◀ Back to NPY
EPHB2 — NPY
Text-mined interactions from Literome
Keffel et al., J Pharmacol Exp Ther 1999
(Leukemia, Erythroblastic, Acute) :
However,
NPY caused a rapid ( already maximal after 30 s ) and concentration dependent ( maximum at 10-100 nM ) activation of extracellular signal regulated kinase (
ERK ) as assessed by immunoblotting with epitope-specific, antiphosphotyrosine antibodies and in some cases enzymatically ...
ERK activation by 100 nM
NPY was abolished by the Y ( 1 ) NPY receptor antagonist BIBP 3226 ( 1 microM ), pertussis toxin treatment ( 100 ng ml(-1) overnight ), the mitogen activated protein kinase ( MAPK ) kinase inhibitor PD 98059 ( 100 microM ), and the phosphatidylinositol-3-kinase inhibitor wortmannin ( 100 nM ) ... However,
NPY activates
ERK by a pathway involving Y ( 1 ) receptors, pertussis toxin-sensitive G proteins, and phosphatidylinositol-3-kinase, whereas PKC may not be involved
Gur et al., Neuroendocrinology 2002
:
Exposure of the cells to the MAPK kinase ( MEK ) inhibitor ( PD98059 ; PD 10, 25 and 50 microM ) completely blocked
NPY induced
ERK activity
Kanevskij et al., Cardiovasc Res 2002
(Translocation, Genetic) :
In contrast,
NPY did not
enhance ERK-activation caused by norepinephrine
Cho et al., Biochem Biophys Res Commun 2004
:
NPY Y1 receptors were expressed on islet and
NPY induced phosphorylation of
ERK1/2 rapidly and transiently ... PD98059 ( MAPK kinase inhibitor ) and BIM-1 ( protein kinase C inhibitor ) inhibited
activation of
ERK1/2 by
NPY , but wortmannin ( phosphatidylinositol 3-kinase inhibitor ) did not
Barnea et al., Brain Res 2004
(MAP Kinase Signaling System) :
We have previously demonstrated that brain derived neurotrophic factor (BDNF) induces persistent
neuropeptide Y (NPY) production in cortical cultures in an
ERK1/2 dependent manner
Chan et al., J Neurochem 2005
(Brain Neoplasms...) :
Stimulation of the Gi-coupled
neuropeptide Y1 and Gq-coupled muscarinic M1 acetylcholine receptors, but not the Gs-coupled dopamine D1 receptor,
led to the activation of extracellular signal regulated kinase (
ERK )
Ruscica et al., Endocrinology 2006
(Disease Progression...) :
In DU145 cells,
NPY stimulated a long lasting
ERK1/2 activation, whereas, in PC3 cells, this effect was rapid and transient and required activation of protein kinase C ... Moreover, in both cell lines, pretreatment with BIBP3226 prevented the
NPY induced
ERK1/2 phosphorylation, further supporting Y1-R involvement