Gene interactions and pathways from curated databases and text-mining

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GPI — VIP

Text-mined interactions from Literome

Rangon et al., J Pharmacol Exp Ther 2005 : The pharmacology of this VPAC(2) receptor seems unconventional because 1 ) PACAP does not mimic VIP effects, 2 ) PHI acts with a comparable potency, and 3 ) PACAP 27 modestly inhibited the VIP-specific binding, whereas for PHI or VIP, inhibition was complete
Nurko et al., Gastroenterology 1989 : On the other hand, VIP and growth hormone releasing factor analogues caused significant antagonism of VIP responses without modifying the responses to PHI-27
Hubel et al., Am J Physiol 1989 : We conclude that 1 ) norepinephrine increases absorption by acting on nerves and enterocytes ; 2 ) the failure of norepinephrine to reduce the Isc response to VIP when the VIP induced increment in Isc is comparable to that caused by EFS is evidence that VIP does not mediate the EFS response ; 3 ) PHI might mediate the EFS response ; and 4 ) VIP , PHI, and histamine affect enterocytes directly ; histamine also affects intrinsic nerves
Turner et al., J Pharmacol Exp Ther 1988 : In this study we have characterized and compared the regulation of the HT29 cell vasoactive intestinal peptide receptor/adenylate cyclase system ( VIP-R/AC ) by the VIP-R agonist peptide histidineisoleucineamide (PHI) and by activators of protein kinase C ( PKC ) including phorbol 12-myristate, 13-acetate ( PMA ) and mezerein ... Also, down-regulation of PKC did not block PHI induced loss of cell surface VIP-R
Shaffer et al., Peptides 1986 : Pharmacology studies indicated that specific 125I-VIP binding was inhibited with high affinity by VIP and low affinity by secretin and PHI
Grider et al., Am J Physiol 1987 : Both secretin and PHI inhibited neurally induced VIP release in the two types of muscle
Jensen et al., Am J Physiol 1981 : In dispersed acini from guinea pig pancreas, PHI , a peptide recently isolated from porcine intestine and found to contain 27 amino acids, inhibited binding of 125I-vasoactive intestinal peptide ( 125I-VIP ), increased cellular cAMP, and stimulated amylase secretion ... From the abilities of PHI to inhibit binding of 125I-VIP , to increase cellular cAMP, and to increase amylase secretion, the apparent affinity of PHI for the VIP preferring receptors on pancreatic acinar cells is approximately 25 times less than that of VIP but 10 times greater than that of secretin
Robberecht et al., Regul Pept 1982 : Effects of PHI on vasoactive intestinal peptide receptors and adenylate cyclase activity in lung membranes