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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 ulating intracellular calcium homeostasis in non-excitable cells.

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

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

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

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

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

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

66 2+ entry, a common pathway for Ca2+ entry in non-excitable tissue, is apparent in the syncytiotrophob

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