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Guidelines for the use and interpretation of assays for monitoring autophagy
TLDR
These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Bax directly induces release of cytochrome c from isolated mitochondria.
TLDR
It is shown that addition of submicromolar amounts of recombinant Bax protein to isolated mitochondria can induce cytochrome c (Cyt c) release, whereas a peptide representing the Bax BH3 domain was inactive, implying that Bax uses an alternative mechanism for triggering release of Cyt c from mitochondria.
Huntingtin Interacting Proteins Are Genetic Modifiers of Neurodegeneration
TLDR
It is demonstrated that high-throughput screening for protein interactions combined with genetic validation in a model organism is a powerful approach for identifying novel candidate modifiers of polyglutamine toxicity.
Coupling Endoplasmic Reticulum Stress to the Cell Death Program
TLDR
It is proposed that any cellular insult that causes prolonged ER stress may induce apoptosis through caspase-7-mediated casp enzyme-12 activation, and the data underscore the involvement of ER and caspases associated with it in the ER stress-induced apoptotic process.
Anti-cancer activity of targeted pro-apoptotic peptides
TLDR
Short peptides composed of two functional domains, one a tumor blood vessel 'homing' motif and the other a programmed cell death-inducing sequence, are designed and synthesized by simple peptide chemistry and may yield new therapeutic agents.
Lysosomal Protease Pathways to Apoptosis
TLDR
Data suggest that Bid represents a sensor that allows cells to initiate apoptosis in response to widespread adventitious proteolysis, supported by the finding that cytosolic extracts from mice ablated in the bid gene are impaired in the ability to release cytochrome c in Response to lysosome extracts.
Inhibition of Calpain Cleavage of Huntingtin Reduces Toxicity
TLDR
Two calpain cleavage sites in Htt are identified and mutation of these sites renders the polyQ expanded Htt less susceptible to proteolysis and aggregation, resulting in decreased toxicity in an in vitro cell culture model, and support the role of calpain-derived Htt fragmentation in HD.
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