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ARG2 — CA2

Text-mined interactions from Literome

Schaeffer et al., Biochem Pharmacol 2001 : Des-Arg ( 10 ) -kallidin increased cytosolic free Ca2+ levels, phosphoinositide turnover, and arachidonic acid release at nanomolar concentrations ( respective EC ( 50 ) values : 16 +/- 2, 4 +/- 2.7, 6 +/- 2 nM )
Waltereit et al., J Neurosci 2001 : Arg3.1/Arc mRNA induction by Ca2+ and cAMP requires protein kinase A and mitogen activated protein kinase/extracellular regulated kinase activation
Eric et al., Eur J Pharmacol 2003 : Des-Arg9-bradykinin increases intracellular Ca2+ in bronchoalveolar eosinophils from ovalbumin sensitized and -challenged mice ... The bronchoalveolar lavage cells of control mice, which were predominantly alveolar macrophages, showed an increase in [Ca2+ ] i in response to bradykinin ( 1 microM ) but not to des-Arg9-bradykinin ( 1 microM ), indicating the presence of functional bradykinin B2 receptors and the absence of B1 receptors ... This des-Arg9-bradykinin induced [ Ca2+ ] i increase was markedly inhibited by the selective bradykinin B1 receptor antagonist, Ac-Lys- [ D-betaNal7, Ile8 ] des-Arg9-bradykinin ( R-715 ; 10 microM )
Lerner et al., Agents Actions 1992 : The stimulatory effect of BK was seen in concentrations at or above 10 ( -8 ) M, with the most pronounced effect at 10 ( -6 ) M. D-Arg0-Hyp3-Thi5,8-DPhe7-BK , a BK B2 receptor antagonist, but not des-Arg9-Leu8-BK, a BK B1 receptor antagonist, blocked BK-induced rise in [Ca2+ ] i
Song et al., J Neurosci 2003 : The internalization was abolished by the MOR antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 ( CTAP ), in the presence of low Ca2+ and by the Na+ channel blocker lidocaine, confirming that it was caused by opioid release and neuronal firing
Azuma et al., J Cardiovasc Pharmacol 2003 : In the presence of 3 x 10 ( -7 ) M Arg-HSA-Spm , the stimulation of catecholamine secretion observed by increasing acetylcholine up to 10 ( -3 ) M did not reach the maximal level observed without Arg-HSA-Spm. Arg-HSA-Spm at 10 ( -5 ) M suppressed both the increase in intracellular free Ca2+ level and the influx of 45Ca2+ induced by 10 ( -4 ) M acetylcholine ... The Arg-HSA-Spm induced suppression of intracellular free Ca2+ level, the influx of 45Ca2+ and catecholamine secretion were not observed in the presence of extracellular K+ at 56 mM
Legaz et al., Eur J Cell Biol 2004 : Ca2+ can not replace Mn2+, but its addition to reaction mixtures in the presence of Mn2+ significantly inhibited arginase activity
Nitschke et al., Pflugers Arch 1991 : d ( CH2 ) 5 [ Tyr ( Me ) 2 ] 2,Arg8vasopressin , a V1 antagonist ( Manning compound, 10 nmol/l ), blocked the ADH effect on [Ca2+ ] i completely ( n = 5 )
Kawanishi et al., J Biol Chem 1991 : In normoxic hepatocytes, phenylephrine ( 50 microM ) and Arg-vasopressin ( 20-40 nM ) induced Ca2+ oscillations in 70 and 40 % of cells, respectively
Doyle et al., Biochem Biophys Res Commun 1985 : The efflux of 45Ca2+ in response to [ Arg8 ] vasopressin could be inhibited by a vasopressin antagonist
O'Brian et al., Biochem Biophys Res Commun 1984 : Protein kinase C phosphorylates the synthetic peptide Arg-Arg-Lys-Ala-Ser-Gly-Pro-Pro-Val in the presence of phospholipid plus either Ca2+ or a phorbol ester tumor promoter
Marsh et al., Br J Pharmacol 1994 : 4. Under calcium-free conditions, des-Arg9-bradykinin induced an increase in [Ca2+ ] i at concentrations of 1 microM and 10 microM
Zhang et al., Proc Natl Acad Sci U S A 1993 : Although neither Asp-85, Asp-212, nor Arg-82 is individually directly involved in the binding of Ca2+ in these two sites, they might all participate in it
Pallone et al., Am J Physiol 1998 : The BK [Ca2+ ] i response was blocked by the selective BK B2-receptor antagonists D-Arg- [ Hyp3,Thi5.8,D-Phe7 ] BK and D-Arg- [ Hyp3,D-Phe7,Leu8 ] BK but not the B1 antagonist des-Arg9- [ Leu8 ] BK. BK vasodilated microperfused OMDVR that had been preconstricted with 10 ( -8 ) M angiotensin II