Sergio Giannattasio

Simultaneous determination of purine nucleotides, their metabolites and beta-nicotinamide adenine dinucleotide in cerebellar granule cells by ion-pair high performance liquid chromatography.

Acid stress adaptation protects Saccharomyces cerevisiae from acetic acid-induced programmed cell death.

An increase in the ATP levels occurs in cerebellar granule cells en route to apoptosis in which ATP derives from both oxidative phosphorylation and anaerobic glycolysis.

Retrograde response to mitochondrial dysfunction is separable from TOR1/2 regulation of retrograde gene expression.

YCA1 participates in the acetic acid induced yeast programmed cell death also in a manner unrelated to its caspase-like activity.

Catalase T and Cu,Zn-superoxide dismutase in the acetic acid-induced programmed cell death in Saccharomyces cerevisiae.

A transient proteasome activation is needed for acetic acid-induced programmed cell death to occur in Saccharomyces cerevisiae.

Cytochrome c is released from coupled mitochondria of yeast en route to acetic acid-induced programmed cell death and can work as an electron donor and a ROS scavenger.

Pleiotropic effects of the yeast Sal1 and Aac2 carriers on mitochondrial function via an activity distinct from adenine nucleotide transport.

Molecular evolution of B6 enzymes: binding of pyridoxal-5'-phosphate and Lys41Arg substitution turn ribonuclease A into a model B6 protoenzyme.

Yeast acetic acid-induced programmed cell death can occur without cytochrome c release which requires metacaspase YCA1.

Knock-out of metacaspase and/or cytochrome c results in the activation of a ROS-independent acetic acid-induced programmed cell death pathway in yeast.

Cytochrome c Trp65Ser substitution results in inhibition of acetic acid-induced programmed cell death in Saccharomyces cerevisiae.

Achievements and perspectives in yeast acetic acid-induced programmed cell death pathways.

Yeast as a tool to study signaling pathways in mitochondrial stress response and cytoprotection.

The role of mitochondria in yeast programmed cell death.

The N-acetylcysteine-insensitive acetic acid-induced yeast programmed cell death occurs without macroautophagy.

Stress-related mitochondrial components and mitochondrial genome as targets of anticancer therapy.

Molecular mechanisms of Saccharomyces cerevisiae stress adaptation and programmed cell death in response to acetic acid.

Yeast growth in raffinose results in resistance to acetic-acid induced programmed cell death mostly due to the activation of the mitochondrial retrograde pathway.

The expanding role of yeast in cancer research and diagnosis: insights into the function of the oncosuppressors p53 and BRCA1/2.

Yeast stress, aging, and death.

Silencing of BRCA2 decreases anoikis and its heterologous expression sensitizes yeast cells to acetic acid-induced programmed cell death.

Mitochondrial dysfunction in cancer chemoresistance.

Yeast as a tool to study mitochondrial retrograde pathway en route to cell stress response.

Differential proteome-metabolome profiling of YCA1-knock-out and wild type cells reveals novel metabolic pathways and cellular processes dependent on the yeast metacaspase.