◀ Back to MTOR
BECN1 — MTOR
Text-mined interactions from Literome
Wang et al., J Biol Chem 2009
:
Inhibition of mTORC1 or mTORC2 by transiently or moderately activated MEK/ERK caused moderately enhanced Beclin 1 resulting in cytoprotective autophagy, whereas inhibition of both mTORC1 and
mTORC2 by sustained MEK/ERK activation
caused strongly pronounced
Beclin 1 leading to cytodestructive autophagy ... Inhibition of
mTORC1 or mTORC2 by transiently or moderately activated MEK/ERK
caused moderately enhanced
Beclin 1 resulting in cytoprotective autophagy, whereas inhibition of both mTORC1 and mTORC2 by sustained MEK/ERK activation caused strongly pronounced Beclin 1 leading to cytodestructive autophagy ... Inhibition of mTORC1 or mTORC2 by transiently or moderately activated MEK/ERK caused moderately enhanced Beclin 1 resulting in cytoprotective autophagy, whereas inhibition of both
mTORC1 and mTORC2 by sustained MEK/ERK activation
caused strongly pronounced
Beclin 1 leading to cytodestructive autophagy ... Our findings thus propose that the
AMPK-MEK/ERK-TSC-mTOR pathway
regulation of
Beclin 1 represents different thresholds responsible for a protective or destructive autophagy
Kang et al., Cell Death Differ 2010
(Carcinoma...) :
Moreover, RAGE sustained autophagy is associated with decreased phosphorylation of
mammalian target of rapamycin (mTOR) and
increased Beclin-1/VPS34 autophagosome formation
Wang et al., J Ethnopharmacol 2013
(Ischemic Attack, Transient...) :
HLJDD also notably elevated the levels of microtubule associated protein1 light chain 3 ( LC3 ),
Beclin-1 , and other autophagy related genes ( Atgs ), promoted the activation of extracellular signal regulated kinases ( ERK ), protein kinase B ( Akt ), 3-phosphoinositide dependent kinase ( PDK1 ), and
inhibited the activation of
mammalian target of rapamycin (mTOR) , c-Jun N-terminal protein kinases (JNK), p38, phosphatase and tensin homolog (PTEN)