Imperial College London

ProfessorJesusGil

Faculty of MedicineInstitute of Clinical Sciences

Professor of Cell Proliferation
 
 
 
//

Contact

 

+44 (0)20 3313 8263jesus.gil

 
 
//

Location

 

ICTEM room 230ICTEM buildingHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Kondoh:2007,
author = {Kondoh, H and Lleonart, ME and Bernard, D and Gil, J},
journal = {Histol Histopathol},
pages = {85--90},
title = {Protection from oxidative stress by enhanced glycolysis; a possible mechanism of cellular immortalization},
volume = {22},
year = {2007}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Reactive oxygen species (ROS) play a crucial role not only in the physiological signal transduction but also in the pathogenesis of several human diseases such as atherosclerosis, neuro-degenerative diseases, metabolic disorders, aging or cancer amongst others. Oxidative stress is also responsible for cellular and organism senescence, in accordance with what Harman initially proposed in the free radical theory of aging. Recent findings support the notion that protection from oxidative stress can increase life span significantly. We reported that enhanced glycolysis could modulate cellular life span with reduction of oxidative stress. Moreover, the tumor suppressor gene p53 controls post-transcriptionally the level of the glycolytic enzyme, phosphoglycerate mutase (PGM). As enhanced glycolysis is a distinctive and prominent feature of cancer cells (termed the Warburg effect), our findings disclosed a novel aspect of the Warburg effect: the connection between senescence and oxidative stress.
AU - Kondoh,H
AU - Lleonart,ME
AU - Bernard,D
AU - Gil,J
EP - 90
PY - 2007///
SP - 85
TI - Protection from oxidative stress by enhanced glycolysis; a possible mechanism of cellular immortalization
T2 - Histol Histopathol
VL - 22
ER -