ライフサイエンスコーパス: Ca2 free

1 otein termed GCAP1, that detects changes in [Ca2+]free.

2 GCAP1 and GCAP2, but not S-100beta, a high [Ca2+]free activator of GC1, competed with the triple mut

3 es were mounted in Ussing-type chambers with Ca2+(-)free and Ca2+(-)rich Tyrode's in the nonpigmented

4 Segments of Ca2+-free and Ca2+ treated thin filaments were sorted by

5 ave determined the solution structure of the Ca2+-free and Ca2+-bound forms of the C2A domain of syna

6 tructure determination of a C2 domain in its Ca2+-free and Ca2+-bound forms.

7 nses to PAF were enhanced 67.0% and 55.7% in Ca2+-free and Ca2+-containing medium, respectively.

8 Although the Ca2+-free and Ca2+-saturated forms of the CaM-IQ domain

9 CAP3 and GCAP2 stimulate GC1 and GC2 in low [Ca2+]free and inhibit GCs when [Ca2+]free is elevated, u

10 ayers in the presence of 0.01 microM to 2 mM Ca2+ (free) and 3 mM ATP (total) on the cytosolic (cis)

11 RYR1) is regulated by calmodulin in both its Ca2+-free (apocalmodulin) and Ca2+-bound (Ca2+ calmoduli

12 dly reduced or completely abolished by using Ca2+-free artificial cerebrospinal fluid (ACSF), ACSF co

13 When the cell was bathed in Ca2+-free Ba2+ Ringer solution, the K+ currents were blo

14 he predominant calmodulin-binding protein in Ca2+-free breast cell lysates and reveal that calmodulin

15 ree bathing solution, and enhanced by either Ca2+-free buffer or addition of lactate.

16 conversion from open (Ca2+-bound) to closed (Ca2+-free) calmodulin is shown to be 4-fold faster than

17 purified recombinant Ca2+-CaM or exposure to Ca2+-free CaM followed by application of Ca2+-containing

18 The effects persisted under an extracellular Ca2+-free condition but were abolished by intracellular

19 p-CPI) induced large contractions even under Ca2+-free conditions and decreased Ca2+ EC50 by more tha

20 efficiency of bipolar NEFO was preserved in Ca2+-free conditions and thus cannot be explained by the

21 Under Ca2+-free conditions designed to block the Ca2+-dependen

22 The large nonselective leak in Ca2+-free conditions was found to be a patch-seal phenom

23 Under the same Ca2+-free conditions, 11.1 mmol/l glucose had no effect

24 Under Ca2+-free conditions, activation of the pancreatic beta-

25 en cells were stepped from -100 to -30 mV in Ca2+-free conditions, small inward currents could be det

26 When, under Ca2+-free conditions, the islets were treated with forsk

27 th physiological external [Ca2+], but not in Ca2+-free conditions.

28 ferences were observed between low and high [Ca2+]free conditions, even when rods were loaded with AT

29 Under these (Ca2+-free) conditions, single-channel Po showed both vol

30 o form intramolecular disulfide bonds in the Ca2+-free conformation of the protein, thus blocking the

31 tivated Ca2+-binding domains in the "closed" Ca2+-free conformation.

32 Cross-linking occurred only to the E2 (Ca2+-free) conformation of SERCA2a, was strongly favored

33 that the inhibition is due to the failure of Ca2+-free CRT to bind the DBD.

34 in bleached vertebrate photoreceptors when [Ca2+]free decreases but is inactivated when cytoplasmic

35 In support of this interpretation, Ca2+-free/EGTA medium induced a greater than 60-fold inc

36 een pre-exposed to thapsigargin/ionomycin in Ca2+-free external solution.

37 ersed near -28 mV and persisted in nominally Ca2+-free extracellular solution, consistent with a nons

38 However, approximately 20% of segments from Ca2+-free filaments fitted best to the high Ca2+ model,

39 ed here suggest a flexible structure for the Ca2+-free form of fibrillin which becomes stabilized, mo

40 The change from a Ca2+-bound to a Ca2+-free form of GCAP1 increased susceptibility of Ca2+

41 roteins from the calmodulin superfamily, the Ca2+-free form of GCAP1 stimulates the effector enzyme.

42 t L between the two allosteric forms, T (the Ca2+-free form) and R (the Ca2+-bound form), without aff

43 f GCAP1 are removed by trypsin, while in the Ca2+-free form, GCAP1 is readily degraded to small fragm

44 he Ca2+ form and s20,w0 = 6.2 +/- 0.1 in the Ca2+-free form.

45 ire an activating conformation only in their Ca2+-free form.

46 ns in yeast cells in both its Ca2+-bound and Ca2+-free form.

47 Ca2+-free forms demonstrated a decrease of 20-30% in len

48 Two-dimensional NMR spectra of the Ca2+-free forms of the mutants have been compared to the

49 ee form of GCAP1 increased susceptibility of Ca2+-free GCAP1 to proteolysis by trypsin.

50 Ca2+-free GCAPs are responsible for activation of photor

51 y converge for strong activation of retGC by Ca2+-free GCAPs.

52 transmission is suppressed by incubation in Ca2+ free/high magnesium saline.

53 Ca2+-free hippocalcin was freely diffusible, as shown by

54 e (1 microM) consistently reduced ICl,vol in Ca2+-free hypotonic bath solutions with strong intracell

55 At 10(-6) M [Ca2+]free, in conditions that inactivated native GCAP1,

56 creases but is inactivated when cytoplasmic [Ca2+]free increase after dark adaptation.

57 C1, competed with the triple mutant at high [Ca2+]free, inhibiting GC1 with similar IC50's.

58 duction of peak Na+ current was similar with Ca2+-free internal solution and in 92 nm internal Ca2+,

59 in patches excised in inside-out mode into a Ca2+-free internal solution and were strongly inhibited

60 GC2 in low [Ca2+]free and inhibit GCs when [Ca2+]free is elevated, unlike GCAP1, which only stimulat

61 In Ca2+-free Krebs-Ringer bicarbonate buffer containing 2.8

62 In Ca2+ -free media, the acid response was curtailed and th

63 g was inhibited when cells were acidified in Ca2+-free media and eliminated by adding 1,2-bis(2-amino

64 Stimulation with thapsigargin in Ca2+-free media revealed that the size of the Ca2+ store

65 First, in both Ca2+-containing and Ca2+-free media serotonin transiently activated a small-

66 odine-sensitive Ca2+ stores were depleted in Ca2+-free media, a return to 2 mM external Ca2+ resulted

67 phenoxy)ethane-N,N,N',N'-tetraacetic acid to Ca2+-free media.

68 inone), and prolonged incubation of cells in Ca2+-free media.

69 Thus, stimulation of parotid acinar cells in Ca2+ -free medium with 0.5 microm carbachol releases app

70 AM loading (to preserve the workload), or in Ca2+-free medium (which also lowers cell workload).

71 rization-evoked Ca2+ increase was present in Ca2+-free medium and also following removal of Na+.

72 noic acid (C14) was significantly reduced in Ca2+-free medium and largely blocked by nicardipine.

73 MP-9 secretion by PGE2 was not diminished in Ca2+-free medium but was suppressed significantly and do

74 Further experiments using Ca2+-free medium demonstrated that the entry of extracel

75 by the finding that the presence of EGTA and Ca2+-free medium did not affect the activation of MAPK b

76 atile application of 0.3 microM histamine in Ca2+-free medium did not cause net loss of Ca2+ from the

77 M) caused a transient increase in [Ca2+]i in Ca2+-free medium in which the peak change was increased

78 sients and mimicked the inhibitory effect of Ca2+-free medium on the [Ca2+]i response to both 12,13-p

79 Pretreatment with Ca2+-free medium or the Ca2+-channel antagonist nicardip

80 tracellular Ca2+ stores (10 min treatment in Ca2+-free medium) and exposed to CaCl2 or MnCl2 had a gr

81 s also carried by external Na+ or Ba2+ (in a Ca2+-free medium) with amplitudes in the order Ca2+ > Ba

82 l growth factor to A-431 cells maintained in Ca2+-free medium, a condition that promotes changes in c

83 or oscillatory Ca2+ elevations; in nominally Ca2+-free medium, a transient Ca2+ rise was generated.

84 c transmission was blocked by perfusing with Ca2+-free medium, DHPG application reliably induced LTD.

85 In Ca2+-free medium, IH-treated cells exhibited higher basa

86 r Ca2+ stores, and small signals remained in Ca2+-free medium, indicating contributions from both ext

87 In Ca2+-free medium, NO reduced the peak Ca2+ rise caused b

88 stage following culture of 8-cell embryos in Ca2+-free medium, or medium containing cytochalasin D or

89 In Ca2+-free medium, pathogenic M. hyopneumoniae still incr

90 m gradually leaked out of the cells into the Ca2+-free medium.

91 ion that were abolished by nifedipine and in Ca2+-free medium.

92 Smaller responses were observed in Ca2+-free medium.

93 ut was abolished by incubation of neurons in Ca2+-free medium.

94 layed toxicity was evident at later times in Ca2+-free medium.

95 Fluorescence and NMR spectra of the Ca2+-free myr-E85Q are identical to those of Ca2+-free w

96 ion of the buried myristate and structure of Ca2+-free Ncs1 are quite different from those in other N

97 In Ca2+-free Ncs1, the N-terminal arm positions the fatty a

98 extracellular Ca2+ from 2.5 mM to nominally Ca2+ free, or by applying the calcium entry blocker SKF

99 1, whereas a lengthy (30 min) incubation in Ca2+-free physiological saline solution similarly reduce

100 also applied during the 30 min incubation in Ca2+-free physiological saline solution.

101 sensitive to diltiazem, and was abolished in Ca2+-free physiological salt solution, and by pretreatme

102 significantly upon application of AP while a Ca2+-free pipette solution completely abolished the elec

103 In ruptured-patch recording using Ca2+-free pipette solution, Ileak was strongly enhanced,

104 questered inside a hydrophobic cavity of the Ca2+-free protein and becomes solvent-exposed in the Ca2

105 not alter the stability and structure of the Ca2+-free protein.

106 region (residues 2-90) is similar to that of Ca2+-free recoverin, whereas the C-terminal region (resi

107 , Y53, F56, F83, and Y86) resembling that of Ca2+-free recoverin.

108 The difference in [Ca2+]free represents the amount of Ca2+ bound to troponi

109 ere confirmed by analysis of Ca2+-loaded and Ca2+-free rotary shadowed fibrillin molecules.

110 sts and hypotonic stimulation were absent in Ca2+ -free saline and were antagonized by the nonselecti

111 ed an increase in [Ca2+]i in both normal and Ca2+-free saline, in part by liberating Ca2+ from a stor

112 iness did not develop if CtVm was applied in Ca2+-free saline.

113 Neither axon seals in Ca2+-free salines.

114 This barrier does not form in Ca2+-free salines.

115 K 8644 was not affected by superfusion with Ca2+-free solution (with 10 mmol/L EGTA) but was suppres

116 The presence of Ca2+-free solution and block of L-type Ca2+ channels by

117 sed Ca2+ influx, because it was abolished in Ca2+-free solution and hypoxia was shown to significantl

118 combination of thapsigargin and ionomycin in Ca2+-free solution and the Ca2+ influx component that oc

119 ter excision or immediately upon exposure to Ca2+-free solution and were not reactivated upon reappli

120 Focal receptor stimulation in Ca2+-free solution by pressure application of agonist-co

121 cells or cells fixed with glutaraldehyde in Ca2+-free solution did not calcify under the same condit

122 Bathing slices in Ca2+-free solution markedly reduced the 5-HT-mediated in

123 he extracellular solution was changed into a Ca2+-free solution that also contained Mg2+ (4 mM) and C

124 IPA treated with thapsigargin (1 microM) in Ca2+-free solution to deplete Ca2+ stores showed sustain

125 th repetitive local activation of release in Ca2+-free solution was markedly slower than that elicite

126 Contractions induced by microcystin in Ca2+-free solution were associated with increased phosph

127 ief applications of ionomycin (25 microM) in Ca2+-free solution were used to release stored Ca2+, rya

128 ic acid (5 micromol/L) in Ca2+-containing or Ca2+-free solution, a significant increase in pulmonary

129 contrast, the [Ca2+]i response, measured in Ca2+-free solution, and inositol triphosphate generation

130 This was prevented in Ca2+-free solution, implying that it was due to Ca2+ ent

131 by the fast Na+ channel blocker TTX or in a Ca2+-free solution, indicating a direct postsynaptic act

132 oxia produced a transient rise in [Ca2+]i in Ca2+-free solution, indicating Ca2+ release from the int

133 Upon addition of MgATP in Ca2+-free solution, recombinant LC17 exchange induced sl

134 transient contraction in Ca2+-containing or Ca2+-free solution, respectively (n=44 vessels from 11 a

135 In Ca2+-free solution, store refilling was similarly depres

136 ned phase of the Ca2+ increase was absent in Ca2+-free solution, suggesting that Ca2+ influx was resp

137 measured with a caffeine pulse in Na+-free/ Ca2+-free solution.

138 activity that was not lost with exposure to Ca2+-free solution.

139 29 +/- 2 mV, which shifted to +7 +/- 5 mV in Ca2+-free solution.

140 from the SR was induced with carbachol in a Ca2+-free solution.

141 er than controls and prolonged incubation in Ca2+ -free solutions did not deplete Ca2+ stores, demons

142 ycin (5 microM) elevated cytosolic [Ca2+] in Ca2+-free solutions even after prior Ni2+ application, i

143 Neither applying Cl-- or Ca2+-free solutions nor increasing intracellular Ca2+ bu

144 we have developed in vitro procedures using Ca2+-free solutions of polyethylene glycol (PEG solution

145 Superfusion of myocytes at 37 degrees C with Ca2+-free solutions with both reduced [Na+] and raised [

146 to acute hypoxia was completely abolished in Ca2+-free solutions.

147 ns, but approximately 10-fold more slowly in Ca2+-free solutions.

148 al Ca2+, and approximately 60% of control in Ca2+-free solutions.

149 Ca2+o but returned to near control levels in Ca2+-free solutions.

150 bilize negatively charged tropomyosin in the Ca2+-free state regardless of Ca2+ levels, an alteration

151 In the Ca2+-free state, the myristoyl group is sequestered in a

152 oyl group less favorable and destabilize the Ca2+-free state.

153 This entrapment did not occur in Ca2+ -free SW (CFSW).

154 ere then transferred to silicone oil, where [Ca2+]free, tension, and sarcomere length were monitored

155 NARE complexes are disrupted in response to [Ca2+]free that trigger maximal fusion.

156 rimental conditions, including low and high [Ca2+]free, the same level of Rho* phosphorylation was me

157 f [Ca2+]i rise following a rapid switch from Ca2+-free to physiological [Ca2+] solution.

158 eries from 208 +/- 10 micron (fully dilated, Ca2+ free) to 116 +/- 7 micron or by 45 % ('myogenic ton

159 Ca2+-free troponin is thought to trap tropomyosin in the

160 The response to hypoxia is abolished with Ca2+-free tyrode buffer containing 10 mM EGTA.

161 aM increases the Kd for the complex from the Ca2+-free value of 2.3 +/- 0.1 microM to a value of 14.4

162 a-ENaC that did not occur when the internal [Ca2+]free was buffered to <10 nM.

163 Ca2+-free myr-E85Q are identical to those of Ca2+-free wild type, indicating that the E85Q mutation d