Keyword search (4,164 papers available)

"Dakik P" Authored Publications:

Title Authors PubMed ID
1 Discovery of fifteen new geroprotective plant extracts and identification of cellular processes they affect to prolong the chronological lifespan of budding yeast. Dakik P, Rodriguez MEL, Junio JAB, Mitrofanova D, Medkour Y, Tafakori T, Taifour T, Lutchman V, Samson E, Arlia-Ciommo A, Rukundo B, Simard É, Titorenko VI 32577164
BIOLOGY
2 Mechanisms by which PE21, an extract from the white willow Salix alba, delays chronological aging in budding yeast. Medkour Y, Mohammad K, Arlia-Ciommo A, Svistkova V, Dakik P, Mitrofanova D, Rodriguez MEL, Junio JAB, Taifour T, Escudero P, Goltsios FF, Soodbakhsh S, Maalaoui H, Simard É, Titorenko VI 31645900
BIOLOGY
3 Lipid metabolism and transport define longevity of the yeast Saccharomyces cerevisiae. Mitrofanova D, Dakik P, McAuley M, Medkour Y, Mohammad K, Titorenko VI 28930594
BIOLOGY
4 Some Metabolites Act as Second Messengers in Yeast Chronological Aging. Mohammad K, Dakik P, Medkour Y, McAuley M, Mitrofanova D, Titorenko VI 29543708
BIOLOGY
5 Yeast Cells Exposed to Exogenous Palmitoleic Acid Either Adapt to Stress and Survive or Commit to Regulated Liponecrosis and Die. Mohammad K, Dakik P, Medkour Y, McAuley M, Mitrofanova D, Titorenko VI 29636840
BIOLOGY
6 Pairwise combinations of chemical compounds that delay yeast chronological aging through different signaling pathways display synergistic effects on the extent of aging delay. Dakik P, McAuley M, Chancharoen M, Mitrofanova D, Lozano Rodriguez ME, Baratang Junio JA, Lutchman V, Cortes B, Simard É, Titorenko VI 30719227
BIOLOGY
7 Quiescence Entry, Maintenance, and Exit in Adult Stem Cells. Mohammad K, Dakik P, Medkour Y, Mitrofanova D, Titorenko VI 31052375
BIOLOGY
8 Mechanisms Through Which Some Mitochondria-Generated Metabolites Act as Second Messengers That Are Essential Contributors to the Aging Process in Eukaryotes Across Phyla. Dakik P, Medkour Y, Mohammad K, Titorenko VI 31057428
BIOLOGY

 

Title:Mechanisms Through Which Some Mitochondria-Generated Metabolites Act as Second Messengers That Are Essential Contributors to the Aging Process in Eukaryotes Across Phyla.
Authors:Dakik PMedkour YMohammad KTitorenko VI
Link:https://www.ncbi.nlm.nih.gov/pubmed/31057428?dopt=Abstract
Publication:
Keywords:
PMID:31057428 Category:Front Physiol Date Added:2019-06-07
Dept Affiliation: BIOLOGY
1 Department of Biology, Concordia University, Montreal, QC, Canada.

Description:

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

Front Physiol. 2019;10:461

Authors: Dakik P, Medkour Y, Mohammad K, Titorenko VI

Abstract

Recent studies have revealed that some low-molecular weight molecules produced in mitochondria are essential contributing factors to aging and aging-associated pathologies in evolutionarily distant eukaryotes. These molecules are intermediates or products of certain metabolic reactions that are activated in mitochondria in response to specific changes in the nutrient, stress, proliferation, or age status of the cell. After being released from mitochondria, these metabolites directly or indirectly change activities of a distinct set of protein sensors that reside in various cellular locations outside of mitochondria. Because these protein sensors control the efficiencies of some pro- or anti-aging cellular processes, such changes in their activities allow to create a pro- or anti-aging cellular pattern. Thus, mitochondria can function as signaling platforms that respond to certain changes in cell stress and physiology by remodeling their metabolism and releasing a specific set of metabolites known as "mitobolites." These mitobolites then define the pace of cellular and organismal aging because they regulate some longevity-defining processes taking place outside of mitochondria. In this review, we discuss recent progress in understanding mechanisms underlying the ability of mitochondria to function as such signaling platforms in aging and aging-associated diseases.

PMID: 31057428 [PubMed]





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