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CASP7 — NGF
Text-mined interactions from Literome
Rong et al., J Neurochem 1999
:
NGF regulated several members of the bcl-2 family and
caspase-3 in a manner consistent with its effect on apoptosis in PC12 cells
Deshmukh et al., J Cell Biol 2000
:
Nerve growth factor (NGF) deprivation
induces a Bax dependent,
caspase dependent programmed cell death in sympathetic neurons
Hughes et al., J Neurosci Res 2001
:
Furthermore, the level of
caspase3-like activity that is rapidly activated by serum withdrawal from PC12 cells is
reduced by both the NGFdelta9/13 protein and
NGF
Jezierski et al., Endocrinology 2001
:
NGF stimulation increases JNK2 phosphorylation and
reduces caspase-3 activity in the olfactory bulb of estrogen replaced animals
Hunsperger et al., J Neurovirol 2003
:
NGF deprivation
stimulates apoptotic signaling by activating the proapoptotic proteolytic enzyme,
caspase-3
Shimoke et al., Neurosci Lett 2005
:
We discovered that the activities of caspase-3, -9 and -12 were increased time-dependently after the treatment with Th, and
NGF suppressed the Th-triggered activation of
caspase-3 , -9 and -12
Hirata et al., J Neurochem 2006
(MAP Kinase Signaling System...) :
Nerve growth factor (NGF) almost completely
prevented rotenone induced but not manganese induced
caspase activation and DNA fragmentation
Yang et al., Neurosci Lett 2008
(Brain Ischemia...) :
NGF/VEGF significantly
inhibited the expression of ERK1 and
caspase-3
Kawashima et al., J Nutr Biochem 2010
:
Phosphorylated-Akt expression was significantly increased in EPA treated cells, and
nerve growth factor withdrawal induced increases in cell death and
caspase-3 activity were
suppressed by EPA treatment
Nguyen et al., Exp Mol Med 2010
:
Both
nerve growth factor (NGF) and brain derived growth factor ( BDNF )
prevent STS induced apoptotic morphology and
caspase-3 activity by upregulating phosphorylation of the tropomyosin receptor kinase ( Trk ) receptor
Holub et al., J Pediatr Surg 2011
(Neuroblastoma) :
Cleaved
caspase-3 expression is further
increased with exogenous
NGF stimulation in the transduced cells