of the Human Neuromuscular Junction

    Ross Jones;Carl Harrison;Samantha L. Eaton;Maria del carmen Llavero hurtado

  • Dysregulation of ubiquitin homeostasis and β-catenin signaling promote spinal muscular atrophy

    Thomas M. Wishart;Chantal A. Mutsaers;Markus Riessland;Michell M. Reimer

  • Progressive abnormalities in skeletal muscle and neuromuscular junctions of transgenic mice expressing the Huntington's disease mutation

    Richard R. Ribchester;Derek Thomson;Nigel I. Wood;Tim Hinks

  • VAPB interacts with and modulates the activity of ATF6

    Christos Gkogkas;Susan Middleton;Anna M. Kremer;Caroline Wardrope

  • Review: neuromuscular synaptic vulnerability in motor neurone disease: amyotrophic lateral sclerosis and spinal muscular atrophy.

    Lyndsay Murray;K. Talbot;T. H. Gillingwater

  • The role of survival motor neuron protein (SMN) in protein homeostasis

    Helena Chaytow;Yu-Ting Huang;Thomas H. Gillingwater;Kiterie M. E. Faller

  • WldS prevents axon degeneration through increased mitochondrial flux and enhanced mitochondrial Ca2+ buffering.

    Michelle A. Avery;Timothy M. Rooney;Jignesh D. Pandya;Thomas M. Wishart

  • riboWaltz: Optimization of ribosome P-site positioning in ribosome profiling data.

    Fabio Lauria;Toma Tebaldi;Paola Bernabò;Ewout J. N. Groen

  • Transcriptional regulation of the AP-1 and Nrf2 target gene sulfiredoxin

    Francesc X. Soriano;Paul Baxter;Lyndsay M. Murray;Michael B. Sporn

  • The contribution of mouse models to understanding the pathogenesis of spinal muscular atrophy.

    James N. Sleigh;Thomas H. Gillingwater;Kevin Talbot;Kevin Talbot

  • Systemic restoration of UBA1 ameliorates disease in spinal muscular atrophy

    Rachael A. Powis;Evangelina Karyka;Penelope Boyd;Julian Come

Frequent Co-Authors

Richard R. Ribchester
Richard R. Ribchester University of Edinburgh
Kevin Talbot
Kevin Talbot University of Oxford
Colin Smith
Colin Smith University of Edinburgh
Michael P. Coleman
Michael P. Coleman University of Cambridge
Giles E. Hardingham
Giles E. Hardingham University of Edinburgh
Rashmi Kothary
Rashmi Kothary Ottawa Hospital
Alessandro Quattrone
Alessandro Quattrone University of Trento
David J. A. Wyllie
David J. A. Wyllie University of Edinburgh
Brunhilde Wirth
Brunhilde Wirth University of Cologne

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