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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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Brain serotonin dysfunction accounts for aggression in male mice lacking neuronal nitric oxide synthase

TL;DR: It is demonstrated that the excessive aggressiveness and impulsiveness of nNOS knockout mice is caused by selective decrements in serotonin (5-HT) turnover and deficient 5-HT(1A) and 5- HT(1B) receptor function in brain regions regulating emotion.
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Stress-induced alterations in parkin solubility promote parkin aggregation and compromise parkin's protective function

TL;DR: It is demonstrated here that several PD-linked stressors, including neurotoxins, paraquat, NO, dopamine and iron, induce alterations in parkin solubility and result in its intracellular aggregation, which provides a link between the influence of environmental and intrinsic factors and genetic susceptibilities in PD pathogenesis.
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An evaluation of the nitric oxide/cGMP/cGMP-dependent protein kinase cascade in the induction of cerebellar long-term depression in culture

TL;DR: In cerebellar cultures made from transgenic mice in which the gene for neuronal nitric oxide synthase has been rendered null, LTD induced by glutamate/depolarization conjunctive stimulation was indistinguishable from that in cultures from wild-type mice in terms of amplitude, rate of onset, and duration.
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Deadly conversations: nuclear-mitochondrial cross-talk.

TL;DR: Observations are consistent with reports of biochemical features of apoptosis in neuronal injury models but modest to no protection by caspase inhibitors, and it is likely that AIF is the effector of the morphologic and biochemical events and is the commitment point to neuronal cell death, events that occur prior to caspases activation, thus accounting for the limited effects of casp enzyme inhibitors.