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CCK — EPHB2

Text-mined interactions from Literome

Piiper et al., Mol Pharmacol 2000 : Cholecystokinin (CCK) activates ERK1/2 by a PKC dependent, and thus presumably PTx-insensitive, pathway ... In the present study, PTx partially inhibited CCK induced ERK1/2 activation in pancreatic AR42J cells, although activation of phospholipase C was not reduced ... PTx also inhibited ERK1/2 activation in response to the PKC activator 12-O-tetradecanoylphorbol-13-acetate ( TPA ) and epidermal growth factor (EGF) as well as activation of c-Raf-1 by EGF and CCK
Kiehne et al., Pancreatology 2002 (Pancreatic Neoplasms) : Differential activation of p42ERK2 and p125FAK by cholecystokinin and bombesin in the secretion and proliferation of the pancreatic amphicrine cell line AR42J ... p42ERK2 and p125FAK were activated by cholecystokinin and bombesin with maximum stimulation at concentrations above 10 nM
Piiper et al., J Biol Chem 2003 : In the present study, we investigated the different mechanisms participating in CCK induced activation of ERK1/2 in pancreatic AR42J cells expressing both CCK ( A ) and CCK ( B ) ... CCK activated ERK1/2 and Raf-1 to a similar extent as epidermal growth factor (EGF) ... Inhibition of EGF receptor (EGFR) tyrosine kinase or expression of dominant negative Ras reduced CCK induced ERK1/2 activation, indicating participation of the EGFR and Ras in CCK induced ERK1/2 activation ... Signal amplification between Ras and Raf in a CCK induced ERK cascade appears to be mediated by activation of protein kinase Cepsilon ( PKCepsilon ), because 1 ) down-modulation of phorbol ester-sensitive PKCs inhibited CCK induced activation of Ras, Raf, and ERK1/2 without influencing Shc-Grb2 complex formation ; 2 ) PKCepsilon, but not PKCalpha or PKCdelta, was detectable in Raf-1 immunoprecipitates, although CCK activated all three PKC isoenzymes ... Together, our data show that different signals emanating from the CCK receptors mediate ERK1/2 activation ; activation of Yes and the EGFR mediate Shc-Grb2 recruitment, and activation of PKC, most likely PKCepsilon, augments CCK stimulated ERK1/2 activation at the Ras/Raf level
Sutton et al., J Neurosci 2004 : The results demonstrate that ERK signaling is necessary for exogenous CCK to suppress food intake in deprived rats and suggest that this pathway may also be involved in natural satiation and the period of satiety between meals through coupling of ERK activation to both cytosolic and nuclear effector mechanisms that have the potential to confer acute and long-term changes in neuronal functioning
Langmesser et al., J Cell Biochem 2007 : Stimulation of ERK1/2 phosphorylation by CCK is mainly mediated by the CCK2 receptor
Choi et al., Am J Physiol Gastrointest Liver Physiol 2007 : We discovered that the upregulation of CCK transcription involves ERK1/2 , PKA, and calmodulin dependent protein kinase mediated pathways
Huang et al., Regul Pept 2007 (Colonic Neoplasms) : The effects of CCK-2i4svR activation on phosphorylation of ERK1/2 , p38 ( MAPK ) and JNK were examined by using immunoblotting
Samuel et al., Pancreatology 2008 (Disease Models, Animal...) : In additional in vitro studies, we show that cholecystokinin- or TNF-alpha stimulated nuclear transcription factor kappa-B activation in AR42J cells is inhibited by dominant negative ERK2
Babic et al., Am J Physiol Regul Integr Comp Physiol 2009 : The aim of this study was to identify the neurochemical phenotypes of the NTS neurons that exhibit CCK induced activation of ERK1/2 ... Using confocal microscopy, we demonstrate that intraperitoneal CCK administration increases the number of neurons that express phosphorylated ERK1/2 ( pERK1/2 ) in the medial and commissural subnuclei of the NTS and that CCK induced expression of ERK1/2 is increased in tyrosine hydroxylase-immunoreactive neurons
Guo et al., Am J Physiol Gastrointest Liver Physiol 2012 : When signaling pathways were evaluated, CCK stimulation increased c-Jun expression, JNK and ERK activity, and AP-1 activation
Campos et al., Endocrinology 2012 (MAP Kinase Signaling System) : Fourth ventricle injection of a competitive NMDA receptor antagonist, prevented CCK induced phosphorylation of ERK1/2 in hindbrain neurons and in vagal afferent endings, as did direct inhibition of MAPK kinase ... We conclude that activation of NMDA receptors in the hindbrain is necessary for CCK induced ERK1/2 phosphorylation in the NTS and consequent reduction of food intake
Nicke et al., Am J Physiol 1999 : In contrast, infection with adenovirus bearing rasN17 increased basal amylase release, inhibited CCK mediated JNK activation, had no effect on CCK activation of ERK , and inhibited DNA synthesis