PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30470900-4 2019 In the general frame of the NCS often observed in crystals of biomolecules, this paper deals with nickel(II)-substituted human carbonic anhydrase(II) (hCAII) and its SAD structure determination at the nickel edge. Nickel(2+) 98-108 carbonic anhydrase 2 Homo sapiens 127-149 31207061-6 2019 For CA I and CA II, the best inhibition enzymes, was the Ni(II) complex with 62.98+-18.41, 86.17+-23.62 Ki values, whereas this inhibition effect showed ligand with 24.53+-2.66 Ki value for the AChE enzyme. Nickel(2+) 57-63 carbonic anhydrase 2 Homo sapiens 13-18 30470900-4 2019 In the general frame of the NCS often observed in crystals of biomolecules, this paper deals with nickel(II)-substituted human carbonic anhydrase(II) (hCAII) and its SAD structure determination at the nickel edge. Nickel(2+) 98-108 carbonic anhydrase 2 Homo sapiens 151-156 29890074-4 2018 By employing energy dispersive X-ray (EDX) spectroscopy, we evaluate the metal content of Ni(II)-bound CP-Ser [oligomer of S100A8(C42S) and S100A9(C3S)] crystals obtained in the absence and presence of Ca(II). Nickel(2+) 90-96 carbonic anhydrase 2 Homo sapiens 202-208 29890074-3 2018 We investigate the effect of Ca(II) ions on the structure and Ni(II)-binding properties of human CP. Nickel(2+) 62-68 carbonic anhydrase 2 Homo sapiens 29-35 29890074-11 2018 This analysis reveals conformational changes associated with coordination of Ca(II) to the EF-hands of S100A9 and that Ca(II) binding affects the coordination number and geometry of the Ni(II) ion bound to the His3Asp site. Nickel(2+) 186-192 carbonic anhydrase 2 Homo sapiens 119-125 29890074-12 2018 In contrast, negligible differences are observed for the Ni(II)-His6 site in the absence and presence of Ca(II). Nickel(2+) 57-63 carbonic anhydrase 2 Homo sapiens 105-111 29218635-5 2018 The magnetic susceptibility anisotropy tensors of cobalt(II) and nickel(II) ions bound to human carbonic anhydrase II in free and inhibited forms have been determined. Nickel(2+) 65-75 carbonic anhydrase 2 Homo sapiens 96-117 11978840-8 2002 These data suggest that SE may persistently convert regular firing cells to intrinsic bursters by selectively increasing the density of a Ni2+-sensitive T-type Ca2+ current. Nickel(2+) 138-142 carbonic anhydrase 2 Homo sapiens 160-163 16609771-6 2006 The amide O-donors of ntam lead to the stabilization of complexes of large metal ions (Pb(II), Cd(II), La(III), Ca(II)) relative to log K1 for the NH3 complexes, while for small metal ions (Ni(II), Cu(II)) the amide O-donors lead to destabilization. Nickel(2+) 190-196 carbonic anhydrase 2 Homo sapiens 112-118 15358810-8 2004 Abolition of this plateau phase by Ni2+ (1 mM) in the presence of extracellular Ca2+ confirmed the existence of an ET1-induced Ca2+ entry. Nickel(2+) 35-39 carbonic anhydrase 2 Homo sapiens 80-83 8930286-8 1996 The hyperpolarization-induced decrease in [Ca2+]i was reduced significantly by 200 microM Cd2+ and 10 microM nimodipine, but was only slightly inhibited by 50 microM Ni2+. Nickel(2+) 166-170 carbonic anhydrase 2 Homo sapiens 43-46 12164389-2 2001 Here we report the synthesis and inhibition studies against the physiologically relevant isozymes CA I, CA II and CA IV, of a series of metal complexes (Co(II), Ni(II) and Cu(II) derivatives) of a Schiff-base ligand, obtained from sulfanilamide and salicylaldehyde. Nickel(2+) 161-167 carbonic anhydrase 2 Homo sapiens 104-109 10964414-10 2000 These data indicate that CA II binds transition metals with high affinity and is much more selective for Zn(2+) over Ni(2+) or Cd(2+) than most small-molecule chelators or other metalloenzymes. Nickel(2+) 117-123 carbonic anhydrase 2 Homo sapiens 25-30 9231716-4 1997 The low [Ca2+]e-induced response is also blocked by replacement of extracellular Ca2+ with Ba2+, Zn2+, or Ni2+, and by 100 microM La3+. Nickel(2+) 106-110 carbonic anhydrase 2 Homo sapiens 9-12 7558146-3 1995 The second phase resulted from transmembrane influx and occurred in the absence of store release and by Ca2+ channels that were inhibited by Ni2+ but not SKF 96365 or econazole. Nickel(2+) 141-145 carbonic anhydrase 2 Homo sapiens 104-107 10456086-6 1996 The LTD was also dependent on Ca2+ influx via voltage-gated Ca2+ channels (VGCCs), because LTD was severely attenuated or blocked by both nimodipine and Ni2+. Nickel(2+) 153-157 carbonic anhydrase 2 Homo sapiens 30-33 10456086-6 1996 The LTD was also dependent on Ca2+ influx via voltage-gated Ca2+ channels (VGCCs), because LTD was severely attenuated or blocked by both nimodipine and Ni2+. Nickel(2+) 153-157 carbonic anhydrase 2 Homo sapiens 60-63 7500154-4 1995 The rises in [Ca2+]i were not due to Ca2+ entry through N-methyl-D-aspartate (NMDA)-activated or non-NMDA-activated glutamate channels, but were reduced by low concentrations of Ni2+. Nickel(2+) 178-182 carbonic anhydrase 2 Homo sapiens 14-17 7962126-6 1994 Addition of 5 mM Ca2+ to cells pretreated with doses of thapsigargin or ionomycin shown to release intracellular Ca2+ stores induced a depolarization which was 1) dependent upon extracellular Ca2+, 2) abolished by 5 mM Ni2+, 3) independent of extracellular Na+, and 4) dependent upon Bapta loading. Nickel(2+) 219-223 carbonic anhydrase 2 Homo sapiens 17-20 7563033-5 1995 Currents were Ca2+ selective with a selectivity sequence of Ca2+ > Sr2+ >> Mg2+ = Mn2+ = Ni2+. Nickel(2+) 98-102 carbonic anhydrase 2 Homo sapiens 14-17 7962126-6 1994 Addition of 5 mM Ca2+ to cells pretreated with doses of thapsigargin or ionomycin shown to release intracellular Ca2+ stores induced a depolarization which was 1) dependent upon extracellular Ca2+, 2) abolished by 5 mM Ni2+, 3) independent of extracellular Na+, and 4) dependent upon Bapta loading. Nickel(2+) 219-223 carbonic anhydrase 2 Homo sapiens 113-116 7962126-6 1994 Addition of 5 mM Ca2+ to cells pretreated with doses of thapsigargin or ionomycin shown to release intracellular Ca2+ stores induced a depolarization which was 1) dependent upon extracellular Ca2+, 2) abolished by 5 mM Ni2+, 3) independent of extracellular Na+, and 4) dependent upon Bapta loading. Nickel(2+) 219-223 carbonic anhydrase 2 Homo sapiens 113-116 8207426-2 1994 Chelation of extracellular Ca2+ with EGTA or inhibition of Ca2+ channels with Ni2+ showed that the plateau phase was dependent upon Ca2+ entry. Nickel(2+) 78-82 carbonic anhydrase 2 Homo sapiens 59-62 7708469-7 1994 Inward currents evoked in Ca2+ were inhibited by other cations with the following order of potency: La3+ > Cd2+ > Co2+ approximately Ni2+ approximately Mn2+. Nickel(2+) 139-143 carbonic anhydrase 2 Homo sapiens 26-29 8207426-2 1994 Chelation of extracellular Ca2+ with EGTA or inhibition of Ca2+ channels with Ni2+ showed that the plateau phase was dependent upon Ca2+ entry. Nickel(2+) 78-82 carbonic anhydrase 2 Homo sapiens 59-62 8006954-2 1994 Depletion of [Ca2+]i stores by the application of thapsigargin, ionomycin or cyclopiazonic acid induced a depolarization which was (i) dependent upon BAPTA-loading, (ii) dependent upon extracellular Ca2+, (iii) independent of extracellular Na+ and (iv) abolished by 5 mM extracellular Ni2+. Nickel(2+) 285-289 carbonic anhydrase 2 Homo sapiens 14-17 1689544-4 1990 In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. Nickel(2+) 231-235 carbonic anhydrase 2 Homo sapiens 83-86 1689544-4 1990 In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. Nickel(2+) 95-99 carbonic anhydrase 2 Homo sapiens 83-86 1689544-4 1990 In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. Nickel(2+) 95-99 carbonic anhydrase 2 Homo sapiens 83-86 1689544-4 1990 In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. Nickel(2+) 95-99 carbonic anhydrase 2 Homo sapiens 83-86 1689544-4 1990 In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. Nickel(2+) 95-99 carbonic anhydrase 2 Homo sapiens 83-86 1689544-4 1990 In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. Nickel(2+) 231-235 carbonic anhydrase 2 Homo sapiens 83-86 1689544-4 1990 In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. Nickel(2+) 231-235 carbonic anhydrase 2 Homo sapiens 83-86 1689544-4 1990 In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. Nickel(2+) 231-235 carbonic anhydrase 2 Homo sapiens 83-86 1689544-7 1990 After depletion of the intracellular pool by stimulation in Ca2(+)-free medium, removal of the agonist and readmission of Ca2+ resulted in a rapid transient increase in [Ca2+]i that could be blocked by Ni2+, La3+, or elevated K+. Nickel(2+) 202-206 carbonic anhydrase 2 Homo sapiens 60-63 1689544-7 1990 After depletion of the intracellular pool by stimulation in Ca2(+)-free medium, removal of the agonist and readmission of Ca2+ resulted in a rapid transient increase in [Ca2+]i that could be blocked by Ni2+, La3+, or elevated K+. Nickel(2+) 202-206 carbonic anhydrase 2 Homo sapiens 122-125 1689544-7 1990 After depletion of the intracellular pool by stimulation in Ca2(+)-free medium, removal of the agonist and readmission of Ca2+ resulted in a rapid transient increase in [Ca2+]i that could be blocked by Ni2+, La3+, or elevated K+. Nickel(2+) 202-206 carbonic anhydrase 2 Homo sapiens 122-125 1689544-9 1990 These results suggest that two separate Ca2(+)-entry mechanisms, one sensitive to Ni2+, La3+, and elevated K+ and responsible for the agonist-induced increase in [Ca2+]i and one insensitive to the blockers and involved in refilling of the intracellular pool, may exist in salt gland cells. Nickel(2+) 82-86 carbonic anhydrase 2 Homo sapiens 40-43 2620798-3 1989 In the presence of Ca(II), the CAM molecule has two binding sites for Ni(II) (K1 = 7.25 x 10(5) M-1; K2 = 3.79 x 10(5) M-1) (Hill coefficient = 1.20 +/- 0.03 SE). Nickel(2+) 70-76 carbonic anhydrase 2 Homo sapiens 19-25 2620798-4 1989 In the absence of Ca(II), a complicated Ni(II)-binding curve is obtained indicating formation of many mutually interacting complex species. Nickel(2+) 40-46 carbonic anhydrase 2 Homo sapiens 18-24 2620798-5 1989 Binding of Ni(II) to CAM in the presence of Ca(II) is inhibited slightly by added MnCl2 (50 microM) and very strongly by CuCl2 and ZnCl2 (10 microM). Nickel(2+) 11-17 carbonic anhydrase 2 Homo sapiens 44-50 2620798-8 1989 Thus, the observed inhibition by Zn(II) of the Ni(II) binding to Ca(II)/CAM does not involve competition for the same binding sites but is rather caused by a conformational arrangement of CAM in its Ca(II)/Zn(II) complex that is different than the Ca(II) complex. Nickel(2+) 47-53 carbonic anhydrase 2 Homo sapiens 65-71 2620798-8 1989 Thus, the observed inhibition by Zn(II) of the Ni(II) binding to Ca(II)/CAM does not involve competition for the same binding sites but is rather caused by a conformational arrangement of CAM in its Ca(II)/Zn(II) complex that is different than the Ca(II) complex. Nickel(2+) 47-53 carbonic anhydrase 2 Homo sapiens 199-205 2620798-8 1989 Thus, the observed inhibition by Zn(II) of the Ni(II) binding to Ca(II)/CAM does not involve competition for the same binding sites but is rather caused by a conformational arrangement of CAM in its Ca(II)/Zn(II) complex that is different than the Ca(II) complex. Nickel(2+) 47-53 carbonic anhydrase 2 Homo sapiens 199-205 2553103-6 1989 Zn2+, Cd2+, Ni2+ and Mn2+ each inhibited Ca2+ inflow through the receptor-activated Ca2+ inflow system. Nickel(2+) 12-16 carbonic anhydrase 2 Homo sapiens 41-44 2553103-6 1989 Zn2+, Cd2+, Ni2+ and Mn2+ each inhibited Ca2+ inflow through the receptor-activated Ca2+ inflow system. Nickel(2+) 12-16 carbonic anhydrase 2 Homo sapiens 84-87 6314846-3 1983 Potentiometric, visible, infrared, electron spin, and nuclear magnetic resonance studies of the complexation of N-(2-acetamido)iminodiacetic acid (H2ADA) by Ca(II), Mg(II), Mn(II), Zn(II), Co(II), Ni(II), and Cu(II) are reported. Nickel(2+) 197-203 carbonic anhydrase 2 Homo sapiens 157-163 6267261-11 1981 Ba2+, Sr2+, Ca2+, Mn2+ and Mg2+ can carry current across the membrane; Ni2+ and Co2+ cannot. Nickel(2+) 71-75 carbonic anhydrase 2 Homo sapiens 12-15 32917908-3 2020 Through a comparative study on the intermediate states of the zinc-bound native CA II and non-native metal-substituted CA IIs, we demonstrate that the characteristic metal ion coordination geometries (tetrahedral for Zn2+, tetrahedral to octahedral conversion for Co2+, octahedral for Ni2+, and trigonal bipyramidal for Cu2+) directly modulate the catalytic efficacy. Nickel(2+) 285-289 carbonic anhydrase 2 Homo sapiens 80-85