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Valina L. Dawson

Researcher at Johns Hopkins University School of Medicine

Publications -  477
Citations -  88024

Valina L. Dawson is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Neurodegeneration & Parkin. The author has an hindex of 136, co-authored 451 publications receiving 76986 citations. Previous affiliations of Valina L. Dawson include University of Baltimore & Hospital of the University of Pennsylvania.

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Methods for amelioration of immunodeficiency virus induced neurodegeneration by covering nitric oxide or superoxide concentration

TL;DR: In this article, agents are administered which reduce nitric oxide production by neurons (e.g., nitricoxide synthase inhibitors, calmodulin inhibitors, immunophilin binding drugs) or lower superoxide concentration (i.e., superoxide dismutase gene).
Journal ArticleDOI

USP39 promotes non-homologous end-joining repair by poly(ADP-ribose)-induced liquid demixing

TL;DR: In this paper, the role of USP39, an inactive deubiquitinating enzyme involved in spliceosome assembly, was characterized and shown to be a molecular trigger for liquid demixing in a PAR-coupled N46-dependent manner, thereby directly interacting with the XRCC4/LIG4 complex.
Book ChapterDOI

Excitotoxic programmed cell death involves caspase-independent mechanisms

TL;DR: Overactivation of poly (ADP-ribose) polymerase-1 (PARP-1) is an early pathological event in excitotoxicity that leads to a unique form of cell death called parthanatos, which is unique in that it does not involve caspase dependent pathways.
Journal ArticleDOI

The Absence of Parkin Does Not Promote Dopamine or Mitochondrial Dysfunction in PolgAD257A/D257A Mitochondrial Mutator Mice

TL;DR: It is shown that Parkin-/-/PolgAD257A/D257A mice, a previously reported PD mouse model, fails to reproduce a Parkinsonian phenotype and is reported that parkin loss does not synergize with mitochondrial dysfunction in mouse models of mitochondrial deficits.
Journal ArticleDOI

The c-Abl inhibitor IkT-148009 suppresses neurodegeneration in mouse models of heritable and sporadic Parkinson’s disease

TL;DR: Karuppagounder et al. as discussed by the authors showed that IkT-148009, a brain-penetrant Abelson tyrosine kinase inhibitor with a favorable toxicology profile, was analyzed for therapeutic potential in animal models of slowly progressive, α-synuclein-dependent Parkinson's disease.