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CA2 — VIP

Text-mined interactions from Literome

Bundey et al., Neuropharmacology 1999 : Pituitary adenylyl cyclase activating polypeptide ( PACAP ) ( 10 nM ), vasoactive intestinal peptide (VIP) ( 1 microM ) and carbachol ( 1 mM ) produced transient increases in intracellular [Ca2+ ]
Jeong et al., J Neurosci 1999 : Likewise, VIP mediated Ca2+ current inhibition, which is mediated by cholera toxin-sensitive G-protein, was also completely suppressed by a number of Galpha subunits overexpressed in neurons
Vanecek et al., Adv Exp Med Biol 1999 : VIP induces [ Ca2+ ] i increase in 14 % of the SCN cells and AVP release is stimulated by Ca2+ ionophore ionomycin
Xiao et al., Am J Physiol Regul Integr Comp Physiol 2004 : PACAP-38 ( 1 nM ), PACAP-27 ( 1 nM ), VIP ( 10 nM ), or forskolin ( 10 microM ) alone did not stimulate [Ca2+ ] i increase, neither did they modulate CCK ( 1 nM ) -induced oscillations ; but when they were added to cells simultaneously exposed to subthreshold CCK ( 10 pM ), calcium spikes emerged
Feth et al., Br J Pharmacol 1992 (Leukemia, Erythroblastic, Acute) : NPY13-36, vasoactive intestinal peptide (VIP) and pancreatic polypeptide (PP) increased intracellular Ca2+ only poorly
Tatsuno et al., Endocrinology 1992 : VIP also increased [ Ca2+ ] i, but required 1 microM or higher concentration for a considerable number of cells to respond
Langer et al., Cell Signal 2005 : Mutations in the carboxy-terminus of the third intracellular loop of the human recombinant VPAC1 receptor impair VIP stimulated [Ca2+ ] i increase but not adenylate cyclase stimulation
Al Kahtane et al., J Neuroendocrinol 2005 (Calcium Signaling) : VIP or the L-type Ca2+ channel activator, Bay K8644 ( Bay ) increased [ Ca2+ ] i in a concentration- and time dependent fashion, an effect abolished by preincubating the cells with R ( - ) -propylnorapomorphine HCl, a D2 dopamine receptor agonist (D2AG) or Verapamil ( VR ), a specific L-type Ca2+ channel blocker
Izzo et al., Regul Pept 1991 : These data demonstrate that ( 1 ) bacitracin decreases the binding of VIP to small intestinal epithelial cells, ( 2 ) both Ca2+ and Mg2+ affect the binding of VIP to its surface receptor and ( 3 ) VIP is internalized into epithelial cells
Kase et al., Pflugers Arch 1991 : VIP in a low concentration can generate cytosolic Ca2+ oscillations via cyclic AMP, but high VIP concentrations inhibit both ACh and VIP evoked Ca2+ signals and this effect is mediated by high intracellular cyclic AMP levels
Li et al., Invest Ophthalmol Vis Sci 2013 (MAP Kinase Signaling System) : Effect of VIP on Intracellular [Ca2+ ], Extracellular Regulated Kinase 1/2, and Secretion in Cultured Rat Conjunctival Goblet Cells
Kumagai et al., Calcif Tissue Int 1989 : The effects of norepinephrine ( NE ), vasoactive intestinal peptide ( VIP ) , and ATP on cytosolic Ca2+ were assessed in a rat osteoblast-like osteosarcoma cell line ( UMR-106 ) responsive to PTH
Zurier et al., Exp Cell Res 1988 : In contrast to other growth promoting neuropeptides, VIP did not induce an increase in cytosolic free Ca2+ or an activation of protein kinase C
Yoshikawa et al., Nihon Naibunpi Gakkai Zasshi 1986 : In studies using a retrograde venous perfusion system of the bovine adrenal gland, marked releases of both VIP-LI and catecholamine ( CA ) were observed immediately after the infusion of potassium solution of a concentration of 56 mM in a Ca2+ dependent manner
Rawlings et al., Endocrinology 1995 : PACAP and VIP stimulated Ca2+ influx responses in individual GH4C1 cells and were equipotent in stimulating cAMP production ( EC50, 15 nM ) in GH4C1 cell populations, but failed to stimulate inositol phospholipid ( PI ) turnover, results consistent with the expression of a PVR3
Zhang et al., J Neurosci Res 1996 : In contrast to astrocytes, when Schwann cells were loaded with fura-2, VIP did not increase cytosolic Ca2+
Hezareh et al., J Neuroendocrinol 1996 : The Ca2+ responses to PACAP38 and VIP were unaffected by overnight treatment of the cells with pertussis toxin ( PTX ; 250 ng/ml ) indicating that these responses are mediated by a PTX-insensitive G-protein
Tiaho et al., Pflugers Arch 1996 : Using the whole-cell patch-clamp technique, we show here that VIP enhances Ca2+ and Ba2+ currents ( IBa ) through voltage dependent L-type Ca2+ channels in adult rat ventricular myocytes
Allescher et al., Am J Physiol 1996 : Basal VIP release was reduced by 65 % by removal of external Ca2+
Nilsson et al., Acta Physiol Scand 1996 (Inflammation) : In the present study the effect of indomethacin and vasoactive intestinal peptide-antiserum ( VIP-antiserum ) on the Ca2+ , HCO ( 3 ) - and fluid secretion in the inflamed gallbladder were tested in a validated experimental model in cats
Xia et al., J Clin Immunol 1996 (Precursor Cell Lymphoblastic Leukemia-Lymphoma) : VIP increased [ cAMP ] i in Tsup-1 cells ( EC50 = 14.4 nM ) and stimulated a rapid and transient increase in [Ca2+ ] i ( EC50 = 30 nM )
Hodges et al., Invest Ophthalmol Vis Sci 1997 : Changes in intracellular [Ca2+ ] ( [ Ca2+ ] i ) were measured on fura-2 loaded acini in response to VIP
Kawasaki et al., Br J Pharmacol 1997 : 1. This study was designed to investigate the mechanism of the relaxation induced by vasoactive intestinal peptide (VIP) in medial strips of the porcine coronary artery, by determining the effect on the cytosolic Ca2+ concentration ([Ca2+]i) , the [ Ca2+ ] i-force relation and the involvement of G-protein
Carbajal et al., Endocrinology 1997 : Basal, VIP- , and DA withdrawal induced cortical F-actin disassembly were dependent on extracellular Ca2+ whereas TRH- and forskolin induced disassembly were not
Low et al., Eur J Pharmacol 1997 : The reintroduction of Ca2+ following VIP induced Ca2+ release did not evoke a Ca2+ response in 5 cells imaged ... Stimulation with VIP caused transient Ca2+ responses in Ca2+-free physiological saline containing 50 microM EGTA
Murthy et al., Am J Physiol 1998 : In muscle cells treated with cAMP dependent protein kinase (PKA) and PKG inhibitors ( H-89 and KT-5823 ), 8-BrcGMP ( 10 microM ), NO ( 1 microM ), and VIP ( 1 microM ) stimulated 45Ca2+ release ( 21 +/- 3 to 30 +/- 1 % decrease in 45Ca2+ cell content ) ; Ca2+ release stimulated by 8-BrcGMP was concentration dependent with an EC50 of 0.4 +/- 0.1 microM and a threshold of 10 nM
Anderova et al., Brain Res 1998 : The effect of VIP on muscarine induced [ Ca2+ ] i signals was mimicked by 8-Br-cAMP, and both were blocked by H-89, a protein kinase A inhibitor