Gene interactions and pathways from curated databases and text-mining

◀ 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