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Neurotoxic reactive astrocytes are induced by activated microglia
TLDR
It is shown that activated microglia induce A1 astrocytes by secreting Il-1α, TNF and C1q, and that these cytokines together are necessary and sufficient to induce A2 astroCytes, which are abundant in various human neurodegenerative diseases. Expand
Mediation of Poly(ADP-Ribose) Polymerase-1-Dependent Cell Death by Apoptosis-Inducing Factor
TLDR
It is shown that PARP-1 activation is required for translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus and that AIF is necessary for PARp-1–dependent cell death. Expand
Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012
TLDR
A functional classification of cell death subroutines is proposed that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic programmed cell death, regulated necrosis, autophagic cell death and mitotic catastrophe. Expand
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018
TLDR
An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed. Expand
PINK1-dependent recruitment of Parkin to mitochondria in mitophagy
TLDR
It is suggested that Parkin, together with PINK1, modulates mitochondrial trafficking, especially to the perinuclear region, a subcellular area associated with autophagy, which may alter mitochondrial turnover which, in turn, may cause the accumulation of defective mitochondria and, ultimately, neurodegeneration in Parkinson's disease. Expand
Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity.
TLDR
Nitric oxide stimulated ADP-ribosylation of PARS in rat brain and blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Expand
Parkin functions as an E2-dependent ubiquitin- protein ligase and promotes the degradation of the synaptic vesicle-associated protein, CDCrel-1.
TLDR
It is suggested that Parkin functions as an E3 ubiquitin-protein ligase through its ring domains and that it may control protein levels via ubiquitination. Expand
Interference by Huntingtin and Atrophin-1 with CBP-Mediated Transcription Leading to Cellular Toxicity
TLDR
It is found that CBP was depleted from its normal nuclear location and was present in polyglutamine aggregates in HD cell culture models, HD transgenic mice, and human HD postmortem brain, suggesting polyglUTamine-mediated interference with CBP-regulated gene transcription may constitute a genetic gain of function, underlying the pathogenesis of polyglutsamine disorders. Expand
PARIS (ZNF746) Repression of PGC-1α Contributes to Neurodegeneration in Parkinson's Disease
TLDR
The identification of PARIS provides a molecular mechanism for neurodegeneration due to parkin inactivation, whose levels are regulated by the ubiquitin proteasome system via binding to and ubiquitination by the E3 ubiquitIn ligase, parkin. Expand
Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures.
TLDR
It is established that NO mediates the neurotoxicity of glutamate and Hemoglobin, which complexes NO, prevents neurotoxic effects of both N-methyl-D-aspartate and sodium nitroprusside. Expand
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