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  • Influence
Mitochondrial complex I deficiency increases protein acetylation and accelerates heart failure.
TLDR
A mechanism connecting mitochondrial dysfunction to the susceptibility to diseases and a potential therapeutic target are described and proposed. Expand
mTOR Inhibition Alleviates Mitochondrial Disease in a Mouse Model of Leigh Syndrome
TLDR
Rapamycin, a drug used clinically as an immunosuppressant and for treatment of certain cancers, delayed the onset and progression of neurological symptoms in a mouse model of Leigh syndrome and significantly extended survival of the animals. Expand
A Putative Cation Channel and Its Novel Regulator: Cross-Species Conservation of Effects on General Anesthesia
TLDR
The anesthetic signature reflects an evolutionarily conserved role for the na orthologs, implying its intimate involvement in drug action, and biochemical studies show that proteins of the UNC-79 family control NA protein levels by a posttranscriptional mechanism. Expand
A stomatin and a degenerin interact in lipid rafts of the nervous system of Caenorhabditis elegans.
TLDR
A low-density, detergent-resistant fraction from cell membranes of C. elegans is isolated and found that the UNC-1 protein is almost totally restricted to this fraction, suggesting lipid rafts may represent a novel class of targets for volatile anesthetics. Expand
Mutations affecting sensitivity to ethanol in the nematode, Caenorhabditis elegans.
  • P. Morgan, M. Sedensky
  • Biology, Medicine
  • Alcoholism, clinical and experimental research
  • 1 December 1995
TLDR
Results indicate that ethanol is similar in its effects to the volatile anesthetics, enflurane and isoflurane, and that ethanol exerts its anesthetic actions at more than one site of action. Expand
Unc-1: a stomatin homologue controls sensitivity to volatile anesthetics in Caenorhabditis elegans.
TLDR
It is postulate that UNC-1 has a direct effect on anesthetic sensitivity in C. elegans and may represent a molecular target for volatile anesthetics. Expand
Mitochondrial Expression and Function of GAS-1 in Caenorhabditis elegans
TLDR
Data indicate that gas-1 is the major 49-kDa protein of complex I and that the GAS-1 protein is critical to mitochondrial function in C. elegans and reveal the importance of mitochondria function in determining not only aging and life span, but also anesthetic sensitivity, in this model organism. Expand
Cell Biology of the Mitochondrion
TLDR
This work focuses on discoveries that were made using C. elegans of cell autonomous and nonautonomous pathways controlling the mitochondrial unfolded protein response, as well as mechanisms for degradation of paternal mitochondria after fertilization. Expand
Mitochondrial Oxidative Phosphorylation Is Defective in the Long-lived Mutant clk-1*
TLDR
It is shown that complexes I and II differ in their ability to use the quinone pool in clk-1, the first direct demonstration of a differential interaction of complex I and complex II with the endogenous quin one pool. Expand
The effects of complex I function and oxidative damage on lifespan and anesthetic sensitivity in Caenorhabditis elegans
TLDR
It is concluded that mitochondrial changes in lifespan appear to be mediated primarily by changes in oxidative damage rather than byChanges in rates of oxidative phosphorylation, and the effects of mitochondrial changes on anesthetic sensitivity appear to been mediated by both altered respiration and oxidative damage. Expand
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