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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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EPHB2 — VIP

Text-mined interactions from Literome

Le Péchon-Vallée et al., Neuroendocrinology 2000 (MAP Kinase Signaling System) : VIP and PACAP38 increased ERK1 and ERK2 phosphorylation and were equipotent stimulators of both kinases ... ERK activation by VIP or PACAP38 and TRH were additive and both sensitive to the MEK inhibitors PD98059 and U0126 ... These results demonstrate for the first time that VIP and PACAP38 activate ERK in GH4C1 cells
Alleaume et al., Neuropeptides 2003 : Under serum-free conditions VIP stimulates HT29 cell proliferation and induced a time- and concentration dependent ERK activation
Romano et al., J Biol Chem 2003 : Experiments involving the expression of the dominant negative mutants of Ras and Rap1 signaling ( RasN17 or Rap1N17 ) indicate that both GTPases Ras and Rap1 are recruited for the ERK activation by VIP and PACAP38, whereas Rap1 is poorly involved in TRH or EGF induced ERK activation
Vlotides et al., Endocrinology 2004 : Both PACAP-38 and VIP also rapidly induced ERK1/2 phosphorylation and their stimulatory effect on NNT-1/BSF-3 mRNA expression was reduced by the MAPK kinase/ERK kinase ( MEK ) inhibitor U0126 ( 10 microm )
Gutiérrez-Cañas et al., Prostate 2005 (Carcinoma, Neuroendocrine...) : VIP induced extracellular signal regulated kinase 1 and 2 ( ERK1/2 ) phosphorylation and NE differentiation by PKA dependent and independent pathways, since the PKA inhibitor H89 partially blocked VIP induced NE differentiation and did not affect ERK1/2 phosphorylation
Falktoft et al., Neuropeptides 2009 (Neuroblastoma) : A pivotal role of PKA was implicated in addition to partial involvement of PKC and ERK1/2 in PACAP induced VIP gene expression as H-89, Bisindolylmaleimide I ( BIS ), Gö6976 and U0126 attenuated the VIP mRNA expression by 93 %, 58 %, 58 % and 40 %, respectively
Yu et al., Neuropeptides 2010 : In addition, VIP treatment induced rapid phosphorylation of ERK1/2 and p38MAPK, and PD98059 and SB203580 were able to inhibit VIP induced phosphorylation of ERK1/2 and p38MAPK, respectively
Persson et al., J Cell Biochem 2011 : In addition, VIP robustly enhanced the phosphorylation of ERK and the stimulatory effect by VIP on rankl mRNA was inhibited by the MEK1/2 inhibitor PD98059
Li et al., Invest Ophthalmol Vis Sci 2013 (MAP Kinase Signaling System) : VIP also increased ERK1/2 activity, VIP stimulated increase in [ Ca ( 2+ ) ] i. Secretion, but not ERK1/2 activity, was inhibited by the protein kinase A inhibitor, H89 ... VIP stimulates a cAMP dependent increase in [ Ca ( 2+ ) ] i and glycoconjugate secretion, but not ERK1/2 activation