ライフサイエンスコーパス: external solution

1 s channel connecting the binding site to the external solution.

2 channel when 1 mm Ca(2+) was present in the external solution.

3 between these sites, to the heme and to the external solution.

4 ation and accelerates Mg2+(o) unblock to the external solution.

5 fter removing glutamate and glycine from the external solution.

6 locations that are relatively exposed to the external solution.

7 t a holding potential of -60 mV in high K(+) external solution.

8 ure, cisternae communicate with salts in the external solution.

9 till be triggered by TLC-S in a calcium-free external solution.

10 its depletion from, and accumulation in, the external solution.

11 A entrapped and the opposite molecule in the external solution.

12 posed to thapsigargin/ionomycin in Ca2+-free external solution.

13 re to thapsigargin/ionomycin in calcium-free external solution.

14 se cells even with 10 mM Ca2+ or Ba2+ in the external solution.

15 ocated at the cell edge, even in Ca(2+)-free external solution.

16 within the protein in excess of that in the external solution.

17 Ca) and STIC tau was not altered in Cl--free external solution.

18 hing of the neurons with nominally Pb2+-free external solution.

19 where little current was evident in control external solution.

20 filling solution inside a nanopipet and the external solution.

21 n ion into the pipet and its egress into the external solution.

22 2 raises vestibular tonicity relative to the external solution.

23 ntaminating glutamate measured in our normal external solutions.

24 ) was compared in various calcium-containing external solutions.

25 ric field" of Kv1.2 between the internal and external solutions.

26 nward Ca2+ current, but without changing the external solution, a mutation, E736K, was introduced int

27 Nominally Ca(2+)-free external solution abolished the SP response.

28 ne of two micropipets ("generator") into the external solution and collected at the second pipet ("co

29 an accept a H(+) and transfer it between the external solution and the central Cl(-) binding site, co

30 m (2 mM Cao2+) or high calcium (10 mM Cao2+) external solutions, application of CCCP (1-2 microM) evo

31 with an oocyte protein whose exposure to the external solution changes during channel gating and whic

32 e of the response was nearly the same in the external solution containing a low Ca2+ concentration; h

33 using standard K+-rich pipette solution and external solutions containing 11.1 mM glucose.

34 In external solutions containing CH(3)SO(3)(-) or gluconate

35 ly significant difference among calcium-free external solutions containing different impermeant anion

36 d hH1 channels inactivated completely if the external solution did not contain sodium ions.

37 ange negatively, whilst acidification of the external solution had the opposite effect.

38 usion of 1 mM BAPTA in nominally Ca(2+)-free external solution, Icat could still be evoked by noradre

39 Nominally calcium-free external solution immediately and reversibly abolished a

40 All three sites are accessible to the external solution in channels with a closed activation g

41 Their exposure to external solution in the TM state indicates that helices

42 reversible in divalent cation-free (0 Ba2+) external solutions in which current was carried by MA+.

43 minobenzoates was modulated by the pH of the external solution; increasing the pH from 7.4 to 10.0 gr

44 Unblock to the external solution is prevented if external permeant ions

45 als, water and protons from the internal and external solutions must be separated by a narrow barrier

46 In external solutions of high osmolarity, release events fo

47 Epidermal peels were subjected to external solutions of varying osmotic potential to shrin

48 ased when Ca2+ was replaced with Ba2+ in the external solution or 5 mM BAPTA was added to the pipette

49 pied and then can either unblock back to the external solution or permeate the channel.

50 3 internalization was blocked in Ca(2+)-free external solution, or by strong buffering of internal Ca

51 Moreover, upon switching to divalent free external solutions, Orai3 currents were considerably mor

52 In response to a sudden change in external solution osmolality from 300 to 600 mOsm, the v

53 Hyposmolar external solutions (osmolarity reduced by 10% to 267 mos

54 a nanowire network/agarose gel sample during external solution pH changes, and (ii) characterizing th

55 e etched electrode was immersed in a dry (no external solution) pool of mercury to produce a TLC.

56 ed by a voltage step, rapid acidification of external solution produced an inward H+ current which ra

57 Hyposmolar external solutions produced a significant reduction in t

58 t remained after washing of the neurons with external solution suggested that Pb2+ acted via an intra

59 In normal NaCl-containing external solution the decay of spontaneous Ca2+-activate

60 When Cl- was the major anion in the external solution, the OFF Idelta was mostly cancelled b

61 In 2 mmol/l calcium external solution, the threshold of voltage-dependent ac

62 urrents were recorded while manipulating the external solution to alter either the total or free prot

63 In divalent cation-free external solution two additional currents were activated

64 p mode with quasi-physiological internal and external solutions, voltage steps from the holding poten

65 hanged when the concentration of Ca2+ in the external solution was decreased from 2 mM to 0.2 mM.

66 The pH of the weakly buffered external solution was recorded during sequential treatme

67 r exposure of the neurons to Pb2+-containing external solution, was not related to changes in Na+-cha

68 With 2 mmol/L Ca2+ in the external solution, we observed sparks at the beginning o

69 sed by exposing the ATPS GVs to a hypertonic external solution, which draws water out of the vesicles