ライフサイエンスコーパス: non-excitable

1 iverse levels of MaxiK channel expression in non-excitable and excitable cells.

2 itive detection of Ca(2+) transients in both non-excitable and excitable cells.

3 cells reported in the literature, which are non-excitable and rely heavily on aerobic glycolysis.

4 ge-gated channel activity in the canonically non-excitable astrocytes are not known.

5 tion potentials at the interface between two non-excitable bioelectric tissues.

6 o-triazole (CAI) is a synthetic inhibitor of non-excitable calcium channels that reversibly inhibits

7 We model the non-excitable cell bioelectrical representation of the e

8 transcript in rabbit kidney, as well as in a non-excitable cell line, LLC-RK1, derived from rabbit ki

9 Ca2+ signalling in the rat megakaryocyte, a non-excitable cell type in which membrane potential can

10 ns was investigated in rat megakaryocytes, a non-excitable cell type recently shown to exhibit depola

11 acellular stores in the rat megakaryocyte, a non-excitable cell type.

12 ment model to simulate calcium transients in non-excitable cells (consisting of a plasma membrane Ca2

13 Y to maintain high input resistance in these non-excitable cells also requires the K(+) channel subun

14 is the predominant Ca(2+) influx pathway in non-excitable cells and is activated in response to depl

15 ium channel Orai regulates Ca(2+) entry into non-excitable cells and is required for proper immune fu

16 1, 4, 5-triphosphate receptor (InsP(3)R) in non-excitable cells and ryanodine receptor (RyR) in exci

17 letal muscle with Ca(2+) entry mechanisms in non-excitable cells are also reviewed.

18 Agonist-activated Ca(2+) signals in non-excitable cells are profoundly influenced by calcium

19 emporal patterns of resting potentials among non-excitable cells as instructive cues in embryogenesis

20 lar Ca2+ stores and mediate Ca2+ influx into non-excitable cells at resting membrane potential.

21 calcium-release-activated current (ICRAC) in non-excitable cells but at present there is little infor

22 In many non-excitable cells Ca2+ influx is mainly controlled by

23 y voltage-regulated Ca2+ channels whereas in non-excitable cells Ca2+ influx is mediated by store-ope

24 to surrounding myocytes, suggesting that the non-excitable cells in the scar closely follow myocyte a

25 AC channel function and SOCE in a variety of non-excitable cells including lymphocytes and other immu

26 was to determine the mechanism through which non-excitable cells influence the spontaneous activity o

27 Receptor-enhanced entry of Ca2+ in non-excitable cells is generally ascribed to a capacitat

28 esults suggest that electrically integrated, non-excitable cells modulate the excitability of cardiac

29 n triggering CICR, and indicate that CICR in non-excitable cells resembles CICR in cardiac myocytes w

30 In non-excitable cells stromal interaction molecule 1 (STIM

31 They also are expressed in non-excitable cells such as macrophages and neoplastic c

32 introduce and analyse a simple model for two non-excitable cells that are dynamically coupled by a ga

33 e adaptation of a multicellular aggregate of non-excitable cells to the electrophysiological perturba

34 e field of agonist-activated Ca(2+) entry in non-excitable cells underwent a revolution some 5 years

35 of such coupling between cardiomyocytes and non-excitable cells when, for example, pathological elec

36 between resting V(mem) and the physiology of non-excitable cells with implications in diverse areas,

37 In non-excitable cells, agonist-induced depletion of intrac

38 isms can yield [Ca(2+)](Cyt) oscillations in non-excitable cells, and, under certain conditions, the

39 In most non-excitable cells, calcium influx is signaled by deple

40 nce for activation of CICR by Ca2+ influx in non-excitable cells, demonstrate a previously unrecogniz

41 usly expressed in electrically excitable and non-excitable cells, either as alpha-subunit (BKalpha) t

42 In electrically non-excitable cells, for example epithelial cells, this

43 anonical' functions of FHFs in excitable and non-excitable cells, including cancer cells, have been r

44 techniques to follow the activation state of non-excitable cells, including lymphocytes.

45 nositol trisphosphate (IP(3)) stimulation of non-excitable cells, including vascular endothelial cell

46 e generation of Ca2+i signals, especially in non-excitable cells, is store-operated Ca2+ entry (SOCE)

47 In non-excitable cells, KCNQ1 forms a complex with KCNE3, w

48 hysiological functions in both excitable and non-excitable cells, reflected in the massive consequenc

49 he sole Ca2+ entry mechanism in a variety of non-excitable cells, store-operated calcium (SOC) influx

50 f RyRs in Ca(2+) signalling and functions in non-excitable cells, such as T lymphocytes, remains poor

51 e characterization of several other types of non-excitable cells, such as the microglia (brain macrop

52 In non-excitable cells, the initial Ca2+ release is typical

53 In non-excitable cells, the major Ca2+ entry pathway is the

54 In many non-excitable cells, the predominant mode of agonist-act

55 In non-excitable cells, these oscillations generally arise

56 In non-excitable cells, thiol-oxidizing agents have been sh

57 ated Calcium Entry (SOCE) is well studied in non-excitable cells.

58 ed as a novel regulator of cell processes in non-excitable cells.

59 raise intracellular Ca(2+) concentration in non-excitable cells.

60 key second messengers in both excitable and non-excitable cells.

61 tivation of discrete downstream responses in non-excitable cells.

62 physiological voltages and calcium levels in non-excitable cells.

63 ch are not physiological conditions for most non-excitable cells.

64 agonist-induced cytosolic Ca(2+) signals in non-excitable cells.

65 ir relation to SOC channels in excitable and non-excitable cells.

66 plays a critical role in Ca2+ signalling in non-excitable cells.

67 pathway responsible for diverse functions in non-excitable cells.

68 llular communication in astrocytes and other non-excitable cells.

69 posed to encode SOCCs responsible for CCE in non-excitable cells.

70 chanical forces regulate membrane traffic in non-excitable cells.

71 and cellular function in both excitable and non-excitable cells.

72 ing membrane potential in both excitable and non-excitable cells.

73 any distinct functions in both excitable and non-excitable cells.

74 functions in both electrically excitable and non-excitable cells.

75 niversal mode of signalling in excitable and non-excitable cells.

76 utine quantification of calcium responses in non-excitable cells.

77 volume decrease (RVD) of both excitable and non-excitable cells.

78 ulating intracellular calcium homeostasis in non-excitable cells.

79 PCR signaling to maintain ion homeostasis in non-excitable cells.

80 been unclear, especially for conventionally non-excitable cells.

81 e behaviour if voltage-gated ion channels in non-excitable channels.

82 However, they are also present in non-excitable eukaryotic cells and prokaryotes, which ra

83 Moreover, they are not applicable to use in non-excitable glial cells.

84 Notwithstanding endothelia being non-excitable in nature, the hypothesis of Ca(2+)-induce

85 Here we present evidence that in non-excitable LNCaP prostate cancer cells, BK channels c

86 on can cause spiking at the edge between two non-excitable media.

87 The present study demonstrates CICR in the non-excitable parotid acinar cells, which resembles the

88 Using the non-excitable rat megakaryocyte as a model system, we no

89 2+ entry, a common pathway for Ca2+ entry in non-excitable tissue, is apparent in the syncytiotrophob

90 play fundamental roles in both excitable and non-excitable tissues and therefore constitute attractiv

91 ions has broad implications in excitable and non-excitable tissues.