TY - JOUR
T1 - Endothelial cells cope with hypoxia-induced depletion of ATP via activation of cellular purine turnover and phosphotransfer networks.
AU - Losenkova, null
AU - Zuccarini, null
AU - Helenius, null
AU - Jacquemet, Guillaume
AU - Gerasimovskaya, null
AU - Tallgren, null
AU - Jalkanen, null
AU - Yegutkin, null
PY - 2018
Y1 - 2018
N2 - H]ADP/ATP. Furthermore, following a period of hypoxia, HUVEC underwent concurrent changes in intracellular signaling manifested in the depletion of putative ATP stores and targeted up-regulation of phospho-p53, p70S6K/mTOR and other tyrosine kinases. The revealed complex implication of both extrinsic and intrinsic mechanisms into a tuned hypoxia-induced control of purine homeostasis and signaling may open up further research for the development of pharmacological treatments to improve endothelial cell function under disease conditions associated with a loss of cellular ATP during oxygen deprivation.
AB - H]ADP/ATP. Furthermore, following a period of hypoxia, HUVEC underwent concurrent changes in intracellular signaling manifested in the depletion of putative ATP stores and targeted up-regulation of phospho-p53, p70S6K/mTOR and other tyrosine kinases. The revealed complex implication of both extrinsic and intrinsic mechanisms into a tuned hypoxia-induced control of purine homeostasis and signaling may open up further research for the development of pharmacological treatments to improve endothelial cell function under disease conditions associated with a loss of cellular ATP during oxygen deprivation.
U2 - 10.1016/j.bbadis.2018.03.001
DO - 10.1016/j.bbadis.2018.03.001
M3 - Artikel
SN - 0925-4439
VL - 1864
SP - 1804
EP - 1815
JO - BBA - Molecular Basis of Disease
JF - BBA - Molecular Basis of Disease
IS - 5 Pt A
ER -