G
Gillian P. Ritson
Researcher at University of Pennsylvania
Publications - 5
Citations - 2258
Gillian P. Ritson is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Neurodegeneration & Frontotemporal lobar degeneration. The author has an hindex of 5, co-authored 5 publications receiving 2064 citations. Previous affiliations of Gillian P. Ritson include St. Jude Children's Research Hospital.
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Journal ArticleDOI
HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS
Udai Bhan Pandey,Zhiping Nie,Yakup Batlevi,Brett A. McCray,Gillian P. Ritson,Natalia B. Nedelsky,Stephanie L. Schwartz,Nicholas A. Diprospero,Melanie Knight,Oren Schuldiner,Ranjani Padmanabhan,Marc Hild,Deborah L. Berry,Dan Garza,Charlotte Hubbert,Tso-Pang Yao,Eric H. Baehrecke,J. Paul Taylor +17 more
TL;DR: It is shown that autophagy acts as a compensatory degradation system when the UPS is impaired in Drosophila melanogaster, and that histone deacetylase 6 (HDAC6), a microtubule-associated de acetylase that interacts with polyubiquitinated proteins, is an essential mechanistic link in this compensatory interaction.
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Expression of Nrf2 in Neurodegenerative Diseases
Chenere P. Ramsey,Charles A. Glass,Marshall B. Montgomery,Kathryn A. Lindl,Gillian P. Ritson,Luis A. Chia,Ronald L. Hamilton,Charleen T. Chu,Kelly L. Jordan-Sciutto +8 more
TL;DR: It is suggested that Nrf2-mediated transcription is not induced in neurons in AD despite the presence of oxidative stress, and in PD, nuclear localization of NRF2 is strongly induced, but this response may be insufficient to protect neurons from degeneration.
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TDP-43 mediates degeneration in a novel Drosophila model of disease caused by mutations in VCP/p97
Gillian P. Ritson,S. K. Custer,Brian D. Freibaum,Jake B. Guinto,D. Geffel,Jennifer Moore,W. Tang,Matthew J. Winton,Manuela Neumann,John Q. Trojanowski,Virginia M.-Y. Lee,Mark S. Forman,J. P. Taylor +12 more
TL;DR: Results show that degeneration associated with VCP mutations is mediated in part by toxic gain of function of TDP-43 in the cytoplasm, which is likely relevant to the pathogenic mechanism of a broad array of T DP-43 proteinopathies, including frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
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VCP Is Essential for Mitochondrial Quality Control by PINK1/Parkin and this Function Is Impaired by VCP Mutations
Nam Chul Kim,Emilie Tresse,Regina-Maria Kolaitis,Amandine Molliex,Ruth E. Thomas,Nael H. Alami,Bo Wang,Aashish Joshi,Rebecca B. Smith,Gillian P. Ritson,Brett J. Winborn,Jennifer Moore,Joo-Yong Lee,Tso-Pang Yao,Leo J. Pallanck,Mondira Kundu,J. Paul Taylor +16 more
TL;DR: A Drosophila model of VCP mutation-dependent degeneration is developed that is reminiscent of PINK1 and parkin mutants, including a pronounced mitochondrial defect, and it is shown that VCP recruitment to damaged mitochondria requires Parkin-mediated ubiquitination of mitochondrial targets.
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Valosin-containing protein and the pathogenesis of frontotemporal dementia associated with inclusion body myopathy
TL;DR: Current literature on IBMPFD is reviewed, focusing on the pathology of the disease and the biology of VCP with respect toIBMPFD, to describe the mechanism whereby mutations in VCP lead to CNS, muscle, and bone disease.