T-cadherin promotes autophagy and survival in vascular smooth muscle cells through MEK1/2/Erk1/2 axis activation

Article ID	Journal	Published Year	Pages	File Type
5509294	Cellular Signalling	2017	13 Pages	PDF

Abstract

T-cadherin increases autophagy-dependent survival in smooth muscle cells via MEK1/2/Ek1/2 axis activation 138

Keywords

PD98059 LC3 eIF2α GPi AMPK FCS N-acetyl-l-cysteine GRP78 LY294002 mTOR NAC RAPA SMC Jnk PBD PI3K BSA c-Jun N-terminal kinase ERK1/2 MAPK MEK1/2 p38 MAPK ROS bovine serum albumin LIR Rapamycin fetal calf serum Smooth muscle cell Rat aortic smooth muscle cell Endothelial cell endoplasmic reticulum eukaryotic translation initiation factor 2α Phosphate buffered saline phosphatidylinositol-3 kinase mammalian target of rapamycin 78 kDa glucose-regulated protein microtubule-associated protein 1A/1B-light chain 3 mitogen activated protein kinase 5′ adenosine monophosphate-activated protein kinase p38 mitogen activated protein kinase Chloroquine extracellular signal-regulated kinase glycosylphosphatidylinositol Reactive oxygen species

Related Topics

Life Sciences Biochemistry, Genetics and Molecular Biology Biochemistry

T-cadherin promotes autophagy and survival in vascular smooth muscle cells through MEK1/2/Erk1/2 axis activation

Authors

Emmanouil Kyriakakis, Agne Frismantiene, Boris Dasen, Dennis Pfaff, Olga Rivero, Klaus-Peter Lesch, Paul Erne, Therese J. Resink, Maria Philippova,