Vladimir I. Titorenko

Acyl-CoA oxidase is imported as a heteropentameric, cofactor-containing complex into peroxisomes of Yarrowia lipolytica.

RNA interference of peroxisome-related genes in C. elegans: a new model for human peroxisomal disorders.

Peroxisome division in the yeast Yarrowia lipolytica is regulated by a signal from inside the peroxisome.

The peroxisome: orchestrating important developmental decisions from inside the cell.

A new definition for the consensus sequence of the peroxisome targeting signal type 2.

Dynamic ergosterol- and ceramide-rich domains in the peroxisomal membrane serve as an organizing platform for peroxisome fusion.

Peroxisome biogenesis: the peroxisomal endomembrane system and the role of the ER.

Lipids and lipid domains in the peroxisomal membrane of the yeast Yarrowia lipolytica.

Overproduction of translation elongation factor 1-alpha (eEF1A) suppresses the peroxisome biogenesis defect in a Hansenula polymorpha pex3 mutant via translational read-through.

A signal from inside the peroxisome initiates its division by promoting the remodeling of the peroxisomal membrane.

Spatiotemporal dynamics of the ER-derived peroxisomal endomembrane system.

Effect of calorie restriction on the metabolic history of chronologically aging yeast.

A novel function of lipid droplets in regulating longevity.

Chemical genetic screen identifies lithocholic acid as an anti-aging compound that extends yeast chronological life span in a TOR-independent manner, by modulating housekeeping longevity assurance processes.

Xenohormetic, hormetic and cytostatic selective forces driving longevity at the ecosystemic level.

Peroxisome metabolism and cellular aging.

In search of housekeeping pathways that regulate longevity.

Lithocholic bile acid selectively kills neuroblastoma cells, while sparing normal neuronal cells.

Dynamics and regulation of lipid droplet formation in lipopolysaccharide (LPS)-stimulated microglia.

Interspecies Chemical Signals Released into the Environment May Create Xenohormetic, Hormetic and Cytostatic Selective Forces that Drive the Ecosystemic Evolution of Longevity Regulation Mechanisms.

Caloric restriction extends yeast chronological lifespan by altering a pattern of age-related changes in trehalose concentration.

Lithocholic acid extends longevity of chronologically aging yeast only if added at certain critical periods of their lifespan.

Integration of peroxisomes into an endomembrane system that governs cellular aging.

The spatiotemporal dynamics of longevity-defining cellular processes and its modulation by genetic, dietary, and pharmacological anti-aging interventions.

Macromitophagy is a longevity assurance process that in chronologically aging yeast limited in calorie supply sustains functional mitochondria and maintains cellular lipid homeostasis.

A network of interorganellar communications underlies cellular aging.

Essential roles of peroxisomally produced and metabolized biomolecules in regulating yeast longevity.

Mitochondrial membrane lipidome defines yeast longevity.

Bile acids induce apoptosis selectively in androgen-dependent and -independent prostate cancer cells.

Macromitophagy, neutral lipids synthesis, and peroxisomal fatty acid oxidation protect yeast from "liponecrosis", a previously unknown form of programmed cell death.

Cells with impaired mitochondrial H2O2 sensing generate less •OH radicals and live longer.

A mitochondrially targeted compound delays aging in yeast through a mechanism linking mitochondrial membrane lipid metabolism to mitochondrial redox biology.

Metabolomic and lipidomic analyses of chronologically aging yeast.

Mechanisms underlying the anti-aging and anti-tumor effects of lithocholic bile acid.

Mechanism of liponecrosis, a distinct mode of programmed cell death.

Quasi-programmed aging of budding yeast: a trade-off between programmed processes of cell proliferation, differentiation, stress response, survival and death defines yeast lifespan.

Origin and spatiotemporal dynamics of the peroxisomal endomembrane system.

The Intricate Interplay between Mechanisms Underlying Aging and Cancer.

Mechanisms by which different functional states of mitochondria define yeast longevity.

Lithocholic bile acid accumulated in yeast mitochondria orchestrates a development of an anti-aging cellular pattern by causing age-related changes in cellular proteome.

Longevity extension by phytochemicals.

A novel approach to the discovery of anti-tumor pharmaceuticals: searching for activators of liponecrosis.

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).

Cell-Nonautonomous Mechanisms Underlying Cellular and Organismal Aging.

Discovery of plant extracts that greatly delay yeast chronological aging and have different effects on longevity-defining cellular processes.

Mitochondria operate as signaling platforms in yeast aging.

Six plant extracts delay yeast chronological aging through different signaling pathways.

Communications between Mitochondria, the Nucleus, Vacuoles, Peroxisomes, the Endoplasmic Reticulum, the Plasma Membrane, Lipid Droplets, and the Cytosol during Yeast Chronological Aging.

Empirical verification of evolutionary theories of aging.

Lithocholic acid induces endoplasmic reticulum stress, autophagy and mitochondrial dysfunction in human prostate cancer cells.

Empirical Validation of a Hypothesis of the Hormetic Selective Forces Driving the Evolution of Longevity Regulation Mechanisms.

A laboratory test of evolutionary aging theories.

Cell-autonomous mechanisms of chronological aging in the yeast .

Specific changes in mitochondrial lipidome alter mitochondrial proteome and increase the geroprotective efficiency of lithocholic acid in chronologically aging yeast.

Mechanisms Underlying the Essential Role of Mitochondrial Membrane Lipids in Yeast Chronological Aging.

Diindolylmethane and its halogenated derivatives induce protective autophagy in human prostate cancer cells via induction of the oncogenic protein AEG-1 and activation of AMP-activated protein kinase (AMPK).

Lipid metabolism and transport define longevity of the yeast Saccharomyces cerevisiae.

Caloric restriction extends yeast chronological lifespan via a mechanism linking cellular aging to cell cycle regulation, maintenance of a quiescent state, entry into a non-quiescent state and survival in the non-quiescent state.

Some Metabolites Act as Second Messengers in Yeast Chronological Aging.

Yeast Cells Exposed to Exogenous Palmitoleic Acid Either Adapt to Stress and Survive or Commit to Regulated Liponecrosis and Die.

Caloric restriction delays yeast chronological aging by remodeling carbohydrate and lipid metabolism, altering peroxisomal and mitochondrial functionalities, and postponing the onsets of apoptotic and liponecrotic modes of regulated cell death.

Yeast chronological aging is linked to cell cycle regulation.

Molecular and Cellular Mechanisms of Aging and Age-related Disorders.

Mechanisms through which lithocholic acid delays yeast chronological aging under caloric restriction conditions.

Pairwise combinations of chemical compounds that delay yeast chronological aging through different signaling pathways display synergistic effects on the extent of aging delay.

Quiescence Entry, Maintenance, and Exit in Adult Stem Cells.

Mechanisms Through Which Some Mitochondria-Generated Metabolites Act as Second Messengers That Are Essential Contributors to the Aging Process in Eukaryotes Across Phyla.

Aging and Age-related Disorders: From Molecular Mechanisms to Therapies.

Mechanisms by which PE21, an extract from the white willow , delays chronological aging in budding yeast.

Discovery of fifteen new geroprotective plant extracts and identification of cellular processes they affect to prolong the chronological lifespan of budding yeast.

Mechanisms that Link Chronological Aging to Cellular Quiescence in Budding Yeast.